MYOSIN LIGHT-CHAIN GENE-EXPRESSION ASSOCIATED WITH DISEASE STATES OF THE HUMAN HEART

被引:30
作者
TRAHAIR, T
YEOH, T
CARTMILL, T
KEOGH, A
SPRATT, P
CHANG, V
DOSREMEDIOS, CG
GUNNING, P
机构
[1] CHILDRENS MED RES FDN, CELL BIOL UNIT, LOCKED BAG 23, WENTWORTHVILLE, NSW 2145, AUSTRALIA
[2] UNIV SYDNEY, DEPT ANAT, MUSCLE RES UNIT, SYDNEY, NSW 2006, AUSTRALIA
[3] ROYAL ALEXANDRA HOSP CHILDREN, CAMPERDOWN, NSW 2050, AUSTRALIA
[4] ST VINCENTS HOSP, DARLINGHURST, NSW 2010, AUSTRALIA
关键词
CONTRACTILE PROTEINS; ISOFORMS; CARDIOMYOPATHY; MYOSIN; HYPERTROPHY; MESSENGER RNA;
D O I
10.1006/jmcc.1993.1067
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
During development of the human heart, the atrial isoform of alkali myosin light chain (MLC1A) is expressed in the ventricle. With maturation of the heart, MLC1A expression is completely replaced by that of the adult ventricular myosin light chain, MLC1V. We have evaluated the re-expression of MLC1A as a marker of different disease states of the human ventricle. RNA was isolated from the ventricles of patients with idiopathic dilated cardiomyopathy (CM) and severe congenital cardiac defects (CCD). Northern blot analysis was used to measure the mRNA levels MLC1A and MLC1V in these samples. As a control, the level of regulatory MLC2V mRNA was also measured. We find that the level of MLC2V mRNA per μg total ventricular RNA is very similar in CM, CCD and normal human samples. In contrast, we find that MLC1V mRNA levels tend to be reduced in both CM and CCD samples. In this case of the CCD samples, this apparent drop in MLC1V is compensated by expression of the developmental MLC1A isoform. However, in CM patients in end-stage failure, expression of MLC1A is barely detectable. The expression of MLC1A in CCD samples may reflect an adaptive mechanism in response to cardiac overload. The failure to detect substantial MLC1A expression in the CM samples may reflect the failure of such an adaptive mechanism. © 1993 Academic Press. All rights reserved.
引用
收藏
页码:577 / 585
页数:9
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