Matrix Metalloproteinase-9 Gene Research Articles

Alterations of the Extracellular Matrix in Colorectal Carcinoma.

Background: The process of proliferation and invasion of tumor cells depends on changes in the extracellular matrix (ECM) through the activation of enzymes and alterations in the profile of ECM components. Our aims were to investigate the mRNA and protein expression profiles of the ECM components, heparanase-1 (HPSE), heparanase-2 (HPSE2), matrix metalloproteinase-9 (MMP-9), and syndecan-1 (SDC1) in neoplastic and nonneoplastic tissues of 24 patients with colorectal carcinoma (CRC) and to test for associations between the expression patterns of these genes with the presence or absence of lymph node metastases. Materials and Methods: This was a cross-sectional study in which 24 adult patients with CRC were admitted for resectional surgery. We analyzed the mRNA and protein expression patterns of the HPSE, HPSE2, MMP-9, and SDC1 genes by quantitative reverse transcription PCR and immunohistochemistry, respectively. Additionally, we investigated whether variations exist in the expression of the ECM components between the affected tissue and nontumoral tissue collected from the same patient. Tissue samples were collected during the surgical resection. Results and Conclusions: The data showed higher mRNA and protein expression levels of HPSE2 (p = 0.0058), MMP-9 (p = 0.0268), and SDC1 (p = 0.0002) in tumor samples when compared to the adjacent non-neoplastic tissues. There was, however, only an increase in the HPSE protein levels in the tumoral tissues. Increased expression of HPSE2 was observed in patients with lymph node metastasis (p = 0.031). This elevation in HPSE2 mRNA expression in patients with lymph node metastases potentially indicates that it may participate in driving colorectal carcinoma progression.

100P Study on the effect of ursolic acid on MMPs and antimetastatic activity in TNBC cells

The matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade multiple components of the extracellular matrix. The significant role of MMPs in tumor invasion, neoangiogenesis and metastasis presented it as ideal pharmacological targets for cancer therapy. The effects of ursolic acid (UA) on matrix metalloproteinase (MMP) gene expression, cell invasion and cell migration were investigated MDA MB- 231 cell line.

Matrix metalloproteinase-7 is increased in lung bases but not apices in idiopathic pulmonary fibrosis.

IntroductionIdiopathic pulmonary fibrosis (IPF) is a progressively fibrotic lung condition with poor prognosis. Matrix metalloproteinase-7 (MMP7) is a protein secreted by epithelial cells in IPF lungs. It is not known if MMP7 expression correlates with fibrotic changes in lung tissue.MethodsTissue samples from lung apices and bases were obtained from 20 IPF patients and 14 non-diseased control (NDC) donors. In formalin-fixed paraffin-embedded sections, histological assessment of fibrosis was performed; overall MMP7 positivity was assessed by immunohistochemistry and MMP7+ cells were quantified using multiplex immunohistochemistry. Protein expression of MMP7 in whole lung lysates was quantified by Western blotting. Bulk tissue transcriptomic profiles of 101 samples were analysed using RNA sequencing technologies.ResultsLung tissue from IPF bases was more fibrotic than in apices. MMP7 protein is elevated in IPF lung base tissue. In IPF whole lung lysates, MMP7 protein levels are increased compared to NDC donors and was increased in IPF lung bases compared to apices. MMP7 protein levels correlated with MMP7 gene expression levels in lung tissue. MMP7 transcript levels were increased in IPF base compared to NDC base lung tissue and increased in IPF base tissue compared to IPF apex tissue.ConclusionsOur cross-sectional study suggests that lung epithelial MMP7 expression increases as the tissue becomes more fibrotic and identifies a potentially nonepithelial or immune-cell source. Mechanisms of disease progression in IPF are still unclear, and our study suggests aberrant MMP7 production may be a histological starting point of lung tissue fibrosis.

Investigation of the effect of gossypin on MMP-2 and MMP-9 genes in prostate cancer cells

Purpose: The aim of this study is to explore the effects of gossypin on matrix metalloproteinases -2 (MMP-2) and MMP-9 genes in prostate cancer cells. Materials and Methods: PC3 cells were grown in culture and treated with three different concentrations of gossypin (25-50-100 µg/ml) and cisplatin (50 µM) as a positive control. First, RNA isolation was performed. Then, cDNA synthesis was performed and RT-PCR was used to evaluate mRNA expression levels of MMP-2 and MMP-9 genes.Results: Gossypin decreased MMP-2 and MMP-9 mRNA expression in prostate cancer cells in a concentration-dependent manner. Three concentrations (25-50-100 µg/ml) of gossypin in PC3 cells reduced the mRNA expression of the MMP-2 gene. While the fold change value of MMP-2 gene expression was 0.3482 ± 0.040 in the 100 µg/ml gossypin group, it was 1.007 ± 0.1425 in the control group. In addition, 50 µg/ml and 100 µg/ml concentrations of gossypin decreased the mRNA expression of the MMP-9 gene. The expression level of the MMP-9 gene in prostate cancer cells was 0.4740 ± 0.038 in the 100 µg/ml gossypin administered group, while it was 1.009 ± 0.1687 in the control group. There was a positive correlation between the expressions of the MMP-2 and MMP-9 genes.Conclusion: According to the results obtained, it is seen that gossypin reduces the expression of MMP-2 and MMP-9 genes in prostate cancer cells and the effects of gossypin on other genetic and epigenetic mechanisms in cancer need to be investigated to reveal the anti-cancer.

Study on the Relationship between MMP-2, MMP-9 Gene Polymorphisms, and the Risk of Colorectal Cancer.

Objective The aim of the study is to explore the relationship between matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) gene polymorphisms and the risk of colorectal cancer. Methods From January 2019 to December 2021, 308 patients with colorectal cancer in our hospital were selected to be included in the colorectal cancer group and 300 normal healthy people were included in the control group. We perform genotyping, compare the genotype frequencies between the colorectal cancer group and the control group, calculate the relationship between MMP-2 and MMP-9 gene polymorphisms and disease risk, and analyze the genotype distribution characteristics of colorectal cancer patients with different pathological stages and lymph node metastasis status. The expression levels of serum MMP-2 and MMP-9 in patients with different genotypes were compared. Results The frequency of CC genotype and C gene at the MMP-2 gene−735 (C/T) locus in the colorectal cancer group was higher than that of the control group, and the frequency of TT genotype and T gene at MMP-9 gene−1562 (C/T) locus was a higher control group (P < 0.05). The comparison of genotype and gene frequency distribution of MMP-2 gene−1306 (C/T), −790 (T/G), and MMP-9 gene R668Q and P574R between the colorectal cancer group and the control group (P > 0.05); MMP-2 gene−735 (C/T) locus CC genotype and MMP-9 gene−1562 (C/T) locus TT genotype are dangerous genotypes for colorectal cancer. OR values were 1.490 (95% CI: 1.085–2.047), 1.519 (95% CI: 1.061–2.174); TNM stage III-IV, the proportion of CC genotype and TT genotype at MMP-9 gene−1562 (C/T) locus in patients with lymph node metastasis is higher than that without lymph node metastasis of TNM stage I-II patients (P < 0.05); MMP-2 gene in colorectal cancer patients. Serum MMP-2 levels in patients with CC genotype at 735 (C/T) locus were higher than those with CT + TT genotype, and serum MMP-9 levels in patients with TT genotype at MMP-9 gene−1562 (C/T) locus were higher CT + CC genotype patients (P < 0.05). Conclusion The CC genotype at −735 (C/T) locus of the MMP-2 gene and the TT genotype at−1562 (C/T) locus of the MMP-9 gene are risk genotypes for the development of colorectal cancer.

ADAM-10 Regulates MMP-12 during Lipopolysaccharide-Induced Inflammatory Response in Macrophages.

A disintegrin and metalloprotease 10 (ADAM-10), a member of the ADAM protease family, has biological activities related to TNF-α activation, cell adhesion, and migration, among other functions. Macrophages are important immune cells that are involved in the inflammatory response of the body. ADAM-10 is involved in inflammatory responses, but the specific regulatory mechanisms are not fully understood. In this study, we investigated the regulatory mechanism of ADAM-10 in the lipopolysaccharide-promoted proliferation (LPS) of the macrophage inflammatory response. Differentially expressed or regulated proteins were identified in interfered ADAM-10 (sh ADAM-10) macrophages using tandem mass tag (TMT) proteomics. The changes and regulatory role of ADAM-10 during LPS-induced inflammatory response in normal, interfering, and overexpressing ADAM-10 (EX ADAM-10) cells were determined. Results indicated that ADAM-10 interference affected inflammation-related pathways and reduced matrix metalloproteinase 12 (MMP-12) protein levels, as identified by TMT proteomics. In normal cells, LPS decreased ADAM-10 gene expression, but promoted ADAM-10 secretion, MMP-12 and TNF-α gene expression, and MMP-12, iNOS, IL-10, and cyclinD1 protein expression. Additionally, ADAM-10 knockdown decreased macrophage viability in sh-ADAM-10 cells. Moreover, an MMP-12 inhibitor had no impact on the viability effect of LPS on cells or the expression of ADAM-10. iNOS expression decreased, whereas IL-10 expression increased after ADAM-10 depletion. ADAM-10 knockdown decreased MMP-12, iNOS, TNF-α, IL-1β, and FKN, while overexpression had an opposite effect. ADAM-10 overexpression further increased MMP-12, iNOS, and TNF-α gene expression in response to LPS. Cell viability was increased in EX ADAM-10 cells, and ADAM-10 secretion was further increased in the EX and LPS groups. Flow cytometry and immunofluorescence staining revealed that EX-ADAM 10 cells had increased iNOS expression, which acted as an IL-6 expression driver. In summary, we found that ADAM-10 is activated by LPS and positively participates in LPS-stimulated macrophage inflammatory responses by positively regulating MMP-12 during the inflammatory process.

Atorvastatin attenuates NS1 (Non-structural protein-1) of dengue type-2 serotype-induced expressions of matrix metalloproteinases in HL-60 cells, differentiated to neutrophils: Implications for the immunopathogenesis of dengue viral disease

BackgroundThe dengue is a vector borne viral infection in humans. Bite of mosquito infected with a dengue virus transmits the disease. The neutrophils support more to the innate immune response by switching to infected tissues and triggering immunomodulatory mechanisms including the release of proteases and host defence peptides. MethodsCell viability by MTT and trypan blue dye exclusion assay, bright field microscopy for assessment of cell morphology, cytokines measurements by ELISA, estimation of protein by Bradford assay were done. Assessments of matrix metalloproteinase genes mRNA expressions were done using real-time PCR. ResultsIn the present study, we have for the first time unveiled that, NS1 antigen of dengue type-2 serotype, induce and stimulate the neutrophils cells to express high levels of matrix metalloproteases. NS1 exposure of HL-60 cells differentiated to neutrophils affected cell morphology and in 24 h of exposure. We have demonstrated that, the NS1 antigen has induced MMP-2, MMP-14 and MMP-9 expressions in neutrophils in a 24hrs exposure time. NS1 exposure has also further upregulated MMP-1, MMP-13, and MMP-8 expressions in neutrophils in a 24hrs exposure time. Notably, treatment with atorvastatin concentrations downregulated the expression profile of the all matrix metalloprotease significantly. Importantly, NS1 antigen has significantly increased the IL-6, IL-13 release by the HL,60 cells which was reversed by atorvastatin. On the other hand, NS1 exposure enhanced the mRNA expressions of VEGF-A and VEGF-D which was reversed by atorvastatin. However, we found that, NS1 exposure reduced the mRNA expressions profile of VEGF-C, which was reversed by atorvastatin. ConclusionIn conclusion, we report that, neutrophils associated matrix metalloprotease are involved in the pathogenesis of dengue viral disease. VEGF growth factors may also be released by the neutrophils which may subsequently participate in the endothelial dysfunctions leading to dengue shock syndrome.

Codon Usage Bias and Cluster Analysis of the MMP-2 and MMP-9 Genes in Seven Mammals.

Matrix metalloproteinase (MMP)-2 and MMP-9 are a family of Zn2+ and Ca2+-dependent gelatinase MMPs that regulate muscle development and disease treatment, and they are highly conservative during biological evolution. Despite increasing knowledge of MMP genes, their evolutionary mechanism for functional adaption remains unclear. Moreover, analysis of codon usage bias (CUB) is reliable to understand evolutionary associations. However, the distribution of CUB of MMP-2 and MMP-9 genes in mammals has not been revealed clearly. Multiple analytical software was used to study the genetic evolution, phylogeny, and codon usage pattern of these two genes in seven species of mammals. Results showed that the MMP-2 and MMP-9 genes have CUB. By comparing the content of synonymous codon bases amongst seven mammals, we found that MMP-2 and MMP-9 were low-expression genes in mammals with high codon conservation, and their third codon preferred the G/C base. RSCU analysis revealed that these two genes preferred codons encoding delicious amino acids. Analysing what factors influence CUB showed that the third base distributors of these two genes were C/A and C/T, and GC3S had a wide distribution range on the ENC plot reference curve under no selection or mutational pressure. Thus, mutational pressure is an important factor in CUB. This study revealed the usage characteristics of the MMP-2 and MMP-9 gene codons in different mammals and provided basic data for further study towards enhancing meat flavour, treating muscle disease, and optimizing codons.

Effects of Lactobacillus kefiri fermentation supernatant on skin aging caused by oxidative stress

• • Lactobacillus kefiri fermentation components(LAF) shows excellent antioxidant effect in vitro. • •Achievements of Lactobacillus kefiri fermentation components providing more possibilities for their application as functional raw materials in cosmetics. • •LAF can regulate the expression of oxidative stress, autophagy, and aging-related genes in damaged cells treated with H 2 O 2 , thereby delaying cell senescence. Lactobacillus kefiri is a beneficial bacteria that is often used to make yogurt only, and is beneficial to human health when it is used in food fermentation. In this article, a fermentation supernatant (LAF) is prepared by culturing Lactobacillus kefiri , and the anti-aging effects of LAF are evaluated at the biochemical, cellular, and molecular biology levels. The antioxidant activity of LAF is comprehensively evaluated by three free radical scavenging tests and the total antioxidant capacity (ABTS method) test. The toxicity of LAF on human skin fibroblasts (HSF) is detected using the MTT method, and the effects of LAF on H 2 O 2 -induced oxidative stress in terms of intracellular reactive oxygen species (ROS), Malondialdehyde (MDA) content, antioxidant enzyme activity are evaluated. The gene expression levels of LC3 and Beclin-1 are detected using the real-time reverse transcription-polymerase chain reaction (qRT-PCR) method, and the protein expression levels of LC3 are detected using the Western blot method to evaluate the effects of LAF on HSF autophagy. The expression of type I collagen (COL-1), Matrix metalloproteinase-1(MMP-1), AKT pathway, MAPK pathway, and other genes are detected by qRT-PCR to study the anti-aging effects of LAF. From the experimental results, it is found that LAF can delay the aging of HSF at the biochemical, cellular, and molecular biology levels, and can be utilized as a functional food ingredient.

The Role of Different Matrixin Gene Expressions on Cerebral Bleeding among Patients with Deficiency of Coagulation Factor XIII.

Enzymes of the matrixin family could be seen as a critical determinant in the breakdown of the extracellular matrix, cell membrane, and tissue regeneration and are interned in the process of brain bleeding. On the other hand, coagulation factor XIII deficiency is a sporadic hemorrhagic disease with an estimated prevalence of 1 in 1-2 million people. Cerebral hemorrhage is the leading cause of death in these patients. This study investigated the relationship between the expression of matrix metalloproteinase 9 and 2 genes with cerebral hemorrhage in these patients. For this purpose, in this case-control study, by examining the clinical and general findings of the studied patients, the Q-Real-time RT-PCR method was used to quantitatively examine the mRNA levels of matrix metalloproteinase 9 and 2 in 42 patients with hereditary deficiency of coagulation factor XIII, including two groups with and without a history of cerebral hemorrhage (case and control groups, respectively). A comparative method (2-ΔΔCT) was used to check the expression level of the target genes. The GAPDH gene expression levels were used to standardize the expression of the measured matrix metalloproteinase genes. The results showed that bleeding from the umbilical cord was the most common clinical symptom among all patients. High levels of MMP-9 gene expression were observed in 13 patients of the case group (69.99%) and three patients of the control group (11.9%). which showed a significant difference (CI: 2.77-95.3, P=0.001) Patients with coagulation factor XIII deficiency show a wide range of clinical symptoms crucial in screening and diagnosing this group of patients. Based on the results of this study, it seems that the increased expression of the MMP-9 gene is due to polymorphism or inflammation related to the pathogenesis of cerebral hemorrhage in this category of patients. It may be conceivable to diminish this impact by utilizing MMP-9 inhibitors and offering assistance to diminishes these patients' hospitalization and passing rates.

Synovial monocytes from psoriatic and rheumatoid arthritis patients are modulated differently by TNF inhibitors and glucocorticoids: an ex-vivo study.

Synovial monocytes (expressing CD14+CD16+) affect pro-inflammatory responses in the synovium microenvironment of psoriatic arthritis (PsA) and rheumatoid arthritis (RA). The effect of various drugs on those cells was evaluated. Synovial fluid mononuclear cells (SFMCs) from PsA (n=29) and RA (n=11) patients were cultured with biologics or glucocorticoids (GCs). CD14+CD16+ cells were analysed by flow cytometry. TNF secretion was assessed by ELISA and changes in cytokine and matrix metalloproteinase-9 (MMP-9) mRNA by qPCR. TNF inhibitors (i) [adalimumab (ADA) and infliximab (IFX)] significantly reduced the %CD14+CD16+ cells (p<0.04 and p<0.02, respectively) compared to IL-17Ai, IL-12/23i, and GCs in PsA patients' SFMCs. Similarly, those TNFi reduced the %CD14+CD16+ cells (p<0.05 and p<0.02, respectively) compared to IL-6Ri, CD20i and GCs in RA patients' SFMCs. TNFi (ADA p<0.01, IFX p=0.0003), and GCs (p<0.05) reduced TNF levels in PsA patients SFMCs supernatants. IFX down-regulated IL-1β mRNA (p<0.005) while GCs betamethasone (BET) (p<0.01) and methylprednisolone acetate (MPA) (p<0.005) led to IL-1β up-regulation. IFX down-regulated IL-8 and MMP-9 (p<0.01) and up-regulated IL-10 (p<0.005), and GCs did so to a greater extent (for IL-8, BET p<0.0001 and MPA p<0.005, for MMP-9, BET and MPA p<0.0001 and for IL-10, BET and MPA p<0.0001). TNFi but not GCs reduced the inflammatory monocytes. Both TNFi and GCs inhibited TNF secretion but differently modulated IL-1β, IL-8, MMP-9 and IL-10 gene expression. Our data point to TNFi as a modulator of synovial monocytes.

Identification of Novel Compound Heterozygous Variants of MMP9 in Fetus With Metaphyseal Anadysplasia Type 2.

Matrix metalloproteinase 9 (MMP9) is an important member of the matrix metalloproteinase family and plays a key role in balancing extracellular matrix proteins. Studies have shown that the homozygous mutations in MMP9 can lead to metaphyseal anadysplasia type 2 (MANDP2, OMIM#613073). The clinical phenotype of this disease is limited and there were only five reported cases of MANDP2 associated with homozygous MMP9 mutations from three families. In this study, we described a case of a fetus with skeletal system malformation. The main clinical manifestations include the short bilateral femur, absence of right fibula, and curved ipsilateral tibia with short length. Importantly, two novel compound heterozygous variants of the MMP9 gene (NM_004,994.3: c.151C > T and c.929del) were found through the trio whole exome sequencing and Sanger sequencing. This is the first report that identified the compound heterozygous variants of the MMP9 gene associated with metaphyseal dysplasia type 2.

Comprehensive bioinformatic analysis of MMP1 in hepatocellular carcinoma and establishment of relevant prognostic model

Matrix metalloproteinase 1 (MMP1) encodes endopeptidases associated with degradation of multiple components of the extracellular matrix. This function has increasingly been considered to play a major proteolysis role in tumor invasion and metastasis. However, the relationship between MMP1 gene expression, tumor-immune microenvironment and prognosis in hepatocellular carcinoma patients remains mostly unclear. This study focused on a comprehensive analysis of MMP1 in hepatocellular carcinoma, specifically the prognosis and tumor-immune microenvironment. MMP1 expression was analyzed using TCGA database and clinical samples. MMP1 associated mechanisms, pathways, mutations and prognosis in hepatocellular carcinoma were evaluated. We also analyzed the tumor-immune microenvironment and corresponding treatments. Our research demonstrated that MMP1 expression was upregulated in patients with hepatocellular carcinoma and correlated with poor survival. A prognostic model was established and its performance evaluated. We also found and report various correlations between MMP1 and immune-related cells/genes, as well the potential therapeutic agents. These findings indicate that MMP1 can potentially be a promising prognostic biomarker and indicator of the tumor-immune microenvironment status in hepatocellular carcinoma.

The Role of Matrix Metalloproteinase Single-Nucleotide Polymorphisms in the Clinicopathological Properties of Breast Cancer.

(1) Background. Breast cancer is the leading cancer type among women. Despite convenient diagnostics at early stages, there is a need for continuous monitoring to predict more aggressive or recurring breast cancer forms. The evidence suggests that the detection of genetic biomarkers could help in improving disease management and reduce mortality. Matrix metalloproteinases (MMPs) are a large family of enzymes that perform physiologically relevant functions and have the potential properties to be biomarkers for cancer assessment. We aimed to evaluate the contribution and association of single-nucleotide polymorphisms (SNPs) in MMP genes (MMP1, MMP2, MMP3, MMP7, MMP8, MMP9) with clinicopathological breast-cancer features. (2) Methods. In this study, 100 breast cancer patients were genotyped by polymerase chain reaction–restriction fragment length polymorphism methodology (PCR–RFLP). (3) Results. The presence of the MMP7 rs11568818 A allele was associated with lower chances for poorly differentiated breast cancer. The lower possibility for HER2-positive breast cancer was associated with the presence of the MMP9 rs3918242 C allele. (4) Conclusions. These results indicate that MMP7 rs11568818 and MMP9 rs3918242 are potential biomarkers for the anticipation of breast cancer aggressiveness.

A new technique for separating platelet-rich plasma by a copolymer device － without a centrifugation process

BackgroundPlatelet-rich plasma (PRP) is beneficial for clinical applications in various medical fields. Although commercial PRP preparation kits are already available in the market, most of these kits employ centrifugation. MethodsWe used a new cationic copolymer coating on a polyurethane (PU) sponge to promote platelet separation from the blood. This copolymer showed no cytotoxicity against cell viability or hemolysis. We further evaluated the efficiency of the new PRP preparation device by comparing it with that of a commercially available kit (RegenKit-THT). ResultsWe demonstrated that PRP obtained using copolymer device contains high concentrations of platelets and angiogenic growth factors (epidermal growth factor, vascular endothelial growth factor-A, growth differentiation factor 2, and interleukin-8). The separated PRP also displayed beneficial effects on cell migration, angiogenesis, and matrix metalloproteinase gene expression. ConclusionBased on these results, we developed a cationic copolymer-coated PU sponge as a PRP preparation device without the need for any centrifugation.

Low Methylation of Matrix Metalloproteinase 1 (MMP1) is Associated with Preterm Labour in Malaysian Mothers

Preterm births comprise 10.6% of livebirths worldwide and account for 35% of deaths among newborn babies. Understanding DNA methylation may offer basic knowledge in the understanding of pathogenesis of preterm labour. The study was undertaken to determine DNA methylation of matrix metalloproteinase 1 (MMP1) promoter in term and preterm labour using methylation-specific polymerase chain reaction (MSP). Thirty maternal venous blood samples (n=15 each) of term and preterm labour was subjected to bisulfite treatment prior to MSP. This result was then validated using DNA sequencing. Evaluation of the sequencing results by CpG islands analysis was performed using the ClustalW and SPSS software. Primers for MMP1 were located between -1226 and -1378 upstream from the transcription start site (TSS) that consisted five CpG islands. Preterm labour group had significantly lower methylated CpG islands with 39 out of total 75 (52%) compared to the term labour that has 49 out of 75 methylated CpG islands (65.33%) (t=0.694, p&lt;0.05). Methylation occurred in 4 out of 5 methylated CpG islands in the MMP1 promoter where it only involved 2 preterm samples (13.33%) and 7 term samples (46.47%). This data suggested there were significant lower percentage of methylated MMP1 in preterm labour. Higher percentage of methylated MMP1 as observed in the term labour, will probably reduce the expression of MMP1, thus maintaining fibrillar collagen strength on the amniotic membrane and subsequently maintain the pregnancy till term. In conclusion, preterm labour has higher percentage of methylated CpG compared with term labour in MMP1 gene.

Systemic correlation between wound and diabetes

The current article provides complete information on the association between wounding and diabetes, as well as a brief overview of Wound, Diabetic wounds as well as treatment options. The Diabetic wounds require special attention like a major clinical and societal challenge. The need of research is increased because of the delayed and compromised healing. New treatment techniques, Single growth factors, skin substitutes, interleukin stimulators, interleukin inhibitors, matrix metalloproteinase inhibitors, gene and stem cell therapies, extracellular matrix, and angiogenesis are only a few examples. stimulators, show that research on delayed healing is moving quickly. Despite the fact that multiple studies show that diabetes causes slowed wound healing, more precise mechanistic understanding into the components involved, and their parts are still being played needed. This review focuses on cytokine (with growth factors) and other molecular cascades previously unknown components that cause slowed wound healing, as well as molecular pathways and recent advancements in wound healing and treatment. Clinicians and academics working in relevant fields were given a briefing on new innovative knowledge on possible molecular targets and therapeutic techniques, including clinical trials, in this article.

Role of matrix metalloproteinase 9 gene polymorphism as genetic risk factor for lung cancer

Lung cancer (LC) is one of the most incident malignancies worldwide. This study investigated the potential role of matrix metalloproteinase9 gene (MMP9) single nucleotide polymorphisms (SNPs) in Lung cancer patients. The study population was included 75 Iraqi patients with confirmed Lung cancer and 25 healthy people as controls. In this study, the -1562 C/T polymorphism in MMP9 gene was detected by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The genotype distribution results of the -1562 C/T SNP of MMP9 gene have shown no significant differences (p&gt;0.05) between controls (CC: n= 15, 60%; CT: n=9, 36%; TT: n=1, 4%) and Lung cancer patients (CC: n= 44, 58.66%; CT: n=30, 40%; TT: n=1, 1.34%). Results of the association analysis between genotype distribution of the -1562 C/T SNP of MMP9 gene and clinicopathological criteria of cases such as histological grading, TNM staging and lymph node metastasis, had shown no significant association (p&gt;0.05). While analysis of the association between genotype distribution of the -1562 C/T SNP of MMP9 gene and smoking status among patients were statically significant (p&lt;0.05). These results suggested that the SNP in MMP9 gene was involved in lung cancer progression, tissue invasion and metastasis involvement.

Состояние глутатионового звена антиоксидантной защиты организма при фунгицидной интоксикации и коррекции витамином А и расторопшей

Background: Breast cancer (BC) is a malignant breast tumor, which occupies a leading place both in the structure of oncological diseases in women and among the causes of female mortality from malignant neoplasms. The role of genetic factors in the formation of breast cancer is beyond doubt. The aim of the study:To study the role of highly penetrant mutations in BRCA1 and CHEK2 genes in the pattern of associations of matrix metalloproteinase genes (MMP) polymorphism with BC. Materials and methods: To solve the research goal, the following three samples were formed: 26 BC patients with highly penetrant mutations in the BRCA1 (c.5266dup (5382insC), c.68_69del (185delAG), 2080delA) and CHEK2 (I157T)) genes, 332 BC patients without germinal mutations in the BRCA1 (c.5266dup (5382insC), c.68_69del (185delAG), 2080delA, 4153delA), BRCA2 (6174delT) and CHEK2 (I157T) genes and 746 women of the control group. Ten polymorphisms of five matrix metalloproteinase genes (MMP1, MMP2, MMP3, MMP8 and MMP9) were studied. The analysis of associations was carried out by the method of logistic regression. Results: The TT rs1940475 MMP8 genotype in BC patients with highly penetrant mutations in the BRCA1 and CHEK2 genes (3.84%) is 6-7 times less common in comparison with both patients without these mutations (22.80% pperm=0.04) and control group individuals (26.18% ORcov=0.11 95%CIcov 0.01-0.81 pperm=0.03). In BC patients who do not have highly penetrant mutations in the BRCA1 and CHEK2 genes, MMP9 gene polymorphisms are associated with the disease: rs17576 (ORcov=0.81 pperm=0.03), rs2250889 (ORcov=0.61-0.66 pperm=0.03), rs3787268 (ORcov=2.03 pperm=0.04) and nine different haplotypes of the six studied MMP9 loci (pperm&lt;0.05). Conclusion: The rs1940475 MMP8 polymorphic locus is associated with the risk of developing BC in women with highly penetrant mutations in the BRCA1 and CHEK2 genes, and polymorphisms of the MMP9 gene are associated with the disease in women without these mutations.

In vitro effects of Eucommia ulmoides and its active components on the growth, lipid metabolism and collagen metabolism of grass carp (Ctenopharyngodon idellus) hepatocyte and intramuscular fibroblast.

Two experiments were conducted to investigate the in vitro effects of Eucommia ulmoides (E. ulmoides) and its active components on the growth, lipid metabolism and collagen metabolism of grass carp's (Ctenopharyngodon idellus) hepatocytes and intramuscular fibroblasts. In experiments 1 and 2 (Expt. 1, 2), hepatocytes and intramuscular fibroblasts were treated with 2.5, 5, 10, 20, 40 and 80 μg ml-1 of Eucommia bark extract (EBE), Eucommia leaf extract (ELE), pinoresinol diglucoside (PDG), chlorogenic acid (CGA), quercetin (QC) and aucubin (AU) for 24 h, respectively, then the cell growth, lipid and collagen metabolism-related gene expressions were evaluated. The results showed that the cell proliferation rate of hepatocytes and intramuscular fibroblasts was significantly improved by the supplementation of EBE, ELE, CGA, QC and AU. Moreover, triglyceride concentration of hepatocytes was significantly decreased by the EBE, ELE, CGA and QC supplementations compared to the control. Meanwhile, EBE, ELE, CGA, QC and AU supplementations significantly upregulated the relative gene expressions of insulin-like growth factor-1 (igf1), protein kinase B (akt), target of rapamycin (tor) and eukaryotic initiation factor 4E binding protein 1 (4ebp1) in hepatocytes, and ribosomal protein S6 kinase 1 (s6k1) transcription was significantly activated by ELE, CGA and QC supplementations. Nonetheless, phosphatidylinositol 3-kinase (pi3k) was unaffected by any of the supplements. In addition, the mRNA expressions of genes associated with lipid metabolism (peroxisome proliferator activated receptor α pparα, carnitine palmitoyltransferase 1 cpt1, adipose triglyceride lipase atgl, hormone-sensitive lipase hsl, peroxisome proliferator activated receptor γ pparγ) were significantly upregulated by EBE, ELE, CGA and QC. In intramuscular fibroblasts, the EBE, ELE, CGA, QC and AU supplementations significantly increased in vitro hydroxyproline concentrations, promoted the relative expressions of transforming growth factor-β1 (tgfβ1), connective tissue growth factor (ctgf), collagen type I alpha 1/2 chain (col1a1, col1a2), lysine oxidase (lox) and tissue inhibitor of matrix metalloproteinase-2 (timp2), and decreased matrix metalloproteinase-2 (mmp2) gene expression. Also, the gene expressions of drosophila mothers against decapentaplegic protein 2/4 (smad2, smad4) and proline hydroxylase (phd) were significantly upregulated by ELE, CGA, QC and AU supplementations. Based on the present in vitro results of grass carp, EBE, ELE, CGA, QC and AU improved the growth and lipid metabolism (except AU) in hepatocytes, and promoted the collagen deposition in intramuscular fibroblast, which is partly attributed to the signalling pathways of AKT/TOR, PPARα and TGF-β/Smads/CTGF.