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MEK1 and MEK2 differentially regulate human insulin- and insulin glargine-induced human bladder cancer T24 cell proliferation

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Chinese Medical Journal 2012年第23期125卷 4197-4201页

作者： LIU Shan-ying LIANG Ying LIN Tian-xin SU Fang LIANG Wei-wen Uwe Heemann LI Yan Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong 510120China Department of Endocrinology Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhouGuangdong 510120China Department of Nephrology Technical University Munich81675 MunichGermany

Background Increased risk of bladder cancer has been reported in diabetic patients. This study was to investigate the roles of mitogen-activated protein kinase kinase （MEK） 1 and 2 in the regulation of human insulin- and insulin glargine-induced proliferation of human bladder cancer T24 cells. Methods In the absence or presence of a selective inhibitor for MEK1 （PD98059） or a specific siRNA for MEK2 （siMEK2）, with or without addition of insulin or glargine, T24 cell proliferation was evaluated by cell counting kit （CCK）-8 assay. Protein expression of MEK2, phosphorylation of ERK1/2 and Akt was analyzed by Western blotting. Results T24 cell proliferation was promoted by PD98059 at 5-20 IJmol/L, inhibited by siMEK2 at 25-100 nmol/L. PD98059 and siMEK2 remarkably reduced phosphorylated ERKI/2. Insulin- and glargine-induced T24 cell proliferation was enhanced by PD98059, suppressed while not blocked by siMEK2. Insulin- and glargine-induced ERKI/2 activation was blocked by PD98059 or siMEK2 treatment, whereas activation of Akt was not affected. Conclusion MEK1 inhibits while MEK2 contributes to normal and human insulin- and insulin glargine-induced human bladder cancer T24 cell proliferation.

关键词： insulin glargine proliferation bladder cancer MEK

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Lipopolysaccharide-enhanced early proliferation of insulin secreting NIT-1 cell is associated with nuclear factor-kappaB- mediated inhibition of caspase 3 cleavage

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Chinese Medical Journal 2011年第22期124卷 3652-3656页

作者： LIU Shan-ying LIANG Qi-jun LIN Tian-xin FAN Xin-lan LIANG Ying Uwe Heemann LI Yan Sun Yat-sen Memorial Hospital Sun Yat-sen University Guangzhou Guangdong 510120 China

Background Increased levels of plasma lipopolysaccharide （LPS） have been found in obesity and diabetes patients. This study was to investigate the effect of LPS on pancreatic beta-cell viability and the involvement of caspase 3 in NIT-1 cell line. Methods Mouse insulinoma NIT-1 cells were treated with LPS for the indicated time and dose. Cell viability was measured by cell counting kit-8 reagent. Toll-like receptor 4 （TLR4）, caspase 3 and cleaved caspase 3 were detected by Western blotting. Insulin was determined by radioimmunoassay （RIA）. Results LPS promoted NIT-1 cell proliferation at 1 μg/ml, peaked at 72 hours of incubation. A reduction in cleavage of caspase 3 was observed upon LPS treatment. Bay11-7082, a specific inhibitor of nuclear factor （NF）-κB, blunted LPS-induced inhibition of caspase 3 cleavage. Reduction in chronic insulin secretion was observed after treatment with LPS at 1 μg/ml for 48 and 72 hours, not for 24 hours. TLR4 protein was upregulated when NIT-1 cells were treated with LPS at 1 μg/ml for 24 hours. Conclusions LPS promotes early NIT-1 cell proliferation in association with NF-KB-mediated inhibition of caspase 3 cleavage. LPS exerts a time-dependent inhibitory effect on chronic insulin secretion from NIT-1 cells.

关键词： lipopolysaccharide NIT-1 cell toll-like receptor 4 nuclear factor-κB caspase 3

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Influence of Progesterone on Chronic Renal Allograft Dysfunction in Rat Model

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器官移植内科学杂志 2009年第3期4卷 134-138页

作者： Hequn Zou Shanying Liu Yousheng Yao Erwei Song Jens Lutz Uwe Heemann Institute of Nephrology and Rheumatology The Third Affiliated Hospital of China Southern MedicalUniversity Guangzhou 510630 China Department of Nephrology University Hospital Essen Germany

Background It is indicated in our recent investigation that oestrogens ameliorate the progression of chronic renal allograft dysfunction. In our present study, we investigated the influence of progesterone on chronic renal allograft dysfunction. Methods The kidneys of female Fisher (F344) rats were orthotopically transplanted into ovariectomized female Lewis recipients. The recipients were divided into two groups and treated with progesterone or vehicle. Animals were harvested 24 weeks after trans- plantation for histological, immunohistological studies and molecular analysis. Results The administration of progesterone resulted in increased urinary protein excretion, profound glomerulosclerosis and mononuclear cell infiltration. Renal allograft damage paralleled intragraft mRNA expression of transforming growth factor-β1 in the two groups. Conclusions It is suggested by our results that progesterone worsened long-term renal allograft outcome.

关键词：细移植转化生长孕酮黄体酮

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MEK1 and MEK2 differentially regulate human insulin- and insulin glargine-induced human bladder cancer T24 cell proliferation

MEK1 and MEK2 differentially regulate human insulin- and ins...

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中华医学会糖尿病学分会第十六次全国学术会议

作者： LIU Shan-ying LIANG Ying LIN Tian-xin SU Fang LIANG Wei-wen Uwe Heemann LI Yan Zhongshan University at SunYixian Memorial Hospital

Objective To investigate the roles of MEKl and MEK2 in the regulation of human insulin- and insulin glargine-induced proliferation of human bladder cancer T24 cells. Methods In the absence or presence of a selective inhibitor for MEKl(PD98059) or a specific siRNA for MEK2(siMEK2),with or without addition of insulin or glargine,T24 cell proliferation was evaluated by CCK-8 assay.Protein expression of MEK2,phosphorylation of ERK1/2 and Akt was analyzed by Western blot.

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Efficacy of estradiol on preventing chronic kidney allograft rejection

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Chinese Medical Journal 1999年第9期 18-18页

作者： Heque Zou and Uwe Heemann

hronic rejection is the main factor to result in the loss of renal allograft In order to look for a potential therapy chronic rejection, we investigated the efficacy of estradiol on preventing renal chronic rejection The kidneys of female F344 rats were orthotopically transplanted into ovatiectomized female Lewis rats and treated for 16 weeks with either estradiol or vehicle Compared with controls treated with vehicle, estradiol treatment reduced urinary protein excretion, glomerular sclerosis, interstitial infiltration and fibrosis, vascular lesions, in parallel to a reduced ICAM 1 and TGF β mRNA expression Our results suggested that estrodiol could significantly decrease the progression of chronic rejection, at least in female recipients, and the reduced adhesion molecule and TGF β gene expression may be involved in the mechanism for estradiol to prevent chronic rejection

关键词： Efficacy of estradiol on preventing chronic kidney allograft rejection

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