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高血压状态下心脏和骨骼肌中的热休克蛋白72

Heat shock protein 72 in cardiac and skeletal muscles during hypertension.

作者信息

Gaia G, Comini L, Pasini E, Tomelleri G, Agnoletti L, Ferrari R

机构信息

Fondazione Clinica del Lavoro, Centro di Fisiopatologia Cardiovascolare S. Maugeri, Gussago, Brescia, Italy.

出版信息

Mol Cell Biochem. 1995 May 10;146(1):1-6. doi: 10.1007/BF00926874.

Abstract

In order to elucidate the relationship between hypertension and hypertrophy in the production of heat shock proteins, we studied the induction of the HSP72 synthesis by the heart and gracilis muscles of normo (WKY) and hypertensive (SHR) rats subjected to hyperthermia (42 degrees C +/- 0.5 for 15 min). Two age groups were investigated in each strain: young (2 months, with developing cardiac hypertrophy) and old (18 months, with fully developed chronic cardiac hypertrophy). The gracilis muscle never developed hypertrophy, independently of hypertension or aging. 72 kDa inducible protein was determined by Western blot analysis using a specific monoclonal antibody. We also used a commercial standard, loaded on each blot, to quantitate densitometrically the signal. The heart of young SHR responds to heat shock more than their normotensive age-matched control (298.8 +/- 24.7% vs 88.3 +/- 8.5%, p < 0.001). This response is not maintained during aging as we did not find any significant difference between normo- and hypertensive old rats after exposure to hyperthermia (43.6 +/- 5.3% vs 65.3 +/- 10.4%). Unlike the heart, the gracilis muscle shows a basal spontaneous HSP72 synthesis in both the SHR (71.4 +/- 10.8%) and WKY (40.6 +/- 11.7%) animals. There was a significant increase in HSP72 synthesis in the gracilis muscle of young SHR with respect to their control (186.2 +/- 18.7% vs 115.8 +/- 9.9%, p < 0.02) which was maintained also during aging (171.9 +/- 17.3% vs 95.2 +/- 10.5%, p < 0.01). In conclusion, these data show that hypertension results in an increased synthesis of HSP72 both in cardiac and gracilis muscle in response to heat shock.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了阐明高血压与肥大在热休克蛋白产生过程中的关系,我们研究了正常血压(WKY)和高血压(SHR)大鼠的心脏和股薄肌在热疗(42℃±0.5℃,持续15分钟)后HSP72合成的诱导情况。每个品系研究了两个年龄组:年轻组(2个月,伴有心脏肥大发展)和老年组(18个月,伴有完全发展的慢性心脏肥大)。股薄肌从未出现肥大,与高血压或衰老无关。使用特异性单克隆抗体通过蛋白质印迹分析测定72 kDa诱导蛋白。我们还在每个印迹上加载了商业标准品,以进行密度定量信号分析。年轻SHR大鼠的心脏对热休克的反应比年龄匹配的正常血压对照大鼠更强烈(298.8±24.7%对88.3±8.5%,p<0.001)。随着衰老,这种反应不再维持,因为在热疗后,我们未发现正常血压和高血压老年大鼠之间有任何显著差异(43.6±5.3%对65.3±10.4%)。与心脏不同,股薄肌在SHR(71.4±10.8%)和WKY(40.6±11.7%)动物中均显示基础自发HSP72合成。年轻SHR大鼠股薄肌中HSP72合成相对于其对照组有显著增加(186.2±18.7%对115.8±9.9%,p<0.02),衰老过程中也保持这种情况(171.9±17.3%对95.2±10.5%,p<0.01)。总之,这些数据表明,高血压导致心脏和股薄肌在热休克反应中HSP72合成增加。(摘要截短至250字)

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