慢性右心衰竭刺激心脏和肝脏中的热休克蛋白72，但不刺激其他组织中的热休克蛋白72。

Right heart failure chronically stimulates heat shock protein 72 in heart and liver but not in other tissues.

作者信息

Comini L, Gaia G, Curello S, Ceconi C, Pasini E, Benigno M, Bachetti T, Ferrari R

机构信息

Fondazione Salvatore Maugeri, Centro di Fisiopatologia Cardiovascolare, Gussago, Brescia, Italy.

出版信息

Cardiovasc Res. 1996 Jun;31(6):882-90.

PMID:8759243

Abstract

OBJECTIVES

During cardiac failure several ontogenically developed adaptional mechanisms are activated. Among these, heat-shock proteins (HSP) are expressed in response to stress. The aim of the present study was to investigate the HSP72 protein expression in lungs, liver, cardiac and skeletal muscles during congestive heart failure (CHF).

METHODS

CHF was induced in Sprague-Dawley rats by a single intraperitoneal injection of monocrotaline (50 mg/kg). Two groups of animals emerged: a CHF group (n = 10) with right ventricular hypertrophy, pleural and peritoneal effusions, and an Hypertrophy group (n = 12) with right ventricular hypertrophy without CHF. The data for each group were compared with those of control (saline infused) age-matched rats. Lungs, liver, right and left ventricles, soleus, extensor digitorum longus and tibialis anterior muscles were excised and analyzed for HSP72 concentration by Western blot analysis using a specific monoclonal antibody. Noradrenaline levels in the heart were also measured using HPLC.

RESULTS

The CHF group showed: (1) reduced right (0.460 +/- 0.090 vs 0.830 +/- 0.070 nmol/ventricle, P < 0.01) and left (1.10 +/- 0.09 vs 2.10 +/- 0.130 nmol/ventricle, P < 0.001) ventricular content of noradrenaline compared to the control; (2) significant activation of HSP72 concentration in right and left ventricles (39.4 +/- 1.6 vs 5 +/- 0.9% and 13 +/- 1.2 vs 3.5 +/- 0.6%, P < 0.001 both) and in the liver (39.8 +/- 11 vs 6 +/- 2%, P < 0.001); (3) no modification in HSP72 concentration in lungs and all of the peripheral muscles considered. The Hypertrophy group showed: (1) unchanged total noradrenaline tissue content as compared to the control; and (2) unmodified HSP72 concentration in all tissues analyzed.

CONCLUSIONS

The present study demonstrates that CHF, but not compensatory hypertrophy, is a specific stimulus for chronic HSP72 induction in the heart and liver. On the contrary, CHF does not affect HSP in lungs and peripheral muscles. HSP 72 induction represents an intracellular marker of stress reaction which can persist chronically.

摘要

目的

在心力衰竭期间，几种发育过程中形成的适应性机制被激活。其中，热休克蛋白（HSP）会在应激反应时表达。本研究的目的是调查充血性心力衰竭（CHF）期间肺、肝、心脏和骨骼肌中HSP72蛋白的表达情况。

方法

通过腹腔单次注射野百合碱（50mg/kg）诱导Sprague-Dawley大鼠发生CHF。出现两组动物：一组CHF组（n = 10），有右心室肥大、胸腔和腹腔积液；另一组肥大组（n = 12），有右心室肥大但无CHF。将每组数据与年龄匹配的对照（输注生理盐水）大鼠的数据进行比较。切除肺、肝、左右心室、比目鱼肌、趾长伸肌和胫骨前肌，使用特异性单克隆抗体通过蛋白质印迹分析来检测HSP72浓度。还使用高效液相色谱法测量心脏中的去甲肾上腺素水平。

结果

CHF组显示：（1）与对照组相比，右心室（0.460±0.090 vs 0.830±0.070nmol/心室，P<0.01）和左心室（1.10±0.09 vs 2.10±0.130nmol/心室，P<0.001）去甲肾上腺素含量降低；（2）左右心室（39.4±1.6 vs 5±0.9%和13±1.2 vs 3.5±0.6%，两者P<0.001）以及肝脏（39.8±11 vs 6±2%，P<0.001）中HSP72浓度显著激活；（3）所研究的肺和所有外周肌肉中HSP72浓度无变化。肥大组显示：（1）与对照组相比，总去甲肾上腺素组织含量未改变；（2）所有分析组织中HSP72浓度未改变。