Relaxin inhibit cardiac fibrosis induced by phorbol 12-myristate 13-acetate.

Author: Yu Peng WANG ¹ ; Ping WANG ² ; Lei DONG ² ; Hui CHEN ² ; Yong Quan WU ² ; Hong Wei LI ² ; Min LI ¹
Author Information

1. Health and Heart Center, the Beijing Friendship Hospital affiliated the Capital Medical University, Beijing 100050, China.
2. Cardiovascular Center, the Beijing Friendship Hospital affiliated the Capital Medical University, Beijing 100050, China.
Publication Type:Letter
MeSH: Animals; Animals, Newborn; Cells, Cultured; Fibroblasts; pathology; Fibrosis; Heart Diseases; chemically induced; pathology; prevention & control; Rats; Rats, Sprague-Dawley; Relaxin; therapeutic use; Tetradecanoylphorbol Acetate; analogs & derivatives
From: Biomedical and Environmental Sciences 2014;27(2):138-141
CountryChina
Language:English
Abstract: Relaxin is known to inhibit cardiac fibrosis. However, it is unclear whether relaxin could regulate the effects of Phorbol 12-myristate 13-acetate (PMA, PKC activator) on cardiac fibrosis. So the influence of relaxin on the cell proliferation and collagen expression induced by PMA in cultured cardiac fibroblasts was studied. It showed that PMA significantly increased cardiac fibroblasts proliferation, Type I pro-collagen protein expression, Type I pro-collagen mRNA expression, and rhRLX absolutely significantly decreased PMA induced effects on cardiac fibroblasts proliferation and Type I pro-collagen expressions, indicating that relaxin could inhibit cardiac fibrosis induced by PMA.