ALTERED SARCOPLASMIC-RETICULUM CA-2+-ATPASE GENE-EXPRESSION IN THE HUMAN VENTRICLE DURING END-STAGE HEART-FAILURE

ALTERED SARCOPLASMIC-RETICULUM CA-2+-ATPASE GENE-EXPRESSION IN THE HUMAN VENTRICLE DURING END-STAGE HEART-FAILURE
复制标题

DOI:
10.1172/jci114429
复制
发表时间:
1990-01-01
影响因子:
15.9
通讯作者:
SCHWARTZ, K
SCHWARTZ, K
中科院分区:
医学1区
文献类型:
--
作者:
MERCADIER, JJ;LOMPRE, AM;SCHWARTZ, K

文献摘要

被引文献

相似文献

最近有报道在实验性心肌肥厚和衰竭时,心肌肌浆网(SR)中编码Ca ~(2+)-ATP酶的mRNA水平降低。为了确定这种缺陷是否发生在人类终末期心力衰竭中,我们使用大鼠心脏SR Ca 2 +-ATP酶cDNA探针比较了13例接受心脏移植的患者(6例特发性扩张型心肌病; 4例冠状动脉疾病伴心肌梗死; 3种不同病因)的左心室(LV)和右心室(RV)标本中SR Ca 2 +-ATP酶mRNA水平与对照心脏样本。我们观察到与对照组相比,心力衰竭患者左室标本中Ca 2 +-ATP酶mRNA相对于18 S核糖体RNA和肌球蛋白重链mRNA显著降低(分别为-48%,P < 0.01和-47%,P < 0.05)。左心室Ca ~(2+)-ATP酶mRNA/18 S RNA比值与心指数呈正相关(P < 0.02)。RV比值与肺动脉收缩压、舒张压和平均肺动脉压呈负相关(分别为P < 0.02、P < 0.02和P < 0.01)。我们认为,减少SR Ca ~(2+)-ATP酶mRNA在心肌中起着重要的作用,在人类终末期心力衰竭期间的Ca ~(2+)运动和心肌舒张的改变报告。
A decrease in the myocardial level of the mRNA encoding the Ca2+-ATPase of the sarcoplasmic reticulum (SR) has been recently reported during experimental cardiac hypertrophy and failure. To determine if such a deficit occurs in human end-stage heart failure, we compared the SR Ca2+-ATPase mRNA levels in left (LV) and right ventricular (RV) specimens from 13 patients undergoing cardiac transplantation (6 idiopathic dilated cardiomyopathies; 4 coronary artery diseases with myocardial infarctions; 3 diverse etiologies) with control heart samples using a rat cardiac SR Ca2+-ATPase cDNA probe. We observed a marked decrease in the mRNA for the Ca2+-ATPase relative to both the 18S ribosomal RNA and the myosin heavy chain mRNA in LV specimens of patients with heart failure compared to controls (-48%, P < 0.01 and -47%, P < 0.05, respectively). The LV ratio of Ca2+-ATPase mRNA to 18S RNA positively correlated with cardiac index (P < 0.02). The RV ratio correlated negatively with systolic, diastolic and mean pulmonary arterial pressures (P < 0.02, P < 0.02, and P < 0.01, respectively). We suggest that a decrease of the SR Ca2+-ATPase mRNA in the myocardium plays an important role in alterations of Ca2+ movements and myocardial relaxation reported during human end-stage heart failure.