刘畅
博士研究生 教授
南京师范大学 生命科学学院
细胞与发育生物学
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- 姓名:刘畅
- 目前身份:在职研究人员
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师
- 职称:高级-教授
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学科领域:
病理学
- 研究兴趣:细胞与发育生物学
刘畅,男,1977年2月出生。南京师范大学生命科学院副院长、博导、教授。2005年7月毕业于南京大学分子医学研究所,获博士学位。2006年3月至2008年4月,在美国密歇根大学生命科学研究所从事博士后研究。近五年来共发表sci论文24篇,其中以通讯作者身份在if>7的顶级学术期刊上发表论文3篇。目前主持国家、省部级科研基金项目12项,金额超过800万。现为中国细胞生物学会医学细胞生物学分会委员,江苏省细胞与发育生物学学会理事暨青年委员会主任,江苏省分子医学生物技术重点实验室主任。被评为第九届江苏省优秀科技工作者(2010),江苏省十大青年科技之星(2012)。
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2012-04-09
刘畅, peixiang zhang, chang liu, chunni zhang, yan zhang, pingping shen, junfeng zhang, chen-yu zhang
febs letters (2005), 579: 1446–1452,-0001,():
-1年11月30日
pgc-1alpha mrna and protein are elevated in islets from multiple animal models of diabetes. overexpression of pgc-1alpha impairs glucose-stimulated insulin secretion (gsis). however, it is not well known which metabolic events lead to upregulation of pgc-1alpha in the beta-cells under pathophysiological condition. in present study, we have investigated effects of chronic hyperlipidemia and hyperglycemia on pgc-1alpha mrna expression in isolated rat islets. isolated rat islets are chronically incubated with 0, 0.2 and 0.4 mm oleic acid/palmitic acid (free fatty acids, ffa) or 5.5 and 25 mm glucose for 72 h. ffa dose-dependently increases pgc-1alpha mrna expression level in isolated islets. ffa also increases pgc-1alpha expression in mouse beta-cell-derived beta tc3 cell line. in contrast, 25 mm glucose decreases expression level of pgc-1alpha. inhibition of pgc-1alpha by sirna improves ffa-induced impairment of gsis in islets. these data suggest that hyperlipidemia and hyperglycemia regulate pgc-1alpha expression in islets differently, and elevated pgc-1alpha by ffa plays an important role in chronic hyperlipidemia-induced beta-cell dysfunction.
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刘畅, zhang, y.*, liu, c.*, zhu, l., jiang, x., chen, qi, liang, jin, s., zhang, p., li, q., wang, d., zeng, k., j., xiang, y., & zhang, c.y.
plos one (2007), 2: e1137.,-0001,():
-1年11月30日
background: oleic acid (oa) stimulates vascular smooth muscle cell (vsmc) proliferation and migration. the precise mechanism is still unclear. we sought to investigate the effects of peroxisome proliferator-activated receptor gamma (ppargamma) coactivator-1 alpha (pgc-1alpha) on oa-induced vsmc proliferation and migration. principal findings: oleate and palmitate, the most abundant monounsaturated fatty acid and saturated fatty acid in plasma, respectively, differently affect the mrna and protein levels of pgc-1alpha in vsmcs. oa treatment resulted in a reduction of pgc-1alpha expression, which may be responsible for the increase in vsmc proliferation and migration caused by this fatty acid. in fact, overexpression of pgc-1alpha prevented oa-induced vsmc proliferation and migration while suppression of pgc-1alpha by sirna enhanced the effects of oa. in contrast, palmitic acid (pa) treatment led to opposite effects. this saturated fatty acid induced pgc-1alpha expression and prevented oa-induced vsmc proliferation and migration. mechanistic study demonstrated that the effects of pgc-1alpha on vsmc proliferation and migration result from its capacity to prevent erk phosphorylation. conclusions: oa and pa regulate pgc-1alpha expression in vsmcs differentially. oa stimulates vsmc proliferation and migration via suppression of pgc-1alpha expression while pa reverses the effects of oa by inducing pgc-1alpha expression. upregulation of pgc-1alpha in vsmcs provides a potential novel strategy in preventing atherosclerosis.
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2012-04-09
刘畅, zhang, y., ba, liu, c., sun, g., ding, l., gao, s., hao, j., yu, z., zhang, zen, k., tong, xiang, & zhang, c.y.
cell res. (2007), 17: 363-73.,-0001,():
-1年11月30日
peroxisome proliferator-activated receptor gamma (ppargamma) coactivator-1 alpha (pgc-1alpha) coactivates multiple transcription factors and regulates several metabolic processes. the current study investigated the role of pgc-1alpha in the induction of apoptosis in human epithelial ovarian cancer cells. the pgc-1alpha mrna level between human ovaries and human ovarian epithelial tumors was examined by quantitative rt-pcr. less pgc-1alpha expression was found in the surface epithelium of malignant tumors compared with normal ovaries. overexpression of pgc-1alpha in human epithelial ovarian cancer cell line ho-8910 induced cell apoptosis through the coordinated regulation of bcl-2 and bax expression. microarray analyses confirmed that pgc-1alpha dramatically affected the apoptosis-related genes in ho-8910 cells. mitochondrial functional assay showed that the induction of apoptosis was through the terminal stage by the release of cytochrome c. furthermore, pgc-1alpha-induced apoptosis was partially, but not completely, blocked by ppargamma antagonist (gw9662), and suppression of ppargamma expression by sirna also inhibited pgc-1alpha-induced apoptosis in ho-8910 cells. these data suggested that pgc-1alpha exerted its effect through a ppargamma-dependent pathway. our findings indicated that pgc-1alpha was involved in the apoptotic signal transduction pathways and downregulation of pgc-1alpha may be a key point in promoting epithelial ovarian cancer growth and progression.
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2012-04-09
刘畅, liu, c., li, s., liu, t., borjigin, j., & lin, j.d.
nature (2007), 447: 477-81.,-0001,():
-1年11月30日
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2012-04-09
刘畅, lin, j.d., liu, c., li, s.
cell cycle (2008), 7: 453-7.,-0001,():
-1年11月30日
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2012-04-09
刘畅, li, s., liu, c., li, n., hao, t., han, hill, d., vidal, m., & lin, j.d.
cell metabolism (2008), 8: 105-17.,-0001,():
-1年11月30日
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2012-04-09
刘畅, li, s., arning, e., liu, c., vitvitsky, v., hernandez, banerjee, r., bottiglieri, t., & lin, j.d.
ajp-endocrinology and metabolism (2009), 296: e543-548.,-0001,():
-1年11月30日
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2012-04-09
刘畅, jiang, x., zhang, y., hou, d., zhu, l., xu, w., ding, qi, sun, g., liu, c., j., zen, k., xiang, c.y.
molecular and cellular endocrinology (2010), 315: 74–80.,-0001,():
-1年11月30日
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2012-04-09
刘畅, qian, j., jiang, f., wang, b., yu, y., zhang, x., yin, z., & liu, c.
j. ethnopharmacol. (2010), 128: 438-445.,-0001,():
-1年11月30日
vessel endothelium injury caused by reactive oxygen species (ros) including h2o2 plays a critical role in the pathogenesis of cardiovascular disorders. therefore, drug targeting ros elimination has highly clinical values in cardiovascular therapy. the plant of radix ophiopogon japonicus is a traditional chinese herbal medicine that has been commonly used for prevention and treatment of cardiovascular diseases for a long history. however, the effective component mediating its beneficial effects remains unknown. in the present study, we investigated the action of ophiopogonin d (op-d), one of the most bioactive components of radix ophiopogon japonicus, in an endothelial injury model induced by h2o2. we found that op-d inhibited mrna levels of antioxidant, inflammatory and apoptotic genes in a dose-dependent manner. h2o2-induced lipid peroxidation and protein carbonylation were reduced by op-d pretreatment. mitochondrial ros generation and cell apoptosis were also attenuated in op-d pretreated cells. in addition, op-d restored cellular total antioxidative capacity and inhibited the release of inflammatory cytokines. furthermore, op-d suppressed the enzymatic activity of catalase, ho-1, and caspases. finally, op-d blocked activation of nf-κb and erk signaling cascades. taken together, our findings provide the first evidence that op-d plays a protective role as an effective antioxidant in h2o2-induced endothelial injury. ophiopogonin d can be therefore developed as a novel drug for the therapy of cardiovascular disorders.
endothelial injury model,, ophiopogonin d,, oxidative stress,, inflammation,, apoptosis
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2012-04-09
刘畅, xu, y., chen, j., yu, x., tao, w., jiang, f., yin, z., & liu, c.
inflamm. res. (2010), 59: 871-877.,-0001,():
-1年11月30日
objective and design: to investigate the potential protective effects of chlorogenic acid (cga) on acute liver injury caused by lipopolysaccharide (lps) in mice. materials and methods: c57bl/6j mice were pretreated with cga (50 mg/kg, intraperitoneally) once per day for five days before an overnight lps challenge (30 mg/kg, intraperitoneally). severity of liver injury was assessed by histological analysis and determination of serum alt and ast levels. expression and activation of key regulators involved in the inflammatory response were respectively determined by real-time rt-pcr and western blotting. results: in contrast to yellow color of the liver in lps-treated mice, cga maintained the normal reddish appearance of the liver. histological analysis indicated that cga attenuated the infiltration of neutrophil cells and the necrosis of hepatocytes. cga also decreased the elevated plasma levels of alt and ast. at the transcriptional level, cga pretreatment suppressed hepatic mrna expression of toll-like receptor 4 (tlr4), tnf-α and nf-κb p65 subunit. in contrast, mrna level of the transcriptional coactivator pgc-1α was restored by cga. finally, cga reduced the phosphorylation of nf-κb p65 subunit in the liver. conclusion: our data suggest that cga has remarkable hepatoprotective effects on lps-induced liver injury and the possible mechanism is related to its anti-inflammatory action.
chlorogenic acid,, liver injury,, lps,, inflammation
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