BMC Molecular and Cell Biology最新文献

{"title":"Mesenchymal stem cells- derived exosomes inhibit the expression of Aquaporin-5 and EGFR in HCT-116 human colorectal carcinoma cell line.","authors":"Amir Hossein Mansourabadi,&nbsp;Azin Aghamajidi,&nbsp;Fatemeh Faraji,&nbsp;Shirin Taghizadeh,&nbsp;Leila Mohamed Khosroshahi,&nbsp;Mona Bahramkiya,&nbsp;Maryam Azimi","doi":"10.1186/s12860-022-00439-0","DOIUrl":"https://doi.org/10.1186/s12860-022-00439-0","url":null,"abstract":"<p><strong>Background: </strong>Aquaporins are channel proteins, form pores in the membrane of biological cells to facilitate the transcellular and transepithelial water movement. The role of Aquaporins in carcinogenesis has become an area of interest. In this study, we aimed to investigate the effects of adipose-derived mesenchymal stem cells secreted exosomes on the expression of aquaporin 5 and EGFR genes in the HCT-116 tumor cell line.</p><p><strong>Methods and results: </strong>Surface antigenic profile of Ad-MSCs was evaluated using specific markers. Exosomes were purified from the Ad-MSc supernatant while the quality and the shape of isolated exosomes were assessed by western blot and transmission electron microscopy (TEM) respectively. HCT-116 cells were co-cultured with MSC-conditioned medium (MSC-CM) and/or with 100 μg/ml of MSC-derived exosomes for 48 h and. Real-time PCR was carried out to determine the expression of aquaporin5 and EGFR in HCT-116. Relative expression levels were calculated using the 2^-ΔΔct method. Our result showed that AQP5 and EGFR mRNA levels were significantly reduced in CM and/or exosomes treated HCT116 compare to the control group (P-value < 0.05).</p><p><strong>Conclusion: </strong>The current study showed that MSC derived exosomes could inhibit expression of two important molecules involved in tumor progression. Hence it seems MSCs-derived exosomes may hold a hopeful future as drug delivery vehicles which need the furtherer investigation.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9479423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40363676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In silico prediction, characterization, docking studies and molecular dynamics simulation of human p97 in complex with p37 cofactor.","authors":"Abolfazl Mirzadeh,&nbsp;George Kobakhidze,&nbsp;Rémi Vuillemot,&nbsp;Slavica Jonic,&nbsp;Isabelle Rouiller","doi":"10.1186/s12860-022-00437-2","DOIUrl":"https://doi.org/10.1186/s12860-022-00437-2","url":null,"abstract":"<p><strong>Background: </strong>The AAA + ATPase p97 is an essential unfoldase/segragase involved in a multitude of cellular processes. It functions as a molecular machine critical for protein homeostasis, homotypic membrane fusion events and organelle biogenesis during mitosis in which it acts in concert with cofactors p47 and p37. Cofactors assist p97 in extracting and unfolding protein substrates through ATP hydrolysis. In contrast to other p97's cofactors, p37 uniquely increases the ATPase activity of p97. Disease-causing mutations in p97, including mutations that cause neurodegenerative diseases, increase cofactor association with its N-domain, ATPase activity and improper substrate processing. Upregulation of p97 has also been observed in various cancers. This study aims towards the characterization of the protein-protein interaction between p97 and p37 at the atomic level. We defined the interacting residues in p97 and p37. The knowledge will facilitate the design of unique small molecules inhibiting this interaction with insights into cancer therapy and drug design.</p><p><strong>Results: </strong>The homology model of human p37 UBX domain was built from the X-ray crystal structure of p47 C-terminus from rat (PDB code:1S3S, G) as a template and assessed by model validation analysis. According to the HDOCK, HAWKDOCK, MM-GBSA binding free energy calculations and Arpeggio, we found that there are several hydrophobic and two hydrogen-bonding interactions between p37 UBX and p97 N-D1 domain. Residues of p37 UBX predicted to be involved in the interactions with p97 N-D1 domain interface are highly conserved among UBX cofactors.</p><p><strong>Conclusion: </strong>This study provides a reliable structural insight into the p37-p97 complex binding sites at the atomic level though molecular docking coupled with molecular dynamics simulation. This can guide the rational design of small molecule drugs for inhibiting mutant p97 activity.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9464413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33458160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activated TRPA1 plays a therapeutic role in TMZ resistance in glioblastoma by altering mitochondrial dynamics.","authors":"Hao Chen,&nbsp;Chunlin Li,&nbsp;Haiyang Hu,&nbsp;Bin Zhang","doi":"10.1186/s12860-022-00438-1","DOIUrl":"https://doi.org/10.1186/s12860-022-00438-1","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GBM) represents nearly one-half of primary brain tumors, and the median survival of patients with GBM is only 14.6 months. Surgery followed by radiation with concomitant temozolomide (TMZ) therapy is currently the standard of care. However, an increasing body of evidence suggests that GBM acquires resistance to TMZ, compromising the effect of the drug. Thus, further exploration into the mechanism underlying this resistance is urgently needed. Studies have demonstrated that TMZ resistance is associated with DNA damage, followed by altered reactive oxygen species (ROS) production in mitochondria. Studies have also showed that Ca²⁺-related transient receptor potential (TRP) channels participate in GBM cell proliferation and metastasis, but the detailed mechanism of their involvement remain to be studied. The present study demonstrates the role played by TRPA1 in TMZ resistance in GBM and elucidates the mechanism of resistance.</p><p><strong>Methods: </strong>U251 and SHG-44 cells were analyzed in vitro. A CCK-8 assay was performed to verify the effect of TMZ toxicity on GBM cells. Intracellular ROS levels were detected by DCFH-DA assay. A MitoSOX Red assay was performed to determine the mitochondrial ROS levels. Intracellular Ca²⁺ levels in the cells were determined with a Fluo-4 AM calcium assay kit. Intracellular GSH levels were determined with GSH and GSSG Assay Kit. MGMT protein, Mitochondrial fission- and fusion-, apoptosis- and motility-related protein expression was detected by western blot assay. A recombinant lentiviral vector was used to infect human U251 cells to overexpress shRNA and generate TRPA1^+/+ and negative control cells. All experiments were repeated.</p><p><strong>Results: </strong>In the U251 and SHG-44 cells, TMZ induced a small increase in the apoptosis rate and intracellular and mitochondrial ROS levels. The expression of antioxidant genes and antioxidants in these cells was also increased by TMZ. However, pretreatment with a TRPA1 agonist significantly decreased the level of antioxidant gene and antioxidants expression and enhanced intracellular and mitochondrial ROS levels. Also TMZ induced the level of MGMT protein increased, and pretreatment with a TRPA1 agonist decreased the MGMT expression. Moreover, Ca²⁺ influx, mitochondrial damage and cell apoptosis were promoted, and the balance between mitochondrial fission and fusion protein expression was disrupted in these GBM cells. Pretreatment with a TRPA1 inhibitor slightly enhanced the level of antioxidant gene expression and reduced the apoptosis rate. TRPA1 gene overexpression in the U251 cells was similar to that after inhibitor intervention, confirming the aforementioned experimental results.</p><p><strong>Conclusion: </strong>The present study proved that activating TRPA1 in glioma cells, which leads to mitochondrial damage and dysfunction and ultimately to apoptosis, may decreas","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40621772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of an inhibitor of the SHH signaling pathway on endometrial cells of patients with endometriosis.","authors":"Yanan He, J Wang, Xinyan Jiang, Jianhua Gao, Yan Cheng, Tian Liang, Jun Zhou, Liyuan Sun, Guangmei Zhang","doi":"10.1186/s12860-022-00426-5","DOIUrl":"10.1186/s12860-022-00426-5","url":null,"abstract":"<p><strong>Background: </strong>Endometriosis is one of the most common gynecological diseases, and seriously reduces the quality of life of patients. However, the pathogenesis of this disease is unclear. Therefore, more studies are needed to elucidate its pathogenesis. Our previous publication found that the Sonic Hedgehog (SHH) signaling pathway was activated in endometriosis. This study tested whether SHH signaling in endometrial stromal cells (ESCs) was critical for the pathogenesis of endometriosis.</p><p><strong>Methods: </strong>To examine the effect of inhibiting the SHH signaling pathway on endometriosis, we first isolated ESCs from eutopic endometrial tissues of patients with or without endometriosis and identified the extracted cells by morphological observation and immunofluorescence. Then, we treated ESCs with the GLI inhibitor GANT61 and used CCK-8, wound healing and invasion assays to detect cell activities, such as proliferation, invasion and metastasis. Furthermore, we detected the expression of key proteins and proliferation markers of the SHH signaling pathway in the lesions of nude mice using immunochemistry.</p><p><strong>Results: </strong>We demonstrated that higher concentrations of GANT61 decreased the proliferation rate and migration distance of ESCs. We observed that GANT61 inhibited the invasion of ESCs. In addition, blockage of the SHH signaling pathway significantly reduced cell proliferation in vitro.</p><p><strong>Conclusions: </strong>Our study suggested that inhibition of the SHH pathway is involved in cell proliferation and invasive growth in the pathogenesis of endometriosis.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9356504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40589998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lack of Nck1 protein and Nck-CD3 interaction caused the increment of lipid content in Jurkat T cells.","authors":"Aussanee Nuiyen,&nbsp;Araya Rattanasri,&nbsp;Piyamaporn Wipa,&nbsp;Sittiruk Roytrakul,&nbsp;Apirath Wangteeraprasert,&nbsp;Sutatip Pongcharoen,&nbsp;Jutaporn Ngoenkam","doi":"10.1186/s12860-022-00436-3","DOIUrl":"https://doi.org/10.1186/s12860-022-00436-3","url":null,"abstract":"<p><strong>Background: </strong>The non-catalytic region of tyrosine kinase (Nck) is an adaptor protein, which is ubiquitously expressed in many types of cells. In T cells, the Nck1 isoform promotes T cell receptor signalling as well as actin polymerisation. However, the role of Nck1 in the lipid metabolism in T cells is unknown. In the present study, we investigated the effect of the Nck1 protein and Nck-CD3 interaction on lipid metabolism and on the physical and biological properties of Jurkat T cells, using a newly developed holotomographic microscope.</p><p><strong>Results: </strong>Holotomographic microscopy showed that Nck1-knocked-out cells had membrane blebs and were irregular in shape compared to the rounded control cells. The cell size and volume of Nck1-deficient cells were comparable to those of the control cells. Nck1-knocked-out Jurkat T cells had a greater lipid content, lipid mass/cell mass ratio, and lipid metabolite levels than the control cells. Interestingly, treatment with a small molecule, AX-024, which inhibited Nck-CD3 interaction, also caused an increase in the lipid content in wild-type Jurkat T cells, as found in Nck1-deficient cells.</p><p><strong>Conclusions: </strong>Knockout of Nck1 protein and hindrance of the Nck-CD3 interaction cause the elevation of lipid content in Jurkat T cells.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9330638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40571220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromatin structure in cancer.","authors":"Meng Wang,&nbsp;Benjamin D Sunkel,&nbsp;William C Ray,&nbsp;Benjamin Z Stanton","doi":"10.1186/s12860-022-00433-6","DOIUrl":"https://doi.org/10.1186/s12860-022-00433-6","url":null,"abstract":"<p><p>In the past decade, we have seen the emergence of sequence-based methods to understand chromosome organization. With the confluence of in situ approaches to capture information on looping, topological domains, and larger chromatin compartments, understanding chromatin-driven disease is becoming feasible. Excitingly, recent advances in single molecule imaging with capacity to reconstruct \"bulk-cell\" features of chromosome conformation have revealed cell-to-cell chromatin structural variation. The fundamental question motivating our analysis of the literature is, can altered chromatin structure drive tumorigenesis? As our community learns more about rare disease, including low mutational frequency cancers, understanding \"chromatin-driven\" pathology will illuminate the regulatory structures of the genome. We describe recent insights into altered genome architecture in human cancer, highlighting multiple pathways toward disruptions of chromatin structure, including structural variation, noncoding mutations, metabolism, and de novo mutations to architectural regulators themselves. Our analysis of the literature reveals that deregulation of genome structure is characteristic in distinct classes of chromatin-driven tumors. As we begin to integrate the findings from single cell imaging studies and chromatin structural sequencing, we will be able to understand the diversity of cells within a common diagnosis, and begin to define structure-function relationships of the misfolded genome.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9331575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40571221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"lncRNA ACTA2-AS1 predicts malignancy and poor prognosis of triple-negative breast cancer and regulates tumor progression via modulating miR-532-5p.","authors":"Yi Peng,&nbsp;Xiaoxi Huang,&nbsp;Hongmei Wang","doi":"10.1186/s12860-022-00432-7","DOIUrl":"https://doi.org/10.1186/s12860-022-00432-7","url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of ACTA2-AS1 and miR-532-5p and their functions in various cancers have been widely reported. Their potential of serving as biomarkers in triple-negative breast cancer (TNBC) remains unknown. This study aimed to evaluate the function of ACTA2-AS1 and miR-532-5p and their potential of serving as biomarkers in TNBC.</p><p><strong>Results: </strong>The TNBC tissues were collected from 119 patients, where the reduced level of ACTA2-AS1 and increased level of miR-532-5p were observed by PCR and showed a significantly negative correlation (P <  0.001). Both ACTA2-AS1 and miR-532-5p were closely associated with the malignant development and poor prognosis of TNBC patients. Moreover, in TNBC cell, overexpressing ACTA2-AS1 was found to suppress cell proliferation and metastasis, which was reversed by the upregulation of miR-532-5p.</p><p><strong>Conclusions: </strong>ACTA2-AS1 and miR-532-5p could act as biomarkers of TNBC predicting the progression and prognosis of patients. ACTA2-AS1 served as a tumor suppressor of TNBC which was mediated by miR-532-5p.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9327331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40550056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDPsBind: a repository of binding sites for intrinsically disordered proteins complexes with known 3D structures.","authors":"CanZhuang Sun,&nbsp;YongE Feng,&nbsp;GuoLiang Fan","doi":"10.1186/s12860-022-00434-5","DOIUrl":"https://doi.org/10.1186/s12860-022-00434-5","url":null,"abstract":"<p><strong>Background: </strong>Intrinsically disordered proteins (IDPs) lack a stable three-dimensional structure under physiological conditions but play crucial roles in many biological processes. Intrinsically disordered proteins perform various biological functions by interacting with other ligands.</p><p><strong>Results: </strong>Here, we present a database, IDPsBind, which displays interacting sites between IDPs and interacting ligands by using the distance threshold method in known 3D structure IDPs complexes from the PDB database. IDPsBind contains 9626 IDPs complexes and 880 intrinsically disordered proteins verified by experiments. The current release of the IDPsBind database is defined as version 1.0. IDPsBind is freely accessible at http://www.s-bioinformatics.cn/idpsbind/home/ .</p><p><strong>Conclusions: </strong>IDPsBind provides more comprehensive interaction sites for IDPs complexes of known 3D structures. It can not only help the subsequent studies of the interaction mechanism of intrinsically disordered proteins but also provides a suitable background for developing the algorithms for predicting the interaction sites of intrinsically disordered proteins.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9327236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40650413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic study of single-cell isolation from musculoskeletal tissues for single-sell sequencing.","authors":"Manman Gao,&nbsp;Peng Guo,&nbsp;Xizhe Liu,&nbsp;Penghui Zhang,&nbsp;Zhongyuan He,&nbsp;Liru Wen,&nbsp;Shaoyu Liu,&nbsp;Zhiyu Zhou,&nbsp;Weimin Zhu","doi":"10.1186/s12860-022-00429-2","DOIUrl":"https://doi.org/10.1186/s12860-022-00429-2","url":null,"abstract":"<p><strong>Background: </strong>The single-cell platform provided revolutionary way to study cellular biology. Technologically, a sophistic protocol of isolating qualified single cells would be key to deliver to single-cell platform, which requires high cell viability, high cell yield and low content of cell aggregates or doublets. For musculoskeletal tissues, like bone, cartilage, nucleus pulposus and tendons, as well as their pathological state, which are tense and dense, it's full of challenge to efficiently and rapidly prepare qualified single-cell suspension. Conventionally, enzymatic dissociation methods were wildly used but lack of quality control. In the present study, we designed the rapid cycling enzymatic processing method using tissue-specific enzyme cocktail to treat different human pathological musculoskeletal tissues, including degenerated nucleus pulposus (NP), ossifying posterior longitudinal ligament (OPLL) and knee articular cartilage (AC) with osteoarthritis aiming to rapidly and efficiently harvest qualified single-cell suspensions for single-cell RNA-sequencing (scRNA-seq).</p><p><strong>Results: </strong>We harvested highly qualified single-cell suspensions from NP and OPLL with sufficient cell numbers and high cell viability using the rapid cycling enzymatic processing method, which significantly increased the cell viability compared with the conventional long-time continuous digestion group (P < 0.05). Bioanalyzer trace showed expected cDNA size distribution of the scRNA-seq library and a clear separation of cellular barcodes from background partitions were verified by the barcode-rank plot after sequencing. T-SNE visualization revealed highly heterogeneous cell subsets in NP and OPLL. Unfortunately, we failed to obtain eligible samples from articular cartilage due to low cell viability and excessive cell aggregates and doublets.</p><p><strong>Conclusions: </strong>In conclusion, using the rapid cycling enzymatic processing method, we provided thorough protocols for preparing single-cell suspensions from human musculoskeletal tissues, which was timesaving, efficient and protective to cell viability. The strategy would greatly guarantee the cell heterogeneity, which is critical for scRNA-seq data analysis. The protocol to treat human OA articular cartilage should be further improved.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9327421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40541701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiogenic ability of human endothelial cells was decreased following senescence induction with hydrogen peroxide: possible role of vegfr-2/akt-1 signaling pathway.","authors":"Nesa Janamo Berenjabad,&nbsp;Vahid Nejati,&nbsp;Jafar Rezaie","doi":"10.1186/s12860-022-00435-4","DOIUrl":"https://doi.org/10.1186/s12860-022-00435-4","url":null,"abstract":"<p><strong>Background: </strong>Many attempts are used to discover mechanisms driving impaired angiogenesis in age-related diseases. Angiogenesis is highly regulated by different signaling pathways. Here, we investigated the angiogenesis potential of human endothelial cells (ECs) upon exposure to hydrogen peroxide (H₂O₂), a cellular senescent factor.</p><p><strong>Results: </strong>Data showed that the wound healing rate of HUVECs decreased upon incubation with H₂O₂ (P < 0.05). LOX activity and NO production were decreased in H₂O₂ treated cells (P < 0.05). Expression of miR-126 and VEGFR-2 up-regulated, while expression of miR-373 and HSP-70 up = regulated in H₂O₂ -induced cells (P < 0.05). In addition, we found that protein levels of p-Akt-1, VCAM-1, MMP-9, and IL-6 decreased in treated cells (P < 0.05).</p><p><strong>Conclusions: </strong>Our data showed that H₂O₂ reduced the angiogenic response of HUVECs in vitro, which may be due to impairment of the VEGFR-2 signaling pathway.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40648823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}