首页> 外文期刊>Reproduction, fertility, and development >Temporal regulation of extracellular signal-regulated kinase 1/2 phosphorylation, heat shock protein 70 and activating transcription factor 3 during prostaglandin F-induced luteal regression in pseudopregnant rats following heat stress
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Temporal regulation of extracellular signal-regulated kinase 1/2 phosphorylation, heat shock protein 70 and activating transcription factor 3 during prostaglandin F-induced luteal regression in pseudopregnant rats following heat stress

机译:细胞外信号调节激酶1/2磷酸化,热休克蛋白70和激活转录因子3在热应激后前列腺素F诱导的患者中的损失回归期间激活转录因子3

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摘要

The aim of the present study was to investigate the effects of heat stress on heat shock protein (HSP) 70 expression and mitogen-activated protein kinase (MAPK) and protein kinase (PK) B signalling during prostaglandin F (PGF)-induced luteal regression. During pseudopregnancy, rats were exposed to heat stress (HS, 40 degrees C, 2h) for 7 days and treated with PGF or physiological saline on Day 7; serum and ovaries were collected 0, 1, 2, 8 or 24h after PGF treatment. The early inhibitory effect of PGF on progesterone was reduced in HS rats. HSP70 expression in response to PGF was significantly enhanced in HS rats. PGF-induced phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was significantly greater in the HS group; however, HS rats exhibited elevated basal levels of phosphorylation of p38 MAPK, but not ERK1/2. PGF treatment increased expression of activating transcription factor (ATF) 3 at 2h, which was inhibited by heat stress. Evaluating PKB signalling revealed that phosphorylation of p-Akt (Thr(308) and Ser(473)) was reduced at 8 and 24h after PGF treatment in both non-heat stress (NHS) and HS groups, but there were no significant differences between the HS and NHS groups at any of the time points. In conclusion, the present study provides further evidence that heat stress may enhance HSP70 and affect ERK1/2 and ATF3 expression, but not Akt activation, during PGF-induced luteal regression in pseudopregnant rats.
机译:本研究的目的是探讨热应激对热休克蛋白(HSP)70表达和丝裂剂活化的蛋白激酶(MAPK)和蛋白激活蛋白激酶(MAPK)和蛋白激酶(PK)B信号传递的影响 - 诱导的肺炎。在假妊娠期间,大鼠暴露于热应激(HS,40℃,2H)7天,并在第7天用PGF或生理盐水处理;在PGF处理后收集血清和卵巢0,1,2,8或24小时。 HS大鼠中,PGF对孕酮的早期抑制作用降低。 HSP70表达响应于PGF的HS大鼠显着增强。在HS组中,PGF诱导的细胞外信号调节激酶(ERK)1/2的磷酸化显着更大;然而,HS大鼠表现出p38 mapk的基础磷酸化升高,但不是ERK1 / 2。 PGF处理在2小时时增加激活转录因子(ATF)3的表达,其被热应激抑制。评估PKB信号传导显示,在非热应激(NHS)和HS组中的PGF处理后,在8和24小时下降低p-AKT(THR(308)和SER(473)的磷酸化,但之间没有显着差异任何时间点的HS和NHS组。总之,本研究提供了进一步的证据,即热应激可以增强HSP70并影响在PGF诱导的伪沉淀大鼠的PGF诱导的肺部回归期间的ERK1 / 2和ATF3表达,但不是AKT活化。

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