Article Sidebar
Published:
Jan 26, 2022Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Retinol exerts therapeutic effect on myocardial infarction through regulation of immune inflammatory cells and Cx43 expression
Abstract
Purpose: To investigate the effect of retinol on cardiac fibroblast proliferation in vitro and on fibrosis formation in mice in vivo.
Methods: Proliferative potential of fibroblasts was determined using cell counting kit-8 assay. Acute myocardial infarction (AMI) was induced in mice via ligation of the left side coronary artery. In myocardial tissues, concentration of TNF-α was determined using enzyme-linked immunosorbent assay (ELISA) assay.
Results: Exposure to retinol significantly suppressed cardiac fibroblast proliferation under ischemia, when compared to untreated fibroblasts (p < 0.05). However, exposure of cardiac fibroblasts to retinol did not produce toxicity at a dose of 10 μM under normal conditions. In contrast, exposure to normal levels of oxygen, glutamine and glucose significantly reversed the inhibitory potential of retinol against fibroblasts during ischemia (p < 0.05). Treatment of mice with retinol at a dose of 5 mg/kg reversed the AMI-mediated increase in hydroxyproline level in myocardial tissues. Retinol treatment of AMI mice caused significant elevation in the number of CD31+ capillaries in myocardial tissues. Increase in TNF-α by AMI in cardiac tissues of mice was reversed by treatment with retinol at a dose of 5 mg/kg. The retinol treatment also caused significant reversal of AMI-induced down-regulation of Cx43 protein (p < 0.05).
Conclusion: Retinol enhanced the proliferation of fibroblasts under ischemic conditions and prevented fibrosis in mice with AMI. Moreover, retinol targeted TNF-α production and upregulated Cx43 expression in myocardial tissues of mice with AMI. Thus, retinol may be useful for the management of myocardial infarction.
