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Relationship between the expressions of lectin-like oxidized low-density lipoprotein receptor-1 and apoptosis associated genes in placenta tissues and the pathogenesis of preeclampsia

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF OBSTETRICS AND GYNECOLOGY
Issue:
6
DOI:
10.3321/j.issn:0529-567X.2008.06.002
Key Word:
先兆子痫;胎盘;清道夫受体,E类;半胱氨酸天冬氨酸蛋白酶;原癌基因蛋白质c-bcl-2;细胞凋亡;Pre-eclampsia;Placenta;Scavenger receptors,class E;Caspases;Proto.oncogene proteins c-bcl-2; Apoptosis

Abstract: Objective To explore the expressions of lectin-like oxidized low-density lipoprotein receptor-1(LOX-1)and apoptosis related genes caspase-3,Bax and bcl-2 in placenta,and their associations with the pathogenesis of preeclampsia.Methods Thirty preeclampsia patients(preeclampsia group),hospitalized in Department of Obstetrics,Shengiing Hospital of China Medical University from June 2005 to December 2006,were selected as the subject group,and 40 normal pregnant women as control group.The expressions of LOX-1 and apoptosis related genes caspase-3.Bax and bel-2 in different gestational weeks'placenta tissues were examined using immunohistochemistry.RT-PCR and western-blot.Results (1)Immunohistochemical detection in preeclampsia group:at 20 w+1-24 w,24 w+1-28 w,28 w+1-32 w.32w+1-36 w+1-36 w+1-40 w,respectively,the results of LOX-1 were 20.1±1.8,25.6±1.3,32.8±1.6,34.3 ±1.5,39.9±1.2;in the control group they respectively were 11.2±0.6,18.5±1.6,26.1±1.8,28.3 4-1.6,32.3±1.6;the difierence was significant(P<0.05).In preeclampsia group,the results of easpase-3 were 12.3±0.9,16.3±0.9,24.4 4-0.8,28.3±0.5,36.3±1.1.and in the control group they respectively were 8.5±1.0,12.3±1.1,17.4±1.2,20.4±stronger than those in normal pregnant women at different gestational weeks(P<0.05).However,the expression tendency of bcl-2 mRNA and proten was converse to the expression tendency of Bax.Conclusion The expressions of LOX-1,caspase-3,and Bax are upregulated in placentas of preeclampsia patients,while bcl-2 iS downregulated,both of which are associated with the pathogenesis of preeclampsia.

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