Gao L, Kennedy J M, Solaro R J
Department of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago 60612, USA.
J Mol Cell Cardiol. 1995 Jan;27(1):541-50. doi: 10.1016/s0022-2828(08)80049-1.
We have investigated developmental transitions of TnI and TnT isoforms in fetal, neonatal, and adult rabbit hearts by western blot analysis. Our results provide the first evidence for the existence of two developmentally regulated isoforms of TnI in rabbit heart. These isoforms comigrate with adult rabbit cardiac TnI (cTnI) and slow skeletal TnI (ssTnI). At 23 days of gestation, ssTnI was the predominant TnI isoform. At 29 days of gestation, there was a significant increase in the relative amount of cTnI, that continued with maturation. The TnI isoform transition was significantly faster in right than left ventricles at gestation 30 and 32 days. Four TnT isoforms were detected in fetal rabbit ventricles. The relative amount of TnT isoforms did not change from 23 to 29 days of gestation. However, the relative amount of the adult TnT isoform increased significantly around the time of birth with the increase being significantly more prominent in left than in right ventricles. Maternal injection of phenylephrine (PHE), an alpha-1 adrenergic agonist, increased fetal cardiac force and arterial blood pressure, facilitated TnT, but not TnI, isoform transition in fetal heart. Our results indicate that the developmental transition of rabbit cardiac TnI and TnT isoforms is not coordinated and might be regulated by different mechanisms. Our results also provide evidence that the TnT isoform population is influenced by adrenergic stimulation and stress on the cardiovascular system during development.
