1. Endothelin-1-induced hypertrophic alterations and heme oxygenase-1 expression in cardiomyoblasts are counteracted by beta estradiol: in vitro and in vivo studies
- Author
-
David D. Haines, Istvan Lekli, Tunde Barta, Agnes Tosaki, György Balla, and Arpad Tosaki
- Subjects
0301 basic medicine ,Male ,In vivo rat ,β-Estradiol (β-E) ,030204 cardiovascular system & hematology ,Pharmacology ,Muscle hypertrophy ,Cell Line ,Rats, Sprague-Dawley ,03 medical and health sciences ,0302 clinical medicine ,In vitro ,In vivo ,Heat shock protein ,Animals ,Viability assay ,H9c2 rat cardiomyoblast ,Endothelin-1 ,Estradiol ,Chemistry ,Gyógyszerészeti tudományok ,Estrogens ,Orvostudományok ,General Medicine ,Hypertrophy ,Endothelin 1 ,Heme oxygenase ,030104 developmental biology ,Heart failure (HF) ,Cell culture ,Endothelin-1 (ET-1) ,Heme oxygenase-1 (HO-1) ,Heme Oxygenase (Decyclizing) ,Original Article ,Myoblasts, Cardiac - Abstract
Endothelin-1 (ET-1), a potent vasoconstrictor normally active in maintaining vascular tone, may mediate significant pathogenic effects, contributing to several serious diseases when aberrantly expressed or regulated. The present study evaluates the capacity of ET-1 to affect endothelin-1-associated hypertrophic activity and decreased expression of heme oxygenase-1 by H9c2 rat cardiomyoblasts in vitro, corresponding to in vivo processes underlying cardiovascular diseases (CVDs). Beta estradiol (β-E) is tested for its capacity to alter the effects of ET-1. H9c2 cells, cultured 48 h, were stimulated with 100-10,000 nM of ET-1 and evaluated for changes in cell size, cell viability, and expression of the cytoprotective heat shock protein heme oxygenase-1 (HO-1), with 200 nM of β-E included in selected cultures to evaluate its effect on ET-1-mediated changes. The application of 100 to 10,000 nM of ET-1 resulted in a significant increase in average cell size and decreases in both cell viability and HO-1 protein content (p more...
- Published
- 2018