The potential role of circulating exosomes in protecting myocardial injury in acute myocardial infarction via regulating miR-190a-3p/CXCR4/CXCL12 pathway.

Exosomes of different origins have been found to be protective against ischemic-induced myocardial injury. This study examined the protective effects of circulating exosomes in the mice model of acute myocardial infarction (AMI) and explored the underlying molecular mechanisms. The effects of exosomes on myocardial injury were assessed in the AMI mice model.

[Urotensin II induces hypertrophy of in vitro cultured neonatal rat cardiac myocytes].

Objective: To examine whether urotensinII (UII) induces hypertrophy of neonatal rat cardiomyocytes cultured in vitro.

Methods: The primary cardiac myocytes cultured for 40 h followed by further culture in serum-free media for another 24 h were subjected to exposure to UII of varied concentrations for 24 h, after which the changes in the size of the cells were analyzed by flow cytometry with (3)H-leucine incorporation also measured.

Results: At the concentration of 1x10(-7) mol/L, UIIcould increase the size of the cultured cardiac myocardial cells (P=0.

[Effects of urotensin II on cultured cardiac fibroblast proliferation and collagen type I mRNA expression].

Objective: To observe the effect of urotensin II on cultured cardiac fibroblast collagen type I mRNA expression and proliferation, thereby to explore the role of urotensin II in myocardial remodeling in the event of cardiac failure.

Methods: Cardiac fibroblasts of neonatal Sprague-Dawley rats isolated by trypsin digestion method were stimulated by urotensin II at varied concentrations when the cells reached growth arrest. MTT assay was employed to measure the proliferation and determine the number of the cells, and reverse transcriptional (RT)-PCR used to detect the collagen mRNA expression.