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GPR15LG regulates psoriasis-like inflammation by down-regulating inflammatory factors on keratinocytes. GPR15LG 通过下调角质形成细胞上的炎症因子来调节牛皮癣样炎症。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR20231347
Caifeng Chen, Renhui Cai, Jun Zhou, Danqun Zhang, Li Chen
{"title":"GPR15LG regulates psoriasis-like inflammation by down-regulating inflammatory factors on keratinocytes.","authors":"Caifeng Chen, Renhui Cai, Jun Zhou, Danqun Zhang, Li Chen","doi":"10.1042/BSR20231347","DOIUrl":"10.1042/BSR20231347","url":null,"abstract":"<p><p>Psoriasis is a common chronic inflammatory skin disease characterized by aberrant proliferation of keratinocytes and infiltration of immune cells. We previously found that GPR15LG protein is highly expressed in psoriasis lesional skin and it positively regulates psoriatic keratinocyte proliferation. Our data also showed that GPR15LG could regulate the activity of NF-κB pathway, which is associated with psoriatic inflammation. In the present study, we demonstrated that Gpr15lg (ortholog of GPR15LG) knockdown attenuated the severity of imiquimod (IMQ)-induced psoriasis-like inflammation in mice. Such an effect was achieved by down-regulating the expression of inflammatory cytokines interleukin (IL)-1α, IL-1β, tumor necrosis factor (TNF)-α and S100A7. Consistently, GPR15LG knockdown in vitro significantly downgraded the expression of inflammatory factors in the cellular model of psoriasis. These results suggested that GPR15LG could be involved in the development of psoriasis by regulating inflammation.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11147810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139929902","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}
引用次数: 0
Expression of Concern: Madecassoside protects retinal pigment epithelial cells against hydrogen peroxide induced oxidative stress and apoptosis through the activation of Nrf2/HO-1 pathway. 表达关注:麦迪卡索苷通过激活 Nrf2/HO-1 通路,保护视网膜色素上皮细胞免受过氧化氢诱导的氧化应激和细胞凋亡。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR-2019-4347_EOC
{"title":"Expression of Concern: Madecassoside protects retinal pigment epithelial cells against hydrogen peroxide induced oxidative stress and apoptosis through the activation of Nrf2/HO-1 pathway.","authors":"","doi":"10.1042/BSR-2019-4347_EOC","DOIUrl":"10.1042/BSR-2019-4347_EOC","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"44 6","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11193161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431297","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}
引用次数: 0
Bioactivity, hemocompatibility, and inflammatory response of calcium incorporated sulfonated polyether ether ketone on mouse-derived bone marrow cells. 钙结合磺化聚醚醚酮对小鼠骨髓细胞的生物活性、血液相容性和炎症反应
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR20232162
Shanmuga Sundar Saravanabhavan, Prabhu Narayanaswamy Venkatesan, Narendranath Jonna, Kamalakannan Vasantha Palaniappan, Zsolt Sarang, Balasubramanian Natesan, Consolato M Sergi
{"title":"Bioactivity, hemocompatibility, and inflammatory response of calcium incorporated sulfonated polyether ether ketone on mouse-derived bone marrow cells.","authors":"Shanmuga Sundar Saravanabhavan, Prabhu Narayanaswamy Venkatesan, Narendranath Jonna, Kamalakannan Vasantha Palaniappan, Zsolt Sarang, Balasubramanian Natesan, Consolato M Sergi","doi":"10.1042/BSR20232162","DOIUrl":"10.1042/BSR20232162","url":null,"abstract":"<p><p>Natural and synthetic polymeric materials, particularly soft and hard tissue replacements, are paramount in medicine. We prepared calcium-incorporated sulfonated polyether-ether ketone (SPEEK) polymer membranes for bone applications. The bioactivity was higher after 21 days of immersion in simulated body fluid (SBF) due to calcium concentration in the membrane. We present a new biomaterial healing system composed of calcium and sulfonated polyether ether ketone (Ca-SPEEK) that can function as a successful biomaterial without causing inflammation when tested on bone marrow cells. The Ca-SPEEK exhibited 13 ± 0.5% clot with low fibrin mesh formation compared to 21 ± 0.5% in SPEEK. In addition, the Ca-SPEEK showed higher protein adsorption than SPEEK membranes. As an inflammatory response, IL-1 and TNF-α in the case of Ca-SPEEK were lower than those for SPEEK. We found an early regulation of IL-10 in the case of Ca-SPEEK at 6 h, which may be attributed to the down-regulation of the inflammatory markers IL-1 and TNF-α. These results evidence the innovative bioactivity of Ca-SPEEK with low inflammatory response, opening venues for bone applications.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11208130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247302","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}
引用次数: 0
Spatiotemporal regulation of the hepatocyte growth factor receptor MET activity by sorting nexins 1/2 in HCT116 colorectal cancer cells. HCT116 大肠癌细胞中肝细胞生长因子受体 MET 活性受分拣 nexins 1/2 的时空调控。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR20240182
Laiyen Garcia Delgado, Amélie Derome, Samantha Longpré, Marilyne Giroux-Dansereau, Ghenwa Basbous, Christine Lavoie, Caroline Saucier, Jean-Bernard Denault
{"title":"Spatiotemporal regulation of the hepatocyte growth factor receptor MET activity by sorting nexins 1/2 in HCT116 colorectal cancer cells.","authors":"Laiyen Garcia Delgado, Amélie Derome, Samantha Longpré, Marilyne Giroux-Dansereau, Ghenwa Basbous, Christine Lavoie, Caroline Saucier, Jean-Bernard Denault","doi":"10.1042/BSR20240182","DOIUrl":"10.1042/BSR20240182","url":null,"abstract":"<p><p>Cumulative research findings support the idea that endocytic trafficking is crucial in regulating receptor signaling and associated diseases. Specifically, strong evidence points to the involvement of sorting nexins (SNXs), particularly SNX1 and SNX2, in the signaling and trafficking of the receptor tyrosine kinase (RTK) MET in colorectal cancer (CRC). Activation of hepatocyte growth factor (HGF) receptor MET is a key driver of CRC progression. In the present study, we utilized human HCT116 CRC cells with SNX1 and SNX2 genes knocked out to demonstrate that their absence leads to a delay in MET entering early endosomes. This delay results in increased phosphorylation of both MET and AKT upon HGF stimulation, while ERK1/2 (extracellular signal-regulated kinases 1 and 2) phosphorylation remains unaffected. Despite these changes, HGF-induced cell proliferation, scattering, and migration remain similar between the parental and the SNX1/2 knockout cells. However, in the absence of SNX1 and SNX2, these cells exhibit increased resistance to TRAIL-induced apoptosis. This research underscores the intricate relationship between intracellular trafficking, receptor signaling, and cellular responses and demonstrates for the first time that the modulation of MET trafficking by SNX1 and SNX2 is critical for receptor signaling that may exacerbate the disease.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11196213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247316","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}
引用次数: 0
UCHL1-dependent control of hypoxia-inducible factor transcriptional activity during liver fibrosis. 肝纤维化过程中 UCHL1 对低氧诱导因子转录活性的依赖性控制
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR20232147
Amy Collins, Rebecca Scott, Caroline L Wilson, Giuseppe Abbate, Gabrielle B Ecclestone, Adam G Albanese, Demi Biddles, Steven White, Jeremy French, John Moir, Wasfi Alrawashdeh, Colin Wilson, Sanjay Pandanaboyana, John S Hammond, Rohan Thakkar, Fiona Oakley, Jelena Mann, Derek A Mann, Niall S Kenneth
{"title":"UCHL1-dependent control of hypoxia-inducible factor transcriptional activity during liver fibrosis.","authors":"Amy Collins, Rebecca Scott, Caroline L Wilson, Giuseppe Abbate, Gabrielle B Ecclestone, Adam G Albanese, Demi Biddles, Steven White, Jeremy French, John Moir, Wasfi Alrawashdeh, Colin Wilson, Sanjay Pandanaboyana, John S Hammond, Rohan Thakkar, Fiona Oakley, Jelena Mann, Derek A Mann, Niall S Kenneth","doi":"10.1042/BSR20232147","DOIUrl":"10.1042/BSR20232147","url":null,"abstract":"<p><p>Liver fibrosis is the excessive accumulation of extracellular matrix proteins that occurs in most types of chronic liver disease. At the cellular level, liver fibrosis is associated with the activation of hepatic stellate cells (HSCs) which transdifferentiate into a myofibroblast-like phenotype that is contractile, proliferative and profibrogenic. HSC transdifferentiation induces genome-wide changes in gene expression that enable the cell to adopt its profibrogenic functions. We have previously identified that the deubiquitinase ubiquitin C-terminal hydrolase 1 (UCHL1) is highly induced following HSC activation; however, the cellular targets of its deubiquitinating activity are poorly defined. Here, we describe a role for UCHL1 in regulating the levels and activity of hypoxia-inducible factor 1 (HIF1), an oxygen-sensitive transcription factor, during HSC activation and liver fibrosis. HIF1 is elevated during HSC activation and promotes the expression of profibrotic mediator HIF target genes. Increased HIF1α expression correlated with induction of UCHL1 mRNA and protein with HSC activation. Genetic deletion or chemical inhibition of UCHL1 impaired HIF activity through reduction of HIF1α levels. Furthermore, our mechanistic studies have shown that UCHL1 elevates HIF activity through specific cleavage of degradative ubiquitin chains, elevates levels of pro-fibrotic gene expression and increases proliferation rates. As we also show that UCHL1 inhibition blunts fibrogenesis in a pre-clinical 3D human liver slice model of fibrosis, these results demonstrate how small molecule inhibitors of DUBs can exert therapeutic effects through modulation of HIF transcription factors in liver disease. Furthermore, inhibition of HIF activity using UCHL1 inhibitors may represent a therapeutic opportunity with other HIF-related pathologies.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11182734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141159986","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}
引用次数: 0
Atox1-cyclin D1 loop activity is critical for survival of tumor cells with inactivated TP53. Atox1-Cyclin D1 环路活动是 TP53 失活肿瘤细胞存活的关键。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-06-26 DOI: 10.1042/BSR20240389
Oleg A Kuchur, Sofya S Pogodaeva, Anna V Shcherbakova, Segrey A Tsymbal
{"title":"Atox1-cyclin D1 loop activity is critical for survival of tumor cells with inactivated TP53.","authors":"Oleg A Kuchur, Sofya S Pogodaeva, Anna V Shcherbakova, Segrey A Tsymbal","doi":"10.1042/BSR20240389","DOIUrl":"10.1042/BSR20240389","url":null,"abstract":"<p><p>The search for relevant molecular targets is one of the main tasks of modern tumor chemotherapy. To successfully achieve this, it is necessary to have the most complete understanding of the functioning of a transcriptional apparatus of the cell, particularly related to proliferation. The p53 protein plays an important role in regulating processes such as apoptosis, repair, and cell division, and the loss of its functionality often accompanies various types of tumors and contributes to the development of chemoresistance. Additionally, the proliferative activity of tumor cells is closely related to the metabolism of transition metals. For example, the metallochaperone Atox1 - a copper transporter protein - acts as a transcription activator for cyclin D1, promoting progression through the G1/S phase of the cell cycle. On the other hand, p53 suppresses cyclin D1 at the transcriptional level, thereby these proteins have divergent effects on cell cycle progression. However, the contribution of the interaction between these proteins to cell survival is poorly understood. This work demonstrates that not only exists a positive feedback loop between Atox1 and cyclin D1 but also that the activity of this loop depends on the status of the TP53 gene. Upon inactivation of TP53 in A549 and HepG2 cell lines, the expression of ATOX1 and CCND1 genes is enhanced, and their suppression in these cells leads to pronounced apoptosis. This fundamental observation may be useful in selecting more precise interventions for combined therapy of p53-negative tumors.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11166628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141174399","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}
引用次数: 0
Temozolomide resistance mechanisms: unveiling the role of translesion DNA polymerase kappa in glioblastoma spheroids in vitro. 替莫唑胺的抗药性机制:揭示体外胶质母细胞瘤球中转运DNA聚合酶Kappa的作用。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-05-29 DOI: 10.1042/BSR20230667
Diego Luis Ribeiro, Marcela Teatin Latancia, Izadora de Souza, Abu-Bakr Adetayo Ariwoola, Davi Mendes, Clarissa Ribeiro Reily Rocha, André Van Helvoort Lengert, Carlos Frederico Martins Menck
{"title":"Temozolomide resistance mechanisms: unveiling the role of translesion DNA polymerase kappa in glioblastoma spheroids in vitro.","authors":"Diego Luis Ribeiro, Marcela Teatin Latancia, Izadora de Souza, Abu-Bakr Adetayo Ariwoola, Davi Mendes, Clarissa Ribeiro Reily Rocha, André Van Helvoort Lengert, Carlos Frederico Martins Menck","doi":"10.1042/BSR20230667","DOIUrl":"10.1042/BSR20230667","url":null,"abstract":"<p><p>Temozolomide (TMZ) is the leading therapeutic agent for combating Glioblastoma Multiforme (GBM). Nonetheless, the persistence of chemotherapy-resistant GBM cells remains an ongoing challenge, attributed to various factors, including the translesion synthesis (TLS) mechanism. TLS enables tumor cells to endure genomic damage by utilizing specialized DNA polymerases to bypass DNA lesions. Specifically, TLS polymerase Kappa (Polκ) has been implicated in facilitating DNA damage tolerance against TMZ-induced damage, contributing to a worse prognosis in GBM patients. To better understand the roles of Polκ in TMZ resistance, we conducted a comprehensive assessment of the cytotoxic, antiproliferative, antimetastatic, and genotoxic effects of TMZ on GBM (U251MG) wild-type (WTE) and TLS Polκ knockout (KO) cells, cultivated as three-dimensional (3D) tumor spheroids in vitro. Initial results revealed that TMZ: (i) induces reductions in GBM spheroid diameter (10-200 µM); (ii) demonstrates significant cytotoxicity (25-200 μM); (iii) exerts antiproliferative effects (≤25 μM) and promotes cell cycle arrest (G2/M phase) in Polκ KO spheroids when compared with WTE counterparts. Furthermore, Polκ KO spheroids exhibit elevated levels of cell death (Caspase 3/7) and display greater genotoxicity (53BP1) than WTE following TMZ exposure. Concerning antimetastatic effects, TMZ impedes invadopodia (3D invasion) more effectively in Polκ KO than in WTE spheroids. Collectively, the results suggest that TLS Polκ plays a vital role in the survival, cell death, genotoxicity, and metastatic potential of GBM spheroids in vitro when subjected to TMZ treatment. While the precise mechanisms underpinning this resistance remain elusive, TLS Polκ emerges as a potential therapeutic target for GBM patients.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875750","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}
引用次数: 0
Induced pluripotent stem cells in cartilage tissue engineering: a literature review. 软骨组织工程中的诱导多能干细胞:文献综述。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-05-29 DOI: 10.1042/BSR20232102
Amani Y Owaidah
{"title":"Induced pluripotent stem cells in cartilage tissue engineering: a literature review.","authors":"Amani Y Owaidah","doi":"10.1042/BSR20232102","DOIUrl":"10.1042/BSR20232102","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a long-term, persistent joint disorder characterized by bone and cartilage degradation, resulting in tightness, pain, and restricted movement. Current attempts in cartilage regeneration are cell-based therapies using stem cells. Multipotent stem cells, such as mesenchymal stem cells (MSCs), and pluripotent stem cells, such as embryonic stem cells (ESCs), have been used to regenerate cartilage. However, since the discovery of human-induced pluripotent stem cells (hiPSCs) in 2007, it was seen as a potential source for regenerative chondrogenic therapy as it overcomes the ethical issues surrounding the use of ESCs and the immunological and differentiation limitations of MSCs. This literature review focuses on chondrogenic differentiation and 3D bioprinting technologies using hiPSCS, suggesting them as a viable source for successful tissue engineering.</p><p><strong>Methods: </strong>A literature search was conducted using scientific search engines, PubMed, MEDLINE, and Google Scholar databases with the terms 'Cartilage tissue engineering' and 'stem cells' to retrieve published literature on chondrogenic differentiation and tissue engineering using MSCs, ESCs, and hiPSCs.</p><p><strong>Results: </strong>hiPSCs may provide an effective and autologous treatment for focal chondral lesions, though further research is needed to explore the potential of such technologies.</p><p><strong>Conclusions: </strong>This review has provided a comprehensive overview of these technologies and the potential applications for hiPSCs in regenerative medicine.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11088306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334615","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}
引用次数: 0
Loci cg06256735 and cg15815843 in the MFAP5 gene regulatory regions are hypomethylated in varicose veins apparently due to active demethylation. MFAP5基因调控区的cg06256735和cg15815843位点在静脉曲张患者中出现低甲基化,这显然是由于主动去甲基化所致。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-05-29 DOI: 10.1042/BSR20231938
Mariya A Smetanina, Valeria A Korolenya, Fedor A Sipin, Igor P Oscorbin, Kseniya S Sevostyanova, Konstantin A Gavrilov, Andrey I Shevela, Maxim L Filipenko
{"title":"Loci cg06256735 and cg15815843 in the MFAP5 gene regulatory regions are hypomethylated in varicose veins apparently due to active demethylation.","authors":"Mariya A Smetanina, Valeria A Korolenya, Fedor A Sipin, Igor P Oscorbin, Kseniya S Sevostyanova, Konstantin A Gavrilov, Andrey I Shevela, Maxim L Filipenko","doi":"10.1042/BSR20231938","DOIUrl":"10.1042/BSR20231938","url":null,"abstract":"<p><p>Varicose vein disease (VVD) is a common health problem worldwide. Microfibril-associated protein 5 (MFAP5) is one of the potential key players in its pathogenesis. Our previous microarray analysis revealed the cg06256735 and cg15815843 loci in the regulatory regions of the MFAP5 gene as hypomethylated in varicose veins which correlated with its up-regulation. The aim of this work was to validate preliminary microarray data, estimate the level of 5-hydroxymethylcytosine (5hmC) at these loci, and determine the methylation status of one of them in different layers of the venous wall. For this, methyl- and hydroxymethyl-sensitive restriction techniques were used followed by real-time PCR and droplet digital PCR, correspondingly, as well as bisulfite pyrosequencing of +/- oxidized DNA. Our microarray data on hypomethylation at the cg06256735 and cg15815843 loci in whole varicose vein segments were confirmed and it was also demonstrated that the level of 5hmC at these loci is increased in VVD. Specifically, among other layers of the venous wall, tunica (t.) intima is the main contributor to hypomethylation at the cg06256735 locus in varicose veins. Thus, it was shown that hypomethylation at the cg06256735 and cg15815843 loci takes place in VVD, with evidence to suggest that it happens through their active demethylation leading to up-regulation of the MFAP5 gene, and t. intima is most involved in this biochemical process.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140921108","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}
引用次数: 0
Expression of Concern: Circular RNA S-7 promotes ovarian cancer EMT via sponging miR-641 to upregulate ZEB1 and MDM2. 关注表达:环状 RNA S-7 通过海绵状 miR-641 上调 ZEB1 和 MDM2 促进卵巢癌 EMT。
IF 4.3 3区 生物学
Bioscience Reports Pub Date : 2024-05-29 DOI: 10.1042/BSR-2020-0825_EOC
{"title":"Expression of Concern: Circular RNA S-7 promotes ovarian cancer EMT via sponging miR-641 to upregulate ZEB1 and MDM2.","authors":"","doi":"10.1042/BSR-2020-0825_EOC","DOIUrl":"10.1042/BSR-2020-0825_EOC","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"44 5","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11065644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854275","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}
引用次数: 0
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