共查询到20条相似文献,搜索用时 15 毫秒
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MicroRNA‐365 Inhibits the Proliferation of Vascular Smooth Muscle Cells by Targeting Cyclin D1 下载免费PDF全文
Myung‐Hyun Kim Onju Ham Se‐Yeon Lee Eunmi Choi Chang Youn Lee Jun‐Hee Park Jiyun Lee Hyang‐Hee Seo Minji Seung Eunhyun Choi Pil‐Ki Min Ki‐Chul Hwang 《Journal of cellular biochemistry》2014,115(10):1752-1761
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MicroRNA‐29b Inhibits Migration and Proliferation of Vascular Smooth Muscle Cells in Neointimal Formation 下载免费PDF全文
Jiyun Lee Soyeon Lim Byeong‐Wook Song Min‐Ji Cha Onju Ham Se‐Yeon Lee Changyoun Lee Jun‐Hee Park Yoonjin Bae Hyang‐Hee Seo Minji Seung Eunhyun Choi Ki‐Chul Hwang 《Journal of cellular biochemistry》2015,116(4):598-608
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Regulation of Mitochondrial Morphology by Positive Feedback Interaction Between PKCδ and Drp1 in Vascular Smooth Muscle Cell 下载免费PDF全文
Soyeon Lim Se‐Yeon Lee Hyang‐Hee Seo Onju Ham Changyeon Lee Jun‐Hee Park Jiyun Lee Minji Seung Ina Yun Sun M. Han Seahyoung Lee Eunhyun Choi Ki‐Chul Hwang 《Journal of cellular biochemistry》2015,116(4):648-660
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Malabaricone C (Mal-C), isolated from nutmeg, is known to exert a variety of pharmacological activities. However, the effect of Mal-C on vascular smooth muscle cells (VSMCs) is unknown. This study examined the effect of Mal-C on proliferation and migration of primary rat aortic smooth muscle cells (RASMCs) as well as its underlying mechanisms. Treatment of RASMCs with Mal-C induced both protein and mRNA expression of heme oxygenase-1 (HO-1) in a dose- and time-dependent manner. Mal-C-mediated HO-1 induction was inhibited by treatment with actinomycin D or by cycloheximide. SB203580 (a p38 inhibitor), SP600125 (a JNK inhibitor), U0126 (a MEK inhibitor), and N-acetylcysteine (NAC, an antioxidant) did not suppress Mal-C-induced HO-1 expression. In contrast, LY294002 (a PI3K inhibitor) blocked Mal-C-induced HO-1 expression. Moreover, RASMCs treated with Mal-C exhibited activation of AKT in a dose- and time-dependent manner. Treatment of RASMCs with Mal-C increased nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2), which is a key regulator of HO-1 expression, and this translocation was also inhibited by LY294002. Consistent with the notion that HO-1 has protective effects against VSMCs, Mal-C remarkably inhibited platelet-derived growth factor (PDGF)-induced proliferation and migration of RASMCs. However, inhibition of HO-1 significantly attenuated the inhibitory effects of Mal-C on PDGF-induced proliferation and migration of RASMCs. Taken together, these findings suggest that Mal-C could suppress PDGF-induced proliferation and migration of RASMCs through Nrf2 activation and subsequent HO-1 induction via the PI3K/AKT pathway, and may be a potential HO-1 inducer for preventing or treating vascular diseases. 相似文献
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Sang‐Wook Kang Min Soo Kim Hyun‐Sung Kim Yunho Kim Daekeun Shin Jung Han Yoon Park Prof. Young‐Hee Kang PhD 《Journal of cellular biochemistry》2013,114(2):398-408
Obesity instigates various health problems such as atherosclerosis, diabetes, and cancer. Resistin, an adipose tissue‐specific secretory adipokine, operates endocrine functions through increasing insulin resistance. Vascular smooth muscle cells (SMC) migrate into the subendothelial space and proliferate, thereby contributing to neointimal formation in atherosclerosis and restenosis. The aim of this study was to elucidate whether celastrol obtained from Tripterygium wilfordii Hook, inhibited human aortic SMC migration. Celastrol capable of antagonizing inflammatory responses attenuated the resistin secretion from THP‐1‐derived macrophages. The macrophage‐conditioned media promoted SMC proliferation and MMP‐2 production, which was dampened by 10–100 nM celastrol. Celastrol encumbered the SMC migration in response to 50 ng/ml resistin, concomitant with the inhibition of induction of connective tissue growth factor and collagen I/IV. In addition, celastrol disabled human aortic SMC exposed to resistin from migrating. The resistin‐induced shedding of integrin β2/β3 expression was demoted by celastrol, thereby contributing to the inhibition of collagen matrix‐SMC interaction. Next, resistin‐induced Toll‐like receptor‐4 (TLR‐4) expression was abrogated by celastrol, indicating that TLR‐4 was the resistin signaling receptor that was blocked by celastrol. Collectively, these results demonstrate that anti‐inflammatory celastrol blunted the macrophage secretion of the adipokine resistin, and suppressed the SMC migration by disturbing the interaction between SMC and intimal collagen matrix. Therefore, celastrol may inhibit atherogenic migration of vascular SMC upon resistin loading by intimal macrophages within atherosclerotic lesions. J. Cell. Biochem. 114: 398–408, 2013. © 2012 Wiley Periodicals, Inc. 相似文献