Connective Tissue Proteins Research Articles

Initiation of Medial Calcification: Revisiting Calcium Ion Binding to Elastin.

Pathological calcification of elastin, a key connective tissue protein in the medial layers of blood vessels, starts with the binding of calcium ions. This Mini-Review focuses on understanding how calcium ions interact with elastin to initiate calcification at a molecular level, and emphasizes water's critical role in mediating this interaction. In the past decade, great strides have been made in understanding and modeling ion-specific hydration and its effects on biomolecule interactions. However, these advances have been largely absent from our understanding of elastin calcification. Historically, charge-neutral backbone carbonyls and negatively charged carboxyl groups have been proposed as elastin's calcium binding sites. Recently, tropoelastin's only four carboxyl groups have been identified as binding sites from classical molecular dynamics (MD). While carboxyl groups have a much higher affinity for binding calcium ions than backbone carbonyls, conflicting evidence persists for both functional group's importance in elastin calcification. This can be attributed to the fact that divalent ions strongly polarize water, leading to a hydration shell that shields electrostatic forces. The hydration shell surrounding both a calcium ion and either of the proposed binding sites must be displaced to enable binding. Providing our own extended X-ray absorption fine structure (EXAFS) data and complementary simulations, we discuss the potential structures of calcium binding in elastin and review prior knowledge regarding the relative importance of the two proposed binding sites.

Корекція пробіотиком пародонтального синдрому у тварин за умов ожиріння і хронічного стресу

The aim of this study was to investigate the effect of obesity and chronic stress on periodontal tissues, both separately and in the combined comorbidity of these conditions in rats, and the role of the probiotic Lactobacillus casei in the correction of periodontal syndrome under these conditions. Methods. The development of periodontal syndrome and the effectiveness of the probiotic Lactobacillus casei IMV B-7280, administered to rats from one month of age intragastrically in a volume of 1 mL (5 · 108 CFU) in two-week courses with breaks of 2 weeks, were studied in a model of glutamate-induced obesity and chronic stress - in combination and separately. In periodontal tissues, the total proteolytic and antitryptic activity, free fucose and glycosaminoglycans (GAG) content, catalase activity, thiobarbiturate active products (TBA reagents), and the content of oxidatively modified proteins (OMP) and molecules of average mass (AMM) were determined; in bone tissue, the molar root exposure coefficient was calculated. The anthropometric parameters of the animals and the Selye triad were studied. Results. We have substantiated the development of periodontal syndrome in animals with glutamate-induced obesity against the background of chronic stress, as evidenced by the activation of free radical oxidation of lipids and proteins, depolymerization of fucoproteins and proteoglycans of periodontal connective tissue, which causes exposure of molar roots by almost 65%. The administration of the probiotic Lactobacillus casei in two-week courses with intervals of 2 weeks to obese rats with chronic stress prevented the development of obesity, as evidenced by a significant decrease in visceral fat mass, Li index, and BMI, as well as the severity of stress syndrome, as evidenced by a decrease in ulcer formation, thymus involution, and adrenal hypertrophy. The periodontoprotective effect of Lactobacillus casei under the combined influence of obesity and chronic stress was proved by significant changes in oxidative stress, free fucose, and GAG content and a 1.5-times decrease in the molar root exposure ratio. Conclusions. Periodic administration of Lactobacillus casei to rats treated with sodium glutamate in the neonatal period against the background of chronic stress prevented the development of obesity, the severity of stress syndromeб and damage to periodontal tissues, as evidenced by the prevention of oxidative stress, increased catabolism of extracellular connective tissue proteins and antiresorptive effect.

Delayed Wound Healing in a Young Patient with TNXB Variants and the Role of WES

After decades of quality improvement efforts, surgical site infections and abnormal wound healing remain intermittent complications in surgery. In both cases, the complication and abnormality may be superficial, restricted to the skin, or deeper within the tissue. The synthesis of connective tissue proteins, critical for structural support as part of the extracellular matrix, is under the control of multiple genes, forming a complex adaptive network. We report an unusual case of delayed and abnormal wound healing with chronic infection in a 16-year-old patient following surgery for scoliosis. Skin patch test showed that he is allergic to cobalt, a component of fixation hardware used in his surgery. He underwent evaluation by clinical genetics with whole exome sequencing (WES) which showed two (maternally and paternally inherited) variants in the TNXB ( Tenasin XB) gene. These two variants are variants of uncertain significance (VUS). TNXB encodes tenascin-XB which is an extracellular matrix glycoprotein located primarily in the basement membrane. Autosomal recessive pathogenic and likely pathogenic variants in TNXB cause TNXB-related classical-like Ehlers-Danlos Syndrome. At present, there are no causal linkages of these VUSs in TNXB to abnormal wound healing. However, as WES becomes more affordable, its use will increase and therefore it is important that we start to document such associations.

Collagen Peptide Supplementation during Training Does Not Further Increase Connective Tissue Protein Synthesis Rates.

Protein supplementation increases post-exercise muscle protein synthesis rates and, as such, supports exercise-induced muscle conditioning. Collagen protein has been suggested as the preferred protein source to stimulate muscle connective protein synthesis rates during recovery from exercise. Here we assessed the effects of hydrolyzed collagen peptide supplementation on both myofibrillar as well as muscle connective protein synthesis rates during one week of strenuous resistance exercise training. In a randomized, double-blind, parallel design, 25 young men (24 ± 3 y, 76.9 ± 6.4 kg) were selected to perform one week of intense resistance-type exercise training. Subjects were randomly assigned into two groups receiving either 15 g hydrolyzed collagen peptides (COL) or a non-caloric placebo (PLA) twice daily during the intervention. Subjects were administered deuterated water (2H2O) daily, with blood and skeletal muscle tissue samples being collected prior to and after the intervention to determine daily myofibrillar and muscle connective protein synthesis rates. Post-absorptive plasma glycine, proline, and hydroxyproline concentrations increased following collagen peptide supplementation (p < 0.05) and showed higher levels when compared to the placebo group (p < 0.05). Daily muscle connective protein synthesis rates during the intervention period exceeded myofibrillar protein synthesis rates (1.99 ± 0.38 versus 1.34 ± 0.23 %/d, respectively; p < 0.001). Collagen peptide supplementation did not result in higher myofibrillar or muscle connective protein synthesis rates (1.34 ± 0.19 and 1.97 ± 0.47 %/d, respectively) when compared to the placebo group (1.34 ± 0.27 and 2.00 ± 0.27 %/d, respectively; p > 0.05). Collagen peptide supplementation (2 x 15 g daily) does not increase myofibrillar or muscle connective protein synthesis rates during one week of intense resistance exercise training in young, recreational athletes.

MicroRNAs in abdominal aortic aneurysms

The abdominal aortic aneurysm (AAA), representing 70% to 90% of all aortic aneurysms, is characterized by a widening of the diameter due to an irreversible weakening of the vascular walls. Risk factors include advanced age, male sex, smoking, hypertension, atherosclerosis, and genetic predisposition. From a pathophysiological point of view, AAA involves alterations in connective tissue proteins, chronic inflammation with the release of cytokines and matrix metalloproteinases, as well as changes in the extracellular matrix. MicroRNAs (miRNAs) have emerged as promising biomarkers and therapeutic targets in the regulation of gene expression and different specific signaling pathways in vascular pathologies. Among which some miRNAs have been highlighted such as: miR-29 and miR-27b-3p, involved in the degradation of the extracellular matrix and inflammatory processes during the progression of AAA. Some diagnostic methods such as computed tomography play a fundamental role, while some innovative therapeutic strategies, such as the inhibition of miRNAs, represent a leading role as possible diagnostic and therapeutic targets. A comprehensive approach includes surveillance and surgical treatment strategies to mitigate the progression and risk of AAA rupture, thus highlighting the relevance of miRNAs in the diagnosis and treatment of this pathology.

Polymorphism in the matrix metallopeptidase genes is associated with coronary artery disease risk with concomitant metabolic syndrome

Background: Metabolic syndrome (MS) and its components are the reasons of the development and progression of cardiovascular diseases. Nowadays, the association between coronary artery disease and MS remains ambiguous. The central role of matrix metallopeptidases (MMP) in the metabolism of connective tissue proteins, cell matrix remodeling, tissue repair and other complex biochemical processes has been shown, which implies their involvement in the pathogenesis of cardiovascular diseases. The aim of the study: To study the associations of polymorphic variants in the MMP genes with the risk of stable coronary artery disease with concomitant metabolic syndrome. Materials and methods: 170 patients with stable coronary artery disease concomitant with a visceral type of obesity in combination with two or more pathological conditions (elevated serum blood glucose level, elevated serum blood cholesterol level, hypertension) were included in the case group. Conditionally healthy volunteers (n=182) were recruited in the control group. Genotyping of five polymorphic sites in the four genes MMP1 (rs514921), MMP3 (rs6796620 and rs626750), MMP9 (rs17576) and TIMP2 (rs2277698) was performed by real-time PCR. The serum blood level of MMP was measured by ELISA. Gene-gene interactions were analyzed using MDR v.3.0.2 software. Results: The frequency of heterozygous C/T genotype in the MMP3 gene (rs626750) was higher in the control group (37.90%) compared to the case group (23.20%), which indicates its protective effect on the risk of coronary artery disease with concomitant metabolic syndrome (OR=0.47, 95%CI 0.29-0.75). 2.6-fold increased risk of coronary artery disease with concomitant metabolic syndrome was demonstrated for carriers of the A/G genotype in the TIMP2 gene (rs2277698) according to the codominant inheritance model. We found no associations of polymorphic variants in the MMP1 (rs514921), MMP3 (rs626750), MMP9 (rs17576) and TIMP2 (rs2277698) genes with the serum blood level of MMP, as well as their inhibitors. Four-loci model of gene-gene interactions (MMP9 (rs17576) – MMP3 (rs626750) – MMP1 (rs514921) – TIMP2 (rs2277698)) characterized by high sensitivity, specificity and risk effect to the coronary artery disease with concomitant metabolic syndrome development was discovered. Conclusion: This study revealed the association of polymorphic variants in the MMP genes and their inhibitors with the risk of coronary artery disease with concomitant metabolic syndrome. In addition, a four-locus model of intergenic interactions with high sensitivity and specificity was obtained.

Investigation of the Presence of Fibrillin in Sea Cucumber (Apostichopus japonicus) Body Wall by Utilizing Targeted Proteomics and Visualization Strategies.

Fibrillin is an important structural protein in connective tissues. The presence of fibrillin in sea cucumber Apostichopus japonicus is still poorly understood, which limits our understanding of the role of fibrillin in the A. japonicus microstructure. The aim of this study was to clarify the presence of fibrillin in the sea cucumber A. japonicus body wall. Herein, the presence of fibrillin in sea cucumber A. japonicus was investigated by utilizing targeted proteomics and visualization strategies. The contents of three different isoforms of fibrillin with high abundance in A. japonicus were determined to be 0.96, 2.54, and 0.15 μg/g (wet base), respectively. The amino acid sequence of fibrillin (GeneBank number: PIK56741.1) that started at position 631 and ended at position 921 was selected for cloning and expressing antigen. An anti-A. japonicus fibrillin antibody with a titer greater than 1:64 000 was successfully obtained. It was observed that the distribution of fibrillin in the A. japonicus body wall was scattered and dispersed in the form of fibril bundles at the microscale. It further observed that fibrillin was present near collagen fibrils and some entangled outside the collagen fibrils at the nanoscale. Moreover, the stoichiometry of the most dominant collagen and fibrillin molecules in A. japonicus was determined to be approximately 250:1. These results contribute to an understanding of the role of fibrillin in the sea cucumber microstructure.

Marfan Syndrome with Atypical Pneumonia: A Case Report

Marfan syndrome (MFS) is an autosomal dominant systemic disorder of the connective tissue. Children impacted by the MFS carry the mutation in one of their two alleles of the gene that codes the connective tissue protein fibrillin-1 (FBN-1). MFS influences their effects upon most organs and tissues, in particular the skeleton, lungs, eyes, heart, and the large blood vessel that distributes blood from the heart to the reminder of the physique. A case report of MFS with atypical pneumonia has been reported with positive Steinberg sign, thumb sign and wrist sign. Existence of long legs with the positive Walker Murdoch sign. There were no complications such as an aortic aneurysm, ocular lens luxation, or mitral valve prolapse were remarked. Since the patient was lacking such complications based on MFS, he was treated only for atypical pneumonia. Keywords: Marfan Syndrome, Fibrillin-1, Thoracic Aortic Aneurysm or Dissection, Ectopia Lentis

Rehabilitation for Marfan Syndrome

Abstract: Marfan syndrome is a spectrum of disorders caused by a heritable genetic defect of connective tissue that has an autosomal dominant mode of transmission. The defect itself has been isolated to the FBN1 gene on chromosome 15, which codes for the connective tissue protein fibrillin. Abnormalities in this protein cause a myriad of distinct clinical problems, of which the musculoskeletal, cardiac, and ocular system problems predominate. The skeleton of patients with Marfan syndrome typically displays multiple deformities. Mitral valve prolapses that requires valve replacement can occur as well. Given the variable expressivity of Marfan Syndrome, no single sign is pathognomonic; the diagnosis is made on clinical grounds on the basis of typical abnormalities. We reported a boy, 12 years old, referred from surgeon with diagnosis pectus carinatum pro brace. Chest protusion appeared since age 6, getting bigger without any complaint but cosmetic. Other complaints on feet which looked flat, sometimes ankle sore after long distance running or futsal. He was the first child and no family history had a condition like him. His hobby was playing futsal, and daily activities were independent without assistive devices. General appearance and vital signs were normal, cardiorespiratory assessment was normal, BMI on percentile 10-25, arm span to height ratio 1.09, lens subluxation of left eye, lens dislocation of right eye, poor standing balance, inadequate toe off, thoracic hyperkyphotic, positive wrist sign, true leg length discrepancy of 1 cm (left&gt;right), bilateral ankle ROM limitation, rigid flat feet suspected bilateral vertical talus, left hallux valgus, Marfan syndrome score 9, and normal echocardiography. In this patient, we gave semi rigid thoraco-lumbo-sacral orthosis (TLSO) with 3 points pressure system and rigid bar on protution area (custom molded). resistance exercise (F: 3x/week, I: moderate fatigue, Borg scale 13-15/20, T: 8-15 reps/ set, 2-3 set/ session, T: major muscle group upper and lower extremities aerobic exercise (F: 3x/week, I: moderate to vigorous, borg scale 13-15/20, T: ≥60 min/session, @5-10 min warming up and cooling down (stretching), T: sport (swimming, running, cycling). The patient was referred to a surgeon for a brace. In conclusion, this case report highlights the multidisciplinary management of patients with Marfan syndrome. Keywords: Marfan syndrome; typical abnormalities; multiple deformities

Bioactive potential of Bio-C Temp demonstrated by systemic mineralization markers and immunoexpression of bone proteins in the rat connective tissue

Intracanal medications are used in endodontic treatment due to their antibacterial activity and ability to induce the periapical repair. Among the intracanal medications, the Calen (CAL; SS. White, Brazil) is a calcium hydroxide-based medication that provides an alkaline pH and releases calcium, exerting an antimicrobial activity. Bio-C Temp (BIO; Angelus, Brazil), a ready-to-use bioceramic intracanal medication, was designed to stimulate the mineralized tissues formation. Here, we investigated the bioactive potential of BIO in comparison to the CAL in the rat subcutaneous. Polyethylene tubes filled with medications, and empty tubes (control group, CG) were implanted in the subcutaneous tissue of rats. After 7, 15, 30 and 60 days, the blood was collected for calcium (Ca+2) and alkaline phosphatase (ALP) measurement, and the capsules around the implants were processed for morphological analyses. The data were submitted to two-way ANOVA and Tukey test (p < 0.05). At 7, 15 and 30 days, the ALP level was grater in BIO and CAL than in CG (p < 0.0001). At 7 and 15 days, greater Ca+2 level was seen in the serum of CAL samples. From 7 to 60 days, an increase in the number of fibroblasts, osteocalcin- and osteopontin-immunolabelled cells was observed in BIO and CAL groups (p < 0.0001). In all periods, BIO and CAL specimens showed von Kossa-positive structures. Moreover, ultrastructural analysis revealed globules of mineralization in the capsules around the BIO and CAL specimens. Thus Bio-C Temp caused an increase in the ALP, osteocalcin and osteopontin, which may have allowed the formation of calcite, suggesting bioactive potential.Graphical

An update review: several extraction methods for collagen isolation in vertebrate fish

Fish are vertebrate animals with a backbone that live in marine environments, presenting a potential source of collagen due to their high protein content. Collagen is a structural protein in the body's connective tissue, contributing 25 to 30% of the total body protein. Collagen sources in fish can be found in the skin, scales, and bones. The isolation of collagen from fish involves several stages, including separation and cleaning, size reduction, removal of non-collagenous components, collagen extraction, and precipitation. The extraction method utilized in collagen isolation impacts the quantity of collagen produced. The aim of this literature review is to identify extraction methods applicable for collagen isolation in vertebrate fish, serving as a reference for selecting extraction methods in future research. The updated review method involved collecting journal data from various literature sources, obtained from national and international journals discussing collagen extraction methods in vertebrate fish. Based on the update review, the isolation of collagen from vertebrate fish is carried out using several extraction methods, including acid soluble collagen extraction, pepsin soluble collagen, water soluble collagen, organic acid ultrasound-assisted, extrusion hydro extraction, deep eutectic solvent, and supercritical fluid extraction.

Investigating the impact of sous vide cooking on the eating quality of spent buffalo (BUBALUS BUBALIS) meat

This study describes the impact of sous vide cooking at different temperatures and time intervals on the eating quality, specifically tenderness of two muscles, bicep femoris (BF) and semitendinosus (ST) from spent buffalo (Bubalus bubalis). Spent buffalo refers to water buffalo that are no longer considered productive following a sixth lactation cycle. Steaks from each muscle were obtained and cooked at three combinations of time and temperature, namely 55 °C-8H, 65 °C-5H, and 95 °C-45 M, respectively. Warner-Bratzler Shear Force (WBSF), cooking loss, cooking yield, color, water activity (aw), total water content (TWC), total collagen content (TCC), heat soluble collagen (HSC), myofibrillar fragmentation index (MFI), and sensory evaluation were measured. The collagen solubilization results showed that temperature and time interacted (P ≤ 0.05), reducing the toughness of the muscles. The tenderization achieved through sous vide cooking was mainly attributed to the thermal denaturation of proteins at the typically lower temperatures and extended time used, weakening of connective tissue through collagen solubilization, and water retention. More cooking loss (P ≤ 0.05) was observed at high temperature treatment of 95 °C-45 M. Meat color, TWC, MFI, and overall acceptability exhibited differences among treatments (P ≤ 0.05). An extended heat interval at lower temperatures caused initial denaturation of myofibrillar proteins, then solubilization of connective tissue proteins. Cooking treatment 55 °C-8H (P ≤ 0.05) reduced the WBSF in both muscles; however, the ST appeared more tender than BF.

Matrix metalloproteinases system profile analysis and their endogenous inhibitors in children with periodontal diseases and various dysplasia phenotypes

Relevance. The search and development of modern non-invasive methods for early periodontal disease detection are of scientific and practical value for a personalized approach to disease course prognosis and explaining the choice of treatment tactics. Morphological immaturity, high intensity of anabolic processes, functional failure of neurohumoral, endocrine and immunological defence systems combined with an imbalance between the synthesis and degradation of extracellular matrix components in children with undifferentiated connective tissue disease (UCTD) significantly increases the risk of developing periodontal diseases. The available data on the activity of salivary matrix metalloproteinases (MMPs), which play a leading role in regulating connective tissue protein metabolism and bone remodelling mechanisms in children with UCTD of various degrees, are scarce and require further study.Purpose. The study aimed to explain the clinical, diagnostic and prognostic value of MMPs as markers of inflammatory periodontal diseases in children with UC TD and dysplastic disorders of various se verity.Material and methods. The study included 67 children with UCTD (main group) and 34 children of health groups I and II (comparison group) aged 12-17. The UCTD severity was established according to the diagnostic criteria by L. N. Abbakumova (2006) and a scale for assessing the significance of phenotypic and visceral signs. The main group was divided into two subgroups: Subgroup 1 (n = 38) – children with mild and moderate UCTD; Subgroup 2 (n=29) – children with severe UCTD. The studied groups had their periodontal status assessed, as well as the concentration of MMP-1, MMP-2, MMP-8, MMP-9 and their tissue inhibitors (TIMP-1, TIMP-2) in the oral fluid identified using the enzyme immunoassay, along with calculation done for the MMP ⁄ TIMP coefficients that set a balance between the degradation and synthesis of collagen.Results. The children with phenotypic signs of UCTD in the oral fluid appeared to show a statistically significant increase in the MMP-1, MMP-2, MMP-8, and MMP-9 levels and an imbalanced ratio in MMP-1⁄TIMP-1, MMP- 2⁄TIMP-2, MMP-8⁄TIMP-1, MMP-9⁄TIMP-1, compared with health groups I, II. An increase in the MMP-1, MMP-2, and MMP-8 concentrations, along with dominating expression of MMP-9 over TIMP-1 in the oral fluid of children of Subgroup 2, causes an increase in intensity and prevalence of periodontal diseases compared to the patients in Sub-group 1 and comparison group.Conclusion. Thus, when children with UCTD don’t demonstrate an increase in specific tissue inhibitors TIMP-1 and TIMP-2 in their oral fluid, along with an increase in the levels of the respective matrixins is the key pathogenetic factor in the degradation of extracellular matrix proteins, which causes a depressing impact on the proliferative activity in the periodontal set of tissues.

A novel view to varicose veins pathogenesis: Proteomic profiling suggests a pivotal role of extracellular matrix degradation.

Although morphological and anatomical studies indicate that venous wall weakening and subendothelial fibrosis characterize varicose veins (VV), the pathogenesis of VV remains poorly understood. The aim of this study is to obtain protein expression profiles in patients with VV and thereby get a step closer to understanding the pathogenesis of VV. Specimens were obtained from total of 10 patients, that is, from 5 patients undergoing VV surgical stripping and from 5 non-VV patients undergoing bypass surgery. Specimens were collected from the same layers of venous wall. Proteins were extracted from each specimen and analyzed by ion mobility spectrometry (IMS-MS). In total, 1387 were identified and 486 proteins were identified in all samples. From these, 15 proteins were differentially expressed between VV and non-VV samples (p < .05) and 12 of these showed a fold change >1.5. Interestingly, among the differentially expressed proteins, only two proteins were significantly increased in the VV tissue, that is, GAPDH (p = .028, fold change 2.74), where several proteins involved in maintaining the homeostasis in the extracellular matrix, that is, the CXXC zinc finger protein 5 (CXXC5) and nucleoporin (SEH1) were prominently downregulated (p = .049, fold change 37.8, and p = .040, fold change 3.46). The downregulation in protein expression of CXXC5 and SEH1 as well as upregulation of GAPDH were validated by Western blotting. The identified differentially expressed proteins suggest an altered profile of the connective tissue proteins as well as an increased proteolytic enzyme activity which both may be central in the pathophysiology of varicose veins.

Analysis of differential expression of genes of structural and regulatory proteins of connective tissue as factors associated with the vaginal prolapse

The article presents data on the differential expression of genes of structural and regulatory proteins of connective tissue (COLIA1, fibronectin, elastin, TGF-β1, LOX) in women with pelvic organ prolapse and stigmas of undifferentiated connective tissue dysplasia (UCTD) compared to patients with prolapse but without UCTD stigmas.&#x0D; Research objectives: analysis of the prognostic significance of differential expression of structural and regulatory genes of connective tissue proteins COLIA1, fibronectin, elastin, TGF-β1, LOX as factors associated with the vaginal prolapse among Ukrainian women.&#x0D; Materials and methods. Vaginal tissue samples were taken from 18 patients at the menopausal age with vaginal prolapse III, IV degree, which required surgical correction during vaginal hysterectomy and/or plastic surgery of vaginal walls. The main group included 11 patients with clinical and anamnestic UCTD stigmas, the comparison group included 7 women without it. Gene expression analysis of structural and regulatory proteins of the extracellular matrix of connective tissue was performed using real-time quantitative polymerase chain reaction. The relative number of transcripts of the studied genes was normalized by the expression level of the GAPDH gene. The data were calculated using the 2–ΔΔCt method.&#x0D; Results. There was decrease in gene expression of the main structural proteins of the extracellular matrix of the connective tissue: COLIA1 (t=-1.7; p=0.044), fibronectin (t=1.66; p=0.047), elastin (t=-1.75, p=0,04), gene of the regulatory protein LOX (t=-1.8, p=0.035) and no statistically significant difference in the TGF-β1 gene in patients with pelvic organ prolapse and clinical and anamnestic UCTD stigmas.&#x0D; Conclusions. Statistically significant lower expression of the genes of the main structural proteins of the extracellular matrix of the connective tissue and the gene of the regulatory protein LOX in patients with pelvic organ prolapse and clinical and anamnestic UCTD stigmas is evidence of the importance of genetically determined pathological remodeling of the connective tissue in the etiology of genital prolapse.

Effects of Wooden Breast Syndrome in Broiler Chicken on Sarcoplasmic, Myofibrillar, and Connective Tissue Proteins and Their Association with Muscle Fiber Area.

This study was conducted on chicken pectoralis major muscle with different wooden breast severity in combination with different sampling locations to investigate the effects of wooden breast syndrome on protein traits and total myofiber area, and their associations. Contents of sarcoplasmic, salt-soluble myofibrillar and salt-insoluble protein and proportion of total myofiber area significantly declined with increasing severity in the superficial part of muscle, whereas the amount of heat-soluble/insoluble collagen and protein denaturation as well as the area of degenerated myofibers, connective tissue and cellular infiltrates increased. Myofibril protein content indicators showed strong positive correlations to total myofiber area. Moreover, PCA results indicated that severe wooden breast is positively linked to muscle collagen content and to protein denaturation. Our results suggest that decrease in sarcoplasmic and myofibrillar proteins is associated with reduction of myofiber area. In turn, the muscle fibers are replaced by connective tissue, accompanied by excessive myofibrillar and sarcoplasmic protein denaturation.

Skin aging-cellular senescence : What is the future?

Cellular senescence is the main cause of skin and organ aging and is associated with awide range of aging-related diseases. To understand which senolytics, senomorphics, and cell-based therapies have been developed to alleviate and even rejuvenate skin aging and reduce cellular senescence. Basic literature for the mode of action of senolytics and senomorphics and their clinical perspectives in daily routine are discussed. Various causes lead to mitochondrial dysfunction and the activation of pro-aging signaling pathways, which eventually lead to cellular senescence with degradation of structural proteins of the dermal connective tissue and severe suppression of regenerative stem cell niches of the skin. Depletion of senescent cells suppress skin aging and enforce rejuvenation of skin and other organs and their function. The removal of senescent cells by cells of the native immune system is severely disturbed during aging. Selected senolytics and senomorphics are approved and are already on the market.

Copper Content in Lumbar Vertebrae across Age Groups

Copper, an essential trace element in bone tissue, plays a crucial role in the active centers of vital enzymes. It is involved in the synthesis of key connective tissue proteins like collagen and elastin, which form the structural matrix of bones and cartilage. This research aims to investigate the copper content in human lumbar vertebrae and explore how it changes with age, with a particular focus on gender differences. The study involved the analysis of the third lumbar vertebrae from 211 individuals spanning ages 0 to 90 years. Copper content was determined using an atomic absorption spectrophotometer C-115M1 (PA “Electron,” Ukraine), while the organic component of bone tissue was calculated using the weighing method. The obtained data were statistically analyzed using ANOVA and independent samples t-tests. The results revealed that copper levels in the spongy bone of human lumbar vertebrae ranged from 2.45 to 6.12 mg/kg dw, and the organic component of bone tissue varied from 6.5% to 49.6%. The statistical analysis demonstrated a positive correlation between the organic component and copper content in the spongy bone tissue for both males (r=0.5195, p&lt;0.01, n=106) and females (r=0.6101, p&lt;0.01, n=105). Our study demonstrated that bone copper levels decrease with age, irrespective of gender. A strong positive correlation was observed between bone copper and organic content in the spongy bone of human lumbar vertebrae.

Expression of Interleukin 17A and 17B in Gingival Tissue in Patients with Periodontitis.

Periodontitis (PD) is a chronic inflammatory disease that is initiated by oral microorganisms. The pathogens induce the production of cytokines, such as interleukin (IL)-17, which enhances the inflammatory response and progression of the disease. The aim of this study was to examine the expression and localization in gingival tissue of IL-17A and IL-17B in patients with periodontitis. This study included 14 patients with periodontal disease and 14 healthy subjects without periodontal disease as a control group. There were no statistically significant differences in the expression of IL-17A mRNA between patients with periodontitis and control subjects. The expression of IL-17B mRNA was statistically significantly lower in patients with periodontitis in comparison with healthy subjects (p < 0.048). The expression of IL-17A correlated significantly with the approximal plaque index. The IL-17B expression in gingival tissue correlated with the clinical attachment level. This correlation reached borderline statistical significance (p = 0.06). In immunohistochemical analysis, we have shown the highest expression of IL-17 protein in inflamed connective tissue, epithelium, and granulation tissue from gingival biopsy specimens from patients with periodontitis. In biopsy specimens from healthy individuals, no IL-17 was found in the epithelium, while an expression of IL-17 was found in the connective tissue. The results of our study confirm the involvement of IL-17 in the pathogenesis of periodontitis. Our results suggest that an increase in IL-17 protein expression in the gingival tissue of patients with periodontitis occurs at the post-translational stage.

Impact on peri-implant connective tissue of laser treated versus traditional healing abutments: a human clinical trials

BackgroundDental implant is the principal treatment for edentulism and the healthiness of the peri-implant tissue has a pivotal role for its longterm success. In addition, it has been shown that also the topography of the healing abutment can influence the outcome of the restoration. The objective of this human clinical trial was to assess the impact of a novel laser-treated healing abutment on peri-implant connective tissue and extracellular matrix proteins compared to the conventional machined surface, which served as the control group.MethodsDuring second surgical stage a customized healing abutment were inserted on 30 single dental implants. Healing abutments were realized with two alternated different surface (two side laser-treated surfaces and two side machined surfaces) in order to be considered both as test and control on the same implant and reduce positioning bias. Following the soft tissue healing period (30 ± 7 days) a 5 mm circular biopsy was retrieved. Immuno-histochemical and quantitative real-time PCR (qPCR) analyses were performed on Collagen, Tenascin C, Fibrillin I, Metalloproteinases (MMPs) and their inhibitor (TIMPs). 15 were processed for qPCR, while the other 15 were processed for immunohistochemical analysis. Paired t-test between the two groups were performed. A value of p < 0.05 was considered statistically significant.ResultsResults revealed that the connective tissue facing the laser-treated surface expressed statistically significant lower amount of MMPs (p < 0.05) and higher level of TIMPs 3 (p < 0.05), compared to the tissue surrounding the machined implant, which, in turn expressed also altered level of extracellular matrix protein (Tenascin C, Fibrillin I (p < 0.05)) and Collagen V, that are known to be altered also in peri-implantitis.ConclusionsIn conclusion, the laser-treated surface holds promise in positively influencing wound healing of peri-implant connective tissue. Results demonstrated that topographic nature of the healing abutments can positively influence mucosal wound healing and molecular expression. Previous studies have been demonstrated how laser treatment can rightly influence integrity and functionality of the gingiva epithelium and cell adhesion. Regarding connective tissue different molecular expression demonstrated a different inflammatory pattern between laser treated or machined surfaces where laser treated showed better response. Targeted interventions and preventive measures on peri- implant topography could effectively minimize the risk of peri-implant diseases contributing to the long-term success and durability of restoration. However, new studies are mandatory to better understand this phenomenon and the role of this surface in the peri-implantitis process. Trial registrationThis trial is registered with ClinicalTrials.gov Identifier: (Registration Number: NCT05754970). Registered 06/03/2023, retrospectively registered.