FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890986550> ?p ?o ?g. }

• W2890986550 abstract "Background The osteogenic differentiation of vascular smooth muscle cell (VSMCs) is important for the development of vascular calcification (VC), particularly in diabetes. Exosomes derived from Mesenchymal Stromal Cells (MSCs) are effective against cardiovascular diseases, yet their role in VC remains unclear. Advanced glycation end products (AGEs) inhibit bone marrow stromal cell osteogenesis by targeting osteogenesis-associated genes. Thus, we investigated the role of exosomes derived from MSCs pretreated with AGE-BSA in VC and its potential mechanisms. Methods Primary VSMCs and MSCs were isolated from the aorta and bone marrow of Sprague-Dawley rats, respectively. VSMCs were cultured with AGEs-BSA to induce osteogenic differentiation. Exosomes were harvested from MSCs by ultracentrifugation. MSCs and VSMCs were cocultured in Transwells, and exosomes were added to VSMC culture medium to assess their effects on osteogenic differentiation. Double luciferase reporter assay was applied to confirm that miR-146a directly targets the 3' UTR of the thioredoxin-interacting protein (TXNIP) gene. Results Pretreatment of VSMCs with AGEs-BSA increased the expression of thioredoxin-interacting protein (TXNIP) by inhibiting that of miR-146a, resulting in enhanced ROS production and VSMC calcification. By contrast, the expression of miR-146a in MSCs was increased by AGEs-BSA treatment. Thus, miR-146a was transferred from AGEs-BSA-pretreated or miR-146a-transfected MSCs to VSMCs via exosomes. After coculture with miR-146a-containing exosomes, the AGEs-BSA-mediated increase in VSMC calcification was diminished, accompanied by decreased TXNIP expression and ROS production. Furthermore, TXNIP overexpression counteracted the anti-calcification effects of MSC-derived miR-146a-containing exosomes. In addition, TXNIP was identified as a target gene of miR-146a, and the results of double luciferase reporter assay confirmed that TXNIP was the direct target gene of miR-146a. Conclusions Exosomes secreted by MSCs pretreated with AGE-BSA contained a high level of miR-146a, which was transferred to VSMCs and inhibited AGEs-BSA-induced calcification in a TXNIP-dependent manner. Thus, miR-146a-containing exosomes may be a potential therapeutic target for VC." @default.
• W2890986550 created "2018-09-27" @default.
• W2890986550 creator A5018863416 @default.
• W2890986550 creator A5032841164 @default.
• W2890986550 creator A5042784783 @default.
• W2890986550 creator A5044079093 @default.
• W2890986550 creator A5084420811 @default.
• W2890986550 date "2018-09-21" @default.
• W2890986550 modified "2023-10-16" @default.
• W2890986550 title "Exosomes Derived From Mesenchymal Stromal Cells Pretreated With Advanced Glycation End Product-Bovine Serum Albumin Inhibit Calcification of Vascular Smooth Muscle Cells" @default.
• W2890986550 cites W1856542144 @default.
• W2890986550 cites W1877686344 @default.
• W2890986550 cites W1967707249 @default.
• W2890986550 cites W1972873840 @default.
• W2890986550 cites W1993760584 @default.
• W2890986550 cites W1995762247 @default.
• W2890986550 cites W1999908383 @default.
• W2890986550 cites W2001614846 @default.
• W2890986550 cites W2006202614 @default.
• W2890986550 cites W2034439984 @default.
• W2890986550 cites W2034712955 @default.
• W2890986550 cites W2037786457 @default.
• W2890986550 cites W2055424631 @default.
• W2890986550 cites W2062011959 @default.
• W2890986550 cites W2074420452 @default.
• W2890986550 cites W2089643746 @default.
• W2890986550 cites W2090335937 @default.
• W2890986550 cites W2096024580 @default.
• W2890986550 cites W2100454719 @default.
• W2890986550 cites W2101995250 @default.
• W2890986550 cites W2104776720 @default.
• W2890986550 cites W2105731956 @default.
• W2890986550 cites W2117412164 @default.
• W2890986550 cites W2143115805 @default.
• W2890986550 cites W2147663252 @default.
• W2890986550 cites W2148300997 @default.
• W2890986550 cites W2154502936 @default.
• W2890986550 cites W2154833555 @default.
• W2890986550 cites W2161537829 @default.
• W2890986550 cites W2177788064 @default.
• W2890986550 cites W2191284640 @default.
• W2890986550 cites W2252804625 @default.
• W2890986550 cites W2278098644 @default.
• W2890986550 cites W2514378411 @default.
• W2890986550 cites W2540434752 @default.
• W2890986550 cites W2559041587 @default.
• W2890986550 cites W2576467391 @default.
• W2890986550 cites W2593816186 @default.
• W2890986550 cites W2596353598 @default.
• W2890986550 cites W2607847191 @default.
• W2890986550 cites W2619411792 @default.
• W2890986550 cites W2729857852 @default.
• W2890986550 cites W2740264541 @default.
• W2890986550 cites W2747746542 @default.
• W2890986550 cites W2755660270 @default.
• W2890986550 cites W2760727189 @default.
• W2890986550 cites W2763871345 @default.
• W2890986550 cites W2765668521 @default.
• W2890986550 cites W2765843771 @default.
• W2890986550 cites W2769740268 @default.
• W2890986550 cites W2770602573 @default.
• W2890986550 cites W2770704239 @default.
• W2890986550 cites W2770992939 @default.
• W2890986550 cites W2775295652 @default.
• W2890986550 cites W2776806294 @default.
• W2890986550 cites W2782372577 @default.
• W2890986550 cites W2782582452 @default.
• W2890986550 cites W2783486838 @default.
• W2890986550 cites W2783976065 @default.
• W2890986550 cites W2790679239 @default.
• W2890986550 cites W2793749852 @default.
• W2890986550 cites W2804706621 @default.
• W2890986550 doi "https://doi.org/10.3389/fendo.2018.00524" @default.
• W2890986550 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6160580" @default.
• W2890986550 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30298051" @default.
• W2890986550 hasPublicationYear "2018" @default.
• W2890986550 type Work @default.
• W2890986550 sameAs 2890986550 @default.
• W2890986550 citedByCount "30" @default.
• W2890986550 countsByYear W28909865502019 @default.
• W2890986550 countsByYear W28909865502020 @default.
• W2890986550 countsByYear W28909865502021 @default.
• W2890986550 countsByYear W28909865502022 @default.
• W2890986550 countsByYear W28909865502023 @default.
• W2890986550 crossrefType "journal-article" @default.
• W2890986550 hasAuthorship W2890986550A5018863416 @default.
• W2890986550 hasAuthorship W2890986550A5032841164 @default.
• W2890986550 hasAuthorship W2890986550A5042784783 @default.
• W2890986550 hasAuthorship W2890986550A5044079093 @default.
• W2890986550 hasAuthorship W2890986550A5084420811 @default.
• W2890986550 hasBestOaLocation W28909865501 @default.
• W2890986550 hasConcept C104317684 @default.
• W2890986550 hasConcept C134018914 @default.
• W2890986550 hasConcept C145059251 @default.
• W2890986550 hasConcept C147990577 @default.
• W2890986550 hasConcept C16930146 @default.
• W2890986550 hasConcept C185592680 @default.
• W2890986550 hasConcept C198826908 @default.
• W2890986550 hasConcept C203014093 @default.
• W2890986550 hasConcept C20518536 @default.

• next