Degradation Of Collagen Fibers Research Articles

Nicotine induces vasa vasorum stenosis in the aortic wall

ABSTRACT Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-α levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation.

Resveratrol activates autophagy and protects from UVA-induced photoaging in human skin fibroblasts and the skin of male mice by regulating the AMPK pathway.

Skin photoaging is mostly caused by ultraviolet A (UVA), although active medications to effectively counteract UVA-induced photoaging have not yet been created. Resveratrol, a naturally occurring polyphenol found in the skin of grapes, has been shown to have various biological functions such as anti-inflammatory and antioxidant characteristics. However, the role of resveratrol in UVA-induced photoaging has not been clarified. We investigated the mechanism of action of resveratrol by UVA irradiation of human skin fibroblasts (HSF) and innovatively modified a mouse model of photoaging. The results demonstrated that resveratrol promoted AMP-activated protein kinase (AMPK) phosphorylation to activate autophagy, reduce reactive oxygen species (ROS) production, inhibit apoptosis, and restore normal cell cycle to alleviate UVA-induced photoaging. In addition, subcutaneous injection of resveratrol not only improved the symptoms of roughness, erythema, and increased wrinkles in the skin of UVA photodamaged mice, but also alleviated epidermal hyperkeratosis and hyperpigmentation, reduced inflammatory responses, and inhibited collagen fiber degradation. In conclusion, our studies proved that resveratrol can treat UVA-induced photoaging and elucidated the possible molecular mechanisms involved, providing a new therapeutic strategy for future anti-aging.

Delving into Matrix Metalloproteinase-1 (MMP-1) and its Significance in Periodontal Diseases

ABSTRACT Matrix metalloproteinase-1 (MMP-1) plays a pivotal role in the pathogenesis of periodontal diseases, particularly periodontitis, by virtue of its collagenolytic activity targeting collagen type I, the primary component of periodontal tissues. This review abstract elucidates the intricate involvement of MMP-1 in periodontal tissue homeostasis and its dysregulation in disease states. Elevated MMP-1 levels, observed in gingival tissues and crevicular fluid of individuals with periodontitis, correlate with the degradation of collagen fibers within the periodontium. This degradation contributes to the detachment of teeth from surrounding tissues and exacerbates alveolar bone resorption, hallmark features of periodontal breakdown. Therapeutically, targeting MMP-1 activity emerges as a promising strategy, prompting ongoing research into MMP inhibitors and host modulation therapies. Understanding MMP-1’s nuanced role in periodontal diseases paves the way for personalized treatment approaches and holds promise in reshaping periodontal disease management for improved patient outcomes and periodontal health.

Leukemia inhibitory factor protects against experimental periodontitis through immuno-modulations of both macrophages and periodontal ligament fibroblasts.

To explore the role of leukemia inhibitory factor (LIF) in periodontitis via in vivo and in vitro experiments. The second upper molar of LIF knockout mice and their wild-type littermates were ligated for 8 days. Micro-computed tomography (micro-CT), histological analysis, and quantitative real-time polymerase chain reaction (qRT-PCR) were performed. The expression levels of proinflammatory cytokines were examined in mouse bone marrow derived macrophages and human periodontal ligament fibroblasts (HPDLFs) after lipopolysaccharide (LPS) treatment. LIF deficiency promoted alveolar bone loss, inflammatory cells infiltration, osteoclasts formation and collagen fiber degradation in ligature-induced mouse, along with higher expressions of proinflammatory cytokines, including interleukin-6 (IL6), IL-1β (IL1B), tumor necrosis factor-α (TNFA), matrix metalloproteinase 13 (MMP13), and RANKL/OPG ratio. Additionally, LIF deletion led to higher expression levels of these proinflammatory cytokines in mouse bone marrow-derived macrophages from both femur and alveolar bone and HPDLFs when treated with LPS. Administration of recombined LIF attenuated TNFA, IL1B, and RANKL/OPG ratio in HPDLFs. These findings indicate that LIF deficiency promotes the progress of periodontitis via modulating immuno-inflammatory responses of macrophages and periodontal ligament fibroblasts, and the application of LIF may be an adjunctive treatment for periodontitis to resolute inflammation.

Markers of Collagen Degradation in Remodeling and Diastolic Dysfunction of Left Ventricle in Patients with Arterial Hypertension

Introduction. Myocardial remodeling is a consequence or predictor of several cardiovascular diseases. The key process in myocardial remodeling is the degradation of collagen fibers, mediated by the activity of matrix metalloproteinases and their tissue inhibitor.The aim of this study was to evaluate serum levels of matrix metalloproteinase type 9 and tissue inhibitor of matrix metalloproteinase type 1 in female patients with arterial hypertension, myocardial remodeling, and diastolic dysfunction.Materials and methods. A cross-sectional study that included 84 postmenopausal women. All patients underwent echocardiography. Left ventricular remodeling was assessed according to Ganau classification, and diastolic function was evaluated using transmittal flow parameters. Serum analysis included the determination of MMP-9 and TIMP-1 levels using an enzyme-linked immunosorbent assay.Results. The median concentration of MMP-9 in the sample was 2 295.00 (923.60–4 114.00) ng/ml, TIMP — 1–17 010.00 (16 780.00–17 170.00) ng/ml. When evaluating the echocardiographic parameters of the patients included in the study, changes were revealed that indicate structural and functional remodeling of the LV and DD. 29 patients (35 %) had normal geometry, 6 patients (7 %) had concentric myocardial remodeling, 21 patients (25 %) had concentric myocardial hypertrophy, 28 cases (33 %) had eccentric myocardial hypertrophy. Statistically significant changes in the activity of MMP-9 and TIMP-1 were revealed in patients with various structural and geometric variants of remodeling. DD was detected in all patients included in the study: I degree was detected in 25 patients (30 %), II degree was determined in 59 cases (70 %). Using one-way analysis of variance, statistically significant differences in the level of MMP-9 in patients with grades I and II DD were determined. MMP-9 and MMP-9/TIMP-1 in patients with grade II DD are significantly higher than in patients with grade I.Discussion. Under pathophysiological conditions, the proteolytic properties of MMP-9 contribute to the stimulation of the immune response, initiating pathogenesis and aggravating the progression of the disease. Evaluation of the activity of MMP-9 and TIMP-1 in patients with arterial hypertension may be a marker of myocardial remodeling.Conclusion. An increase in the activity of matrix metalloproteinase type 9 and a decrease in the activity of a tissue inhibitor of matrix metalloproteinases type 1 were revealed in patients with arterial hypertension, myocardial remodeling and LV diastolic dysfunction. The level of MMP-9 is associated with the degree of diastolic dysfunction and the structural-geometric type of LV remodeling.

Transcriptomic analysis reveals the early body wall regeneration mechanism of the sea cucumber Holothuria leucospilota after artificially induced transverse fission

BackgroundSea cucumbers exhibit a remarkable ability to regenerate damaged or lost tissues and organs, making them an outstanding model system for investigating processes and mechanisms of regeneration. They can also reproduce asexually by transverse fission, whereby the anterior and posterior bodies can regenerate independently. Despite the recent focus on intestinal regeneration, the molecular mechanisms underlying body wall regeneration in sea cucumbers still remain unclear.ResultsIn this study, transverse fission was induced in the tropical sea cucumber, Holothuria leucospilota, through constrainment using rubber bands. Histological examination revealed the degradation and loosening of collagen fibers on day-3, followed by increased density but disorganization of the connective tissue on day-7 of regeneration. An Illumina transcriptome analysis was performed on the H. leucospilota at 0-, 3- and 7-days after artificially induced fission. The differential expression genes were classified and enriched by GO terms and KEGG database, respectively. An upregulation of genes associated with extracellular matrix remodeling was observed, while a downregulation of pluripotency factors Myc, Klf2 and Oct1 was detected, although Sox2 showed an upregulation in expression. In addition, this study also identified progressively declining expression of transcription factors in the Wnt, Hippo, TGF-β, and MAPK signaling pathways. Moreover, changes in genes related to development, stress response, apoptosis, and cytoskeleton formation were observed. The localization of the related genes was further confirmed through in situ hybridization.ConclusionThe early regeneration of H. leucospilota body wall is associated with the degradation and subsequent reconstruction of the extracellular matrix. Pluripotency factors participate in the regenerative process. Multiple transcription factors involved in regulating cell proliferation were found to be gradually downregulated, indicating reduced cell proliferation. Moreover, genes related to development, stress response, apoptosis, and cell cytoskeleton formation were also involved in this process. Overall, this study provides new insights into the mechanisms of whole-body regeneration and uncover potential cross-species regenerative-related genes.

The Role of ADAMTS Proteoglycanases in Thoracic Aortic Disease.

Thoracic aortic aneurysm and dissection (TAAD) are complex disease states with high morbidity and mortality that pose significant challenges to early diagnosis. Patients with an aneurysm are asymptomatic and typically present to the emergency department only after the development of a dissection. The extracellular matrix (ECM) plays a crucial role in regulating the aortic structure and function. The histopathologic hallmark termed medial degeneration is characterised by smooth muscle cell (SMC) loss, the degradation of elastic and collagen fibres and proteoglycan (PG) accumulation. Covalently attached to the protein core of PGs are a number of glycosaminoglycan chains, negatively charged molecules that provide flexibility, compressibility, and viscoelasticity to the aorta. PG pooling in the media can produce discontinuities in the aortic wall leading to increased local stress. The accumulation of PGs is likely due to an imbalance between their synthesis by SMCs and decreased proteolysis by A Disintegrin-like and Metalloproteinase with Thrombospondin motifs (ADAMTS) proteoglycanases in the ECM. Mouse models of TAAD indicated that these proteases exert a crucial, albeit complex and not fully elucidated, role in this disease. This has led to a mounting interest in utilising ADAMTS proteoglycanases as biomarkers of TAAD. In this review, we discuss the role of ADAMTSs in thoracic aortic disease and their potential use in facilitating the clinical diagnosis of TAAD and disease progression.

Senkyunolide I ameliorates thoracic aortic aneurysm and dissection in mice via inhibiting the oxidative stress and apoptosis of endothelial cells

BackgroundThoracic aortic aneurysm and aortic dissection (TAAD) is one of the most fatal cardiovascular diseases. Senkyunolide I (SEI) is a component of traditional Chinese medicine with remarkable anti-inflammatory properties and exhibits remarkable protective effects, but its impact on TAAD remains unclear. Our study aimed to explore the role of SEI in a murine model of TAAD and further explore the immunopharmacological mechanism. Methods and materialsThe in vivo model were assessed using echocardiography, gross anatomy, and tissue staining. Western blot and immunofluorescence were performed to evaluate the effects of SEI in vivo and in vitro. A SEI solution injection containing 1 % dimethyl sulfoxide (DMSO) was administered intraperitoneally to the TAAD model group, while a normal saline injection comprising 1 % DMSO was administered to the sham group. ResultsSEI prevented TAAD formation induced by BAPN/Ang II and reduced the TAAD incidence in mice. SEI treatment significantly inhibited the degradation of collagen and elastin fibers in the extracellular matrix. Furthermore, it reduced the expression of inflammatory factors in the aortic intima. Western blot analysis revealed that SEI-treated mice showed a significant decrease in apoptosis-related protein levels in the aorta compared with the TAAD group. PI3K, Akt, and mTOR in the SEI treatment group were significantly lower than in the model group. SEI could also attenuate H2O2-induced Human umbilical vein endothelial cells (HUVECs) damage and reverse the decline in migrant cells. The apoptosis of HUVECs was considerably reduced by the SEI treatment. ConclusionsConclusively, SEI may alleviate the progression of TAAD by suppressing the PI3K/Akt/NF-κB signaling pathway. The SEI's ability to inhibit inflammation and oxidative stress opens the way to restore the function of endothelial cells and vascular homeostasis, and thus to provide novel and promising options for the treatment of TAAD patients.

Corneal stromal regeneration-keratoconus cell therapy: a review.

Keratoconus is a corneal ectatic disease caused by stromal thinning leading to astigmatism and progressive loss of vision. Loss of the keratocytes and excessive degradation of collagen fibres by matrix metalloproteinases are the molecular signatures of the disease. Despite several limitations, corneal collagen cross-linking and keratoplasty are the most widely used treatment options for keratoconus. In the pursuit of alternative treatment modalities, clinician scientists have explored cell therapy paradigms for treating the condition. Articles pertaining to keratoconus cell therapy with relevant key words were used to search in PubMed, Researchgate, and Google Scholar. The articles were selected based on their relevance, reliability, publication year, published journal, and accessibility. Various cellular abnormalities have been reported in keratoconus. Diverse cell types such as mesenchymal stromal cells, dental pulp cells, bone marrow stem cells, haematopoietic stem cells, adipose-derived stem cells apart from embryonic and induced pluripotent stem cells can be used for keratoconus cell therapy. The results obtained show that there is a potential for these cells from various sources as a viable treatment option. There is a need for consensus with respect to the source of cells, mode of delivery, stage of disease, and duration of follow-up, to establish a standard operating protocol. This would eventually widen the cell therapy options for corneal ectatic diseases beyond keratoconus.

Effect and mechanism of fish scale extract natural hydrogel on skin protection and cell damage repair after UV irradiation

Skin lesions caused by ultraviolet radiation exposure seriously reduce people's life quality, safe natural products development to prevent and repair ultraviolet damage is an effective strategy. We investigated the protective and reparative effects of the natural composite gel (SE-gel) derived from fish scales on UV-irradiated skin by inhibiting reactive oxygen species (ROS) -mediated oxidative stress and inflammatory responses. Our results showed that SE-gel rich in glycine and proline had good ultraviolet absorption, water absorption, moisturizing and free radical scavenging abilities. In vitro, SE-gel could improve UV-irradiated L929 cell viability by 1.24 times via inhibiting 50% ROS production and malondialdehyde, and improving superoxide dismutase activity to reduce oxidative stress caused by UV irradiation. In UV-irradiated mouse skin damage model, SE-gel prevent UV-induced skin erythema, epidermal thickening, collagen fiber degradation and disruption, and reduced UV-induced inflammatory response via NF-κB signaling pathway, showing potential application in UV-irradiated skin damage prevention and repair.

Preparation of Cod Skin Collagen Peptides/Chitosan-Based Temperature-Sensitive Gel and Its Anti-Photoaging Effect in Skin.

Photoaging decreases quality of life and increases the risk of skin cancer, underscoring the urgent need to explore natural, high-efficacy, anti-skin photoaging (SP) active substances. In this study, a gel (CS/CSCPs/β-GP gel) was prepared using chitosan (CS) and sodium β-glycerophosphate (β-GP) through crosslinking with small molecular CSCPs as the carried drug. We evaluated its structural characteristics and properties. The effect of CS/CSCPs/β-GP gel on the degree of ultraviolet (UV)-induced skin aging of mice was investigated through comparative analysis of skin damage, the integrity of collagen tissues and elastic fibers, levels of reactive oxygen species (ROS) and key inflammatory factors (tumor necrosis factor [TNF]-α and interleukin [IL]-1β, IL-6, and IL-10), and tissue expression of matrix metalloproteinase-3 (MMP-3) after repeated UV irradiation in a nude mice SP model. The results showed that CS/CSCPs/β-GP gel was successfully prepared and had the desired characteristics. Compared with CSCPs alone, the CS/CSCPs/β-GP gel more evidently improved typical photoaging characteristics on mouse dorsal skin. It also increased the moisture content, causing the skin to become glossy and elastic. Pathological skin analysis revealed that this peptide-carrying gel can effectively inhibit epidermal thickening, reduce tissue inflammatory infiltration, suppress collagen fiber degradation, increase the collagen content, alleviate structural elastic fiber damage, and significantly inhibit abnormal MMP-3 expression. In addition, biochemical analysis showed that the CS/CSCPs/β-GP gel can effectively inhibit the elevated expressions of ROS and key proinflammatory factors (TNF-α, IL-1β, IL-6) in photoaging skin tissues and promote expression of the anti-inflammatory factor IL-10. SP can cause many clinical skin diseases, such as solar freckle-like nevus, solar keratosis, cutaneous melanoma, and squamous cell carcinoma. CSCPs are a high-efficacy anti-SP natural active substance and CS/CSCPs/β-GP gel can synergistically enhance the CSCPs' anti-SP effect. The mechanism is likely related to the inhibited activation of ROS/nuclear transcription factor-κB signaling and the expression of downstream inflammatory factors.

Tricaprin can prevent the development of AAA by attenuating aortic degeneration

Medical therapeutic options to prevent rupture of abdominal aortic aneurysm (AAA), a critical event, must be developed. Moreover, further understanding of the process of AAA development and rupture is crucial. Previous studies have revealed that aortic hypoperfusion can induce the development of AAA, and we successfully developed a hypoperfusion-induced AAA animal model. In this study, we examined the effects of medium-chain triglycerides (MCTs), tricaprylin (C8-TG) and tricaprin (C10-TG), on hypoperfusion-induced AAA rat model. We estimated the effects of MCTs on aortic pathologies, mechanical properties of the aorta, and development of AAA. C10-TG, but not C8-TG, significantly suppressed AAA development and completely prevented the rupture. We observed that C10-TG prevented the development and rupture of AAA, but not C8-TG. Additionally, regression of AAA diameter was observed in the C10-TG group. Pathological analysis revealed C10-TG improved the hypoperfusion-induced increase in hypoxia-inducible factor-1α levels, medial smooth muscle cells (SMCs) loss, degeneration of aortic elastin and collagen fibers, and loss of aortic wall elasticity. In addition, regression of the formed AAA was observed by administration of C10-TG after AAA formation. C10-TG administration after AAA formation improved degeneration of AAA wall including degradation of aortic elastin and collagen fibers, stenosis of vasa vasorum, and loss of medial SMCs. These data suggest C10-TG can prevent AAA by attenuating aortic hypoperfusion and degeneration. Considering the clinical safety of C10-TG, C10-TG can be a promising AAA drug candidate.

Synergistic effects of heating and traction during fibrous tissue elongation

Fibrosis involves the abnormal accumulation of components of the extracellular matrix, such as collagen, and can lead to organ failure, which accounts for approximately one-third of all deaths worldwide. Accordingly, there is an urgent need to develop low-invasive treatment strategies for fibrosis as there is currently a lack of anti-fibrotic pharmacological agents available. In the present study, we tested the hypothesis that applying traction to fibrous tissues while using heat to denature proteins can be used to adjust the shape and flexibility of tissues. Bovine Achilles tendon samples as a model of fibrous tissue contracted by approximately 25% compared to the original length in response to heating, in line with previous findings. In contrast, the application of traction during heating and cooling increased tissue length by 25% and decreased Young’s modulus by 16%. Tissue staining and detection of unfolded collagen using collagen-hybridizing peptide demonstrated thermal degradation of collagen fibers and conversion to gelatinous material throughout samples, confirming that traction, and heating damages collagen. These results indicate that this technique can be used to alter the shape and reduce the rigidity of organs affected by fibrosis.

Textural modification of Chinese traditional stewed pig trotter: Effect of acid or alkaline-induced degradation of collagen fibers.

This study aimed to investigate the effects of acid or alkaline treatments on the textural properties of Chinese traditional stewed pig trotter in relation to the degradation of collagen fibers. Pig trotters were subjected to different pHs of 4, 5, 6, 7, and 8 and then stewed at 95°C for 60 min. Textural parameters (springiness, chewiness, hardness, and gumminess) of pig trotters and Raman spectroscopy, cross-links, decorin, and glycosaminoglycans contents of collagen fibers were assessed. The acid or alkaline treatments at pH 4, 5, 6, and 8 improved the textural properties evidenced by lower chewiness, hardness, and gumminess, and promoted the unfolding of the secondary structure evidenced by a loss of α-helix paralleled with an increase of random coil, as well as induced a breakage to the covalent cross-links evidenced by the reduction of cross-links, decorin, and glycosaminoglycans. This study thus concluded positive effects of acid or alkaline treatments on the textural modification of Chinese traditional stewed pig trotter in relation to the induced degradation of the collagen fibers.

Effects of thermal processing on the texture and collagen characteristics of ready-to-eat chicken claw.

The effects of thermal processing on the texture and collagen properties of ready-to-eat chicken claws were investigated and the relationship between the texture of chicken claws and the collagen properties of connective tissue was further discussed. The texture, sensory and collagen characteristics (content, solubility, and structure), and the degradation of insoluble collagen of chicken claws underwent thermal processing at 90°C/30 min, 100°C/30 min, 115°C/15 min, and 121°C/10 min were measured. The results showed that thermal processing significantly reduced the textural parameters (hardness, springiness, cohesiveness, chewiness, and resilience) of chicken claws, and the textural deterioration intensified with the increase in temperature. Thermal processing aggravated the degradation of collagen fibers in cooked chicken claws, resulting in decreased insoluble collagen content and increased collagen solubility. Moreover, higher thermal processing temperature produced more soluble collagen components composed of low-molecular weight peptides. The textural deterioration of chicken claws caused by thermal processing was related to the decrease of insoluble collagen content and the increase of content of soluble collagen composed of low-molecular weight peptides. On the one hand, the decreased of insoluble collagen content led to the weakening of connective tissue. On the other hand, low-molecular weight peptides hindered the cooling renaturation of soluble collagen, leading to the formation of gels with poor mechanical properties.

Radiologic findings associated with mucoid degeneration of the anterior cruciate ligament.

Mucoid degeneration (MD) of the anterior cruciate ligament (ACL) is a well-recognized pathology characterized by the degradation of collagen fibers and infiltration of a mucoid-like substance. This study is to determine the anatomical associated factors for MD-ACL using radiographic and magnetic resonance imaging (MRI). This was a retrospective study on patients who had undergone knee arthroscopy between 2011 and 2020. The patients with MD-ACL were defined and enrolled by the MRI and arthroscopy. Eventually, 52 patients in the MD-ACL group (group 1) and 52 patients in the control group (group 2) were enrolled, following sex and age matching. Radiologic evaluation included the assessment of Kellgren-Lawrence (K-L) grade, mechanical hip-knee-ankle (HKA) angle, posterior tibial slope (PTS) angle, and Insall-Salvati ratio. The notch width index and transverse notch angle were measured on MRI, and the grade of trochlear dysplasia was defined. Logistic regression analysis, receiver operating characteristic (ROC) curves, and area under curve (AUC) were performed. The ROM was significantly decreased in group 1, whereas the PTS angle was significantly larger in group 1. Combined ganglion cysts of ACL were found in 42/52 patients (80.7%) in group 1. The risk of MD-ACL was associated with a steeper PTS angle, increased Insall-Salvati ratio, male sex, higher K-L grade, and decreased transverse notch angle and notch width index. The cutoff values in ROC analysis were found to be ≤ 28.27% for the notch width index (AUC, 0.849; p < 0.001), > 12.2° for the PTS angle (AUC, 0.765; p < 0.001), and ≤ 47.4° for the transverse notch angle (AUC, 0.711; p < 0.001), but not significant for Insall-salvati ratio. A steeper PTS angle, decreased notch width index, and transverse notch angle are significantly associated with the presence of MD-ACL. These factors should be considered during diagnosis or when determining the treatment strategy for symptomatic MD-ACL patients. Level IIIb.

Association of fatal and non-fatal adverse health outcomes with urinary peptides reflecting collagen I turnover

Abstract Background Imbalance of collagen I (COL1) turnover, featured by increased synthesis and decreased degradation of collagen fibers, is a hallmark of fibrosis in the heart and blood vessels that associates with poor cardiovascular outcomes. Such as imbalance of COL1 turnover could be reflected in urine and serve as fingerprint for future adverse outcomes in general population, and high risk subjects. Purpose We hypothesize that imbalance of proteomic signatures of urinary peptides (UPs) reflecting COL1 turnover relate to adverse health outcomes in participants from a general population Methods We randomly recruited 776 participants (51.2% women; 50.5 years) from the Flemish Study on Environment, Genes and Health Outcomes cohort and measured UPs proteome by capillary electrophoresis coupled with mass spectrometry. Our analyses focused on 148 peptides of COL1 alpha-1 (COL1A1) chain that retained ≥70% signal in the whole sample. The primary endpoint included fatal and nonfatal cardiovascular endpoints. Secondary endpoints consisted of total mortality, fatal and nonfatal cardiac, coronary, and heart failure endpoints. Multivariate Cox proportional models, partial least squares analysis (PLS), log-likelihood test, and receiver operating characteristics (ROC) curve were applied. Results Over a median follow up of 12.4 years, 110 primary endpoints occurred, 61 participants died, 81, 41 and 24 experienced cardiac, coronary, and heart failure endpoints; respectively. In PLS analyses, upregulation of UPs signatures closer to C- and N-terminal locations of the COL1A1 chain whereas downregulation of mid-region UPs were associated with lower risk of adverse health outcomes. This pattern was inverted in subjects with cardiovascular disease, as upregulation of terminal and downregulation of mid region UPs increased risk. Adding UPs to a basic model including sex, age and usual cardiovascular risk factors significantly improved model performance between 2.54% to 4.93% (P≤0.001) for prediction of adverse health outcomes. In ROC plots, adding UPs to the basic model increased the area under the curve up to 4.00% (P&amp;lt;0.012). Conclusions UPs reflecting COL1 turnover predicted adverse health outcomes. The inverted up- and down regulations of UPs in between participants with and without previous cardiovascular diseases might be explained by a shift in the UPs signatures of COL1 fragments linked to distinct fibrotic processes. Urinary proteomic might have clinical importance in documenting the extent of collagen accumulation that relates to adverse health outcomes. In patients at high cardiovascular risk, modification of collagen I fibers turnover might be a potential treatment target Funding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): The European Union the European Research Council and the European Research Area Net for Cardiovascular Diseases.

The Texture Change of Chinese Traditional Pig Trotter with Soy Sauce during Stewing Processing: Based on a Thermal Degradation Model of Collagen Fibers.

In order to clarify the influence of the thermal degradation of collagen fibers on the texture profile analysis (TPA) parameters of pig trotter stewed with soy sauce (PTSWSS), TPA (springiness, chewiness, hardness, and gumminess), the secondary structures, the cross-linkage, decorin (DCN) and glycosaminoglycan (GAG) levels, and the histochemical morphology of collagen fibers during the stewing process (0, 30, 60, 120 min) were assessed. The springiness and hardness increased after 30 min of stewing, along with the denaturation of collagen proteins. TPA parameters improved with the prolonged stewing times of 60 and 120 min, along with the ultra-structural dissolution of collagen fibers, and a substantial reduction in cross-linkage, DCN, and GAG levels, and the unfolded triple-helix structure. This study concluded that the TPA parameters of PTSWSS were dependent on the stewing time, and that the improvement in TPA parameters with longer stewing time could primarily be attributed to the thermal degradation of collagen fibers.

Contribution of secondary bonds to the storage stability of ready-to-eat sea cucumber

To explore the contribution of secondary bonds on storage stability of RSC, urea, n-propanol and sodium nitrite (NaNO2) were used for the breakdown of hydrogen bonds, hydrophobic bonds, side-chain groups, respectively. The impact of the breakdown of secondary bonds before and after storage on texture properties and microstructure were investigated. The breakdown of hydrogen bonds, especially before storage, significantly reduced the hardness (from 3.12 to 2.21 N), chewiness (from 1.82 to 1.05 mJ), and springiness (from 2.57 to 1.57 mJ) of RSC, while the breakdown of hydrophobic bonds and side-chain groups had a slight effect. Similarly, degradation of collagen fibers by breaking hydrogen bonds before storage was more serious than other groups. Furthermore, moisture content and water activity decreased and the degradation degree of collagen in RSC body wall increased with hydrogen bonds breaking. The results showed that hydrogen bonds were essential for the storage stability of RSC.

Do osmotic pressure and hygroscopicity of areca nut related products drive extracellular fluid loss and condensation of collagen bundles in oral submucous fibrosis?

Increased production and decreased degradation of collagen fibers are the two of hallmarks of oral submucous fibrosis (OSMF). To date pathogenesis of OSMF has been perceived from the perspective of chemical constituents of the betel quid (BQ) and their impact on the signaling pathways related to fibrosis. In the present paper, physical properties such as osmotic pressure and hygroscopicity of the BQ amalgamation formed in the oral cavity are proposed as the causative mechanisms for OSMF. The detailed mechanism of osmotic pressure gradient development between extracellular fluid and the amalgamated BQ in the oral cavity has been deliberated. In addition, the hygroscopicity of BQ is also projected as a complementary mechanism to the osmotic pressure mechanism for OSMF development. Various laboratory experiments, cell culture models, and animal studies are proposed to evaluate the hypothesis. Since OSMF can also occur in only areca nut chewing individuals, we put forth the proposed mechanism as complementary to the already known pathogenesis. This novel hypothesis addresses the age-old problem related to the management of OSMF and extracellular fluid restoration strategies would drastically change and probably improve the clinical status and reduce the malignant potential of OSMF.