[Effects of rosuvastatin in homocysteine induced mouse vascular smooth muscle cell dedifferentiation and endoplasmic reticulum stress and its mechanisms]
| Autor: | Chang-Zuan, Zhou, Sun-Lei, Pan, Hui, Lin, Li-Ping, Meng, Zheng, Ji, Ju-Fang, Chi, Hang-Yuan, Guo |
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| Rok vydání: | 2018 |
| Předmět: |
X-Box Binding Protein 1
TOR Serine-Threonine Kinases Calcium-Binding Proteins Microfilament Proteins Myocytes Smooth Muscle Membrane Proteins Ribosomal Protein S6 Kinases 70-kDa Cell Dedifferentiation Endoplasmic Reticulum Stress Actins Muscle Smooth Vascular Mice Animals Rosuvastatin Calcium Endoplasmic Reticulum Chaperone BiP Homocysteine Cells Cultured Heat-Shock Proteins |
| Zdroj: | Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology. 34(1) |
| ISSN: | 1000-6834 |
| Popis: | To investigate the effect of rosuvastatin on homocysteine (Hcy) induced mousevascular smooth muscle cells(VSMCs) dedifferentiation and endoplasmic reticulum stress(ERS).VSMCs were co-cultured with Hcy and different concentration of rosuvastatin (0.1, 1.0 and 10 μmol/L). Cytoskeleton remodeling, VSMCs phenotype markers (smooth muscle actin-α, calponin and osteopontin) and ERS marker mRNAs (Herpud1, XBP1s and GRP78) were detected at predicted time. Tunicamycin was used to induce, respectively 4-phenylbutyrate(4-PBA) inhibition, ERS in VSMCs and cellular migration, proliferation and expression of phenotype proteins were analyzed. Mammalian target of rapamycin(mTOR)-P70S6 kinase (P70S6K) signaling agonist phosphatidic acid and inhibitor rapamycin were used in Rsv treated VSMCs. And then mTOR signaling and ERS associated mRNAs were detected.Compared with Hcy group, Hcy+ Rsv group (1.0 and 10 μmol/L) showed enhanced α-SMA and calponin expression (Rosuvastatin could inhibit Hcy induced VSMCs dedifferentiation |
| Databáze: | OpenAIRE |
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