摘要
热休克（４２℃，２ｈ）或Ｈ＿２Ｏ＿２预处理，均能在蛋白翻译合成水平使牛肺动脉内皮细胞（ＢＰＡＥＣｓ）中ＨＳＰ７０增多；在基因转录水平使ＢＰＡＥＣｓ中ＨＳＰ７０ｍＲＮＡ含量增加。蛋白激酶Ｃ（ＰＫＣ）抑制剂──Ｓｔａｕｒｏｓｐｏｒｉｎｅ（ＳＴＰ）能显著减少热休克和Ｈ＿２Ｏ＿２诱导的ＨＳＰ７０合成及ＨＳＰ７０ｍＲＮＡ转录的增加。提示ＰＫＣ在热休克和Ｈ＿２Ｏ＿２诱导的热休克基因表达的信息传递中具有重要作用。
he study found that the bovine pulmonary endothelial cells (BPAECs)heat-shocked(42℃2h)or treated with hydrogen peroxide(H_2O_2,0.25mmol·L-1 for 30min)had two function,ie.they displayed ropid synthesis of heat shock proteins(HSPs),detected by SDS-PAGE(5%～15%acrylamide gradient)of the[35S]methionine labeled protein,and incredsed level of mRNAcoding for heat shock protein 70kD(HSP70)revealed by northern blot analysis. lf BPAECs wereincubated with staurosporine──a potent protein kinase C(PKC)inhibitor during treatment withheat shock and H_2O_2 the synthesis of HSPs and the transcription of HSP70 mRNA were both re-duced.These results suggest that both heal shock and H2O2 can induce heat shock gene expres-sion in BPAECs,and PKC might be,as ainformation transfer involved in the regulation of heatshock gene expression.
出处
《湖南医科大学学报》
CSCD
1996年第6期487-489,共3页
Bulletin of Hunan Medical University
基金
国家自然科学基金
及湖南省自然科学基金
关键词
热休克蛋白
基因表达
蛋白激酶C
病理生理
heat-shock proteins
genes
protein kinase C
pulmonary artery
endothelium:cells:cattle
