Key result
Treatment with phenylephrine significantly increased beta-MHC expression to 55% compared to 34.5% in contracting cardiomyocytes, whereas mechanical arrest with KCl or BDM did not.
Hormonal factors such as adrenergic stimulation, rather than mechanical stress or calcium, appear to qualitatively regulate myosin heavy chain gene expression in neonatal cardiomyocytes.
Answers are grounded in this paper and cite their sources.
Should not change clinical practice; leaves open adrenergic regulation of MHC expression for human translation.
It is generally accepted that mechanical stress of cardiomyocytes increases RNA and protein synthesis of myosin heavy chain (MHC) quantitatively but it is still a matter of debate whether MHC gene expression is also changed qualitatively. We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)]. Relative distribution of MHC mRNA isoforms (alpha and beta) was studied by quantitative polymerase chain reaction. Expression of MHC isoenzymes was the same in contracting (34.5% beta-MHC) and arrested (40.5% and 33.0% beta-MHC in KCl and BDM, respectively) cardiomyocytes. However, treatment with phenylephrine for the same period increased significantly beta-MHC expression to 55%. We conclude that hormonal factors rather than Ca2+ or mechanical stress regulate qualitatively MHC gene expression.
No takes yet. Share an insight, caveat, or question.
Luther et al. (1997) studied Neonatal cardiomyocytes. Phenylephrine vs. Spontaneously contracting cardiomyocytes was evaluated on Expression of beta-MHC isoenzymes. Treatment with phenylephrine significantly increased beta-MHC expression to 55% compared to 34.5% in contracting cardiomyocytes, whereas mechanical arrest with KCl or BDM did not.
Synapse has enriched 10 related papers. Consider them for comparative context: