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An alpha-cardiac myosin heavy chain gene mutation impairs contraction and relaxation function of cardiac myocytes.
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- Author(s): Kim SJ;Kim SJ; Iizuka K; Kelly RA; Geng YJ; Bishop SP; Yang G; Kudej A; McConnell BK; Seidman CE; Seidman JG; Vatner SF
- Source:
The American journal of physiology [Am J Physiol] 1999 May; Vol. 276 (5), pp. H1780-7.- Publication Type:
Journal Article; Research Support, U.S. Gov't, P.H.S.- Language:
English - Source:
- Additional Information
- Source: Publisher: American Physiological Society Country of Publication: United States NLM ID: 0370511 Publication Model: Print Cited Medium: Print ISSN: 0002-9513 (Print) Linking ISSN: 00029513 NLM ISO Abbreviation: Am J Physiol Subsets: MEDLINE
- Publication Information: Publication: Bethesda, MD : American Physiological Society
Original Publication: Washington [etc.] American Physiological Society. - Subject Terms: Muscle Fibers, Skeletal/*enzymology ; Myocardial Contraction/*physiology ; Myocardium/*metabolism ; Myosin Heavy Chains/*genetics ; Myosin Heavy Chains/*metabolism; Action Potentials/physiology ; Animals ; Blotting, Northern ; Calcium/metabolism ; Calcium-Transporting ATPases/metabolism ; Cells, Cultured ; DNA Primers ; Heart Ventricles/cytology ; Heart Ventricles/metabolism ; Male ; Mice ; Mice, Transgenic ; Muscle Fibers, Skeletal/cytology ; Mutation/physiology ; Myocardium/cytology ; RNA, Messenger/analysis
- Abstract: Left Ventricular (LV) myocytes were isolated from 15-wk-old male mice bearing the Arg403 --> Gln alpha-cardiac myosin heavy chain missense mutation (alpha-MHC403/+), a model of familial hypertrophic cardiomyopathy. LV myocytes were classified morphologically: type I, rod shaped with parallel myofibrils; type II, irregularly shaped, shorter and wider than wild-type (WT) control cells, with parallel myofibrils; and type III, irregularly shaped with disoriented myofibrils. Compared with WT myocytes, alpha-MHC403/+ myocytes had fewer type I cells (WT = 74 +/- 3%, alpha-MHC403/+ = 41 +/- 4%, P < 0.01) and more type III cells (WT= 12 +/- 3%, alpha-MHC403/+ = 49 +/- 7%, P < 0.01). In situ histology also demonstrated marked myofibrillar disarray in the alpha-MHC403/+ hearts. With the use of video edge detection, myocytes were paced at 1 Hz (37 degrees C) to determine the effects of the mutation on myocyte function. End-diastolic length was reduced in mutant myocytes, but fractional shortening (% contraction) and sarcomere length were not. Velocity of contraction (-dL/dtmax) was depressed in mutant cells, but more in type II and III cells (-31%) than in type I cells (-18%). Velocity of relaxation (+dL/dt) was also depressed more in type II and III cells (-38%) than in type I cells (-16%). Using fura 2 dye with intracellular Ca2+ transients, we demonstrated that in alpha-MHC403/+ myocytes, the amplitude of the Ca2+ signal during contraction was unchanged but that the time required for decay of the signal to decrease 70% from its maximum was delayed significantly (WT = 159 +/- 8 ms; alpha-MHC403/+ = 217 +/- 14 ms, P < 0.01). Sarco(endo)plasmic reticulum Ca2+-ATPase mRNA levels in alpha-MHC403/+ and WT mice were similar. These data indicate that the altered cardiac dysfunction of alpha-MHC403/+ myocytes is directly due to defective myocyte function rather than to secondary changes in global cardiac function and/or loading conditions.
- Grant Information: HL-33107 United States HL NHLBI NIH HHS; HL-37404 United States HL NHLBI NIH HHS; HL-59139 United States HL NHLBI NIH HHS
- Contributed Indexing: Keywords: Non-programmatic
- Accession Number: 0 (DNA Primers)
0 (RNA, Messenger)
EC 3.6.4.1 (Myosin Heavy Chains)
EC 7.2.2.10 (Calcium-Transporting ATPases)
SY7Q814VUP (Calcium) - Publication Date: Date Created: 19990518 Date Completed: 19990603 Latest Revision: 20191210
- Publication Date: 20240104
- Accession Number: 10.1152/ajpheart.1999.276.5.H1780
- Accession Number: 10330263
- Source:
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