李晖
一直从事心血管疾病尤其是缺血性心脏病发病的分子机制及心肌保护因素作用的研究。
个性化签名
- 姓名:李晖
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
生物化学
- 研究兴趣:一直从事心血管疾病尤其是缺血性心脏病发病的分子机制及心肌保护因素作用的研究。
李晖,女,博士,博士生导师。生物化学与分子生物学教研室副主任。1994年获医学遗传学硕士学位,1997年获医学博士学位。1997年9月至1999年12月哈尔滨医科大学临床药理学博士后流动站进行博士后工作,1999年12月完成博士后研究报告,研究课题:反义PAI-1核酸基因治疗的研究。2000年1月到美国耶鲁大学细胞与分子生理学系和LSU医学中心做博士后工作。2003年1月结束访问与科研工作,回国任教。
自1994年以来李晖教授一直从事心血管疾病尤其是缺血性心脏病发病的分子机制及心肌保护因素作用的研究。2000年1月进入美国耶鲁大学生理系,主要从事肾小管上皮细胞钠离子通道(ENaC)基因表达和功能调节、A6细胞系ENaC磷酸化调节机制的研究和人类胎盘组织中血管内皮细胞、成纤维细胞、血管周细胞中基因表达差异及低氧条件下表达调控的研究。并相继在J General Physiology、Placenta 、Hypertension in pregnancy等学术刊物上发表多篇研究论文。1999年4月和2001年分别获得黑龙江省科技进步二等奖和国家教育部科学技术进步二等奖。
先后主持国家自然基金项目《SCN5A基因突变与克山病易感性的研究》、黑龙江省教育厅海外学人重点项目资助《大鼠缺血性心律失常及Na+通道基因SCN5A的研究》、黑龙江省自然科学基金项目《缺氧大鼠心肌细胞Na+通道基因SCN5A表达的研究》及市科技局项目《抗心律失常药物靶点miRNA与Na+通道作用机制的研究》等科研项目。目前,部分课题实验工作基本完成,已发表论文多篇,并正在积极申报科研成果。
李晖教授在回国的短短几年中,先后培养了硕士研究生7人,博士研究生1人,七年制学生3人,高等学校教师3人;在读硕士研究生10人,博士研究生2人,七年制学生1人,并指导七年制学生完成科研实习训练。
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李晖, H.Li a, B. Gu a, Y.Zhang a, D.F.Lewis a and Y.Wanga, b, *
Placenta (2005), 26, 210-217,-0001,():
-1年11月30日
Objective: Placental trophoblast cells (TCs) produce soluble Flt-1 (sFlt-1). Hypoxia induces placental oxidative stress and modulates trophoblast function. The aim of this study was to investigate whether hypoxia mediates TC sFlt-1 production and whether increased sFlt-1 production correlates with increased oxidative stress in placental TCs. Methods: Placentas were obtained immediately after delivery from normal pregnant women (n=8). Placental TCs were isolated by Dispase digestion of villous tissue and purified by Percoll gradient centrifugation. Isolated TCs were cultured under normoxia (21% O2: 5%CO2/95% air) and hypoxia (2% O2/5% CO2/93% N2) conditions for 3 days in vitro. TC productions of sFlt-1, VEGF, and PlGF were measured by enzyme-linked immunosorbent assay (ELISA). Lipid peroxide production and superoxide dismutase (CuZn-SOD) levels were evaluated. Messenger RNA expressions of Flt-1, VEGF and PlGF were determined by RT-PCR. Messenger RNA expressions for superoxide dismutase (CuZn-SOD) and heme oxygenase-1 (HO-1) were also determined. Data are expressed as meanGSE. A p level less than 0.05 was considered statistically different. Results: Our results show that sFlt-1 production was significantly increased by TCs cultured under hypoxia condition that correlates with increased lipid peroxide production. We also found that under hypoxia condition: (1) the ratio of PlGF/VEGF production was reversed; (2) the ratio of lipid peroxides to superoxide dismutase production was increased. The increased mRNA expressions for Flt-1 and VEGF and the decreased mRNA expression for PlGF in TCs were consistent with the protein productions under hypoxia condition. Conclusion: We concluded that upregulation of sFlt-1 and unbalanced PlGF/VEGF production associated with increased oxidative stress are consequences of hypoxia in placental TCs. Our results suggest that placental TCs are major sources of sFlt-1 and VEGF levels in the maternal circulation in women with preeclampsia. Placenta (2005), 26, 210e217
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李晖, Y. Wanga, b, *, Y. Zhanga, D. F. Lewis a, Y.Gu a, H. Li a, D. N. Granger b and J. S. Alexander b
Placenta (2003), 24, 851-861,-0001,():
-1年11月30日
Objectives: Soluble endothelial-cell adhesion molecules (ICAM, VCAM and PECAM) are markers of endothelial activation, and are elevated in the maternal circulation during pregnancy and even further increased in pregnancies complicated by pre-eclampsia (PE). To identify possible sources of endothelial activators during pregnancy, we addressed whether factors released from placental trophoblast cells (TCs) activate endothelial cells (ECs) to enhance adhesion molecule expression on ECs. We also examined whether proteases released by placental cells induce the endothelial cell surface molecule expression in PE. Methods: Confluent ECs were co-cultured with placental TCs derived from normal (n=9) or PE (n=8) pregnancies or with placental conditioned media (CM) derived from PE placental cultures (n=7). ICAM, VCAM, P-selectin and E-selectin were quantified using an enzyme-linked immunosorbent assay (ELISA). The protease inhibitors 2-macroglobulin ( 2M), thrombin inhibitor (TI) and chymotrypsin inhibitor (CI) were tested in the co-culture system. mRNAs for ICAM, VCAM, P-selectin and E-selectin were determined by RNase protection assay (RPA). NF- B activity in ECs was also determined. Results: (1) ICAM and VCAM expression was significantly increased on ECs co-cultured with both normal-TCs and PE-TCs, compared to control ECs (P<0.01). ICAM and VCAM expression in ECs co-cultured with normal-TCs did not differ from ECs co-cultured with PE-TCs. (2) E-selectin expression was increased on ECs co-cultured with normal-TCs (P<0.05) and further increased in ECs co-cultured with PE-TCs (P<0.01). (3) P-selectin expression was increased on ECs co-cultured with PE-TCs, but not ECs co-cultured with normal-TCs compared to control ECs (P<0.05). (4) 2M and TI did not alter the ICAM, VCAM, P-selectin and E-selectin expression on ECs induced by PE-CM. (5) CI blocked the upregulation of P-selectin and E-selectin (P<0.05), but not ICAM and VCAM expression, in ECs cultured with PE-CM. (6) Changes in mRNA for ICAM, VCAM, P-selectin and E-selectin paralleled the increases in protein expression on ECs cultured with PE-CM. (7) NF- B activity was alsoincreased in cells challenged with PE-CM. Conclusions: (1) Factor(s) released from both normal-TCs and PE-TCs promote ICAM and VCAM expression on ECs. (2) Factor(s) released from PE-TCs significantly increase EC P-selectin and E-selectin expression. (3) CI blocks the upregulation of P-selectin and E-selectin on ECs induced by factors released from PE placental cells, suggesting that chymotrypsin is responsible for the increased endothelial expression of P-selectin and E-selectin in pre-eclampsia. Placenta (2003), 24, 851-861
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【期刊论文】硒对异丙肾上腺素致损伤大鼠心肌SCN5A基因表达的影响
李晖, 李凤兰, 范启明, 杨宝峰, 于卓, 陈诗慧, 金剑峰, 马宁
中国地方病学杂志,2005,24(3):285~287,-0001,():
-1年11月30日
目的研究异丙肾上腺素(ISP)致大鼠心肌损伤模型中,编码电压门控Na+通道α亚单位基因SCN5A表达的变化,以及硒对其表达的影响。方法24只Wistar大鼠雌雄各半,随机分为3组,即对照组、ISP组、硒+ISP组。测定心肌丙二醛(MDA)的水平;采用逆转录聚合酶链反应(RT-PCR)和Western-blot方法检测心肌SCN5A基凶的表达变化。结果与ISP组比较,硒+ISP组MDA显著降低(P<0.05),但高于对照组(P<0.05);ISP组SCN5A基凶mRNA和蛋白的表达均较对照组显著增加,而硒+ISP组降低其表达。结论异丙肾上腺素可使心肌SCN5A基因mRNA和蛋白的表达显著增高:硒对异丙肾上腺素致大鼠心肌损伤有保护作用并能逆转ISP引起的SCN5A基凶表达的改变。
基因, SCN5A, 基凶表达, 异丙肾上腺素, 亚硒酸钠
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李晖, 钱素娟, 于维汉, 王守智, 刘秀萍, 高旭, 周令望
中国地方病学杂志,1999,18(4):265~267,-0001,():
-1年11月30日
目的探讨阿霉素对肝细胞的损伤机制及亚硒酸钠对肝细胞的保护作用。方法通过复制大鼠阿霉素性心肌损伤的动物模型,以亚硒酸钠作为保护因素,应用原位末端标记法(TUNEL)和免疫组化技术检测大鼠肝细胞凋亡和肝细胞转化生长因子1表达,并观察了大鼠血清中脂质过氧化含量。结果阿霉素组大鼠肝组织可见细胞凋亡和肝细胞中转化生长因子1的异常表达;阿霉素组大鼠血清中脂质过氧化物明显升高;亚硒酸钠对阿霉素的损伤有明显的保护作用。结论阿霉素诱导肝细胞凋亡可能是其肝脏损伤机制之一,并且细胞凋亡与转化生长因子1的高表达和血清中脂质过氧化水平升高有密切关系。
阿霉素, 细胞凋亡, 亚硒酸钠, 转化生长因子—
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【期刊论文】纤溶酶原激活物抑制剂1反义RNA对猪主动脉内皮细胞中成纤维细胞生长因子的影响
李晖, 富路, 梅宇
中华病理学杂志,2001,30(3):215~216,-0001,():
-1年11月30日
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【期刊论文】PAI-1反义RNA对人主动脉平滑肌细胞中血管内皮生长因子的影响
李晖, 富路, 梅宇
,-0001,():
-1年11月30日
目的探讨纤溶酶原激活物抑制剂-1(plasminogenactivatorinhibitor-1,pai-1)反义RNA对离体培养的主动脉平滑肌细胞(smoothmusclecell,SMC)PAI-1表达的作用及对血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)表达的影响。方法PCR扩增PAI-1第2外显子,将PCR产物纯化克隆后连入真核细胞表达载体pcDNA3。1,构建PAI-1反义RNA重组质粒。将pcDNA3。1-反义PAI-1重组质粒转染SMC中。通过免疫组化。Western印迹,ELISA检测细胞中PAI-1表达的改变;通过免疫荧光技术观察细胞中PAI-1表达量的变化对VEGF的影响。结果转染后第3天,细胞中PAI-1含量最低,VEGF也相应增加。第7天,PAI-1含量接近于正常,CEGF也增加至正常水平。结论反义PAI-1RNA能有效阻断SMC中PAI-1的蛋白合成,同时抑制细胞中VEGFDE的表达。
纤溶酶原激活物抑制剂-1, 反义RNA, 血管内皮生长因子, 平滑肌细胞
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