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The adipokine Retnla deficiency increases responsiveness to cardiac repair through adiponectin-rich bone marrow cells

Title
The adipokine Retnla deficiency increases responsiveness to cardiac repair through adiponectin-rich bone marrow cells
Authors
Kim Y.S.Cho H.H.Cho D.I.Jeong H.-Y.Lim S.Jun J.H.Kim M.R.Kang B.G.Cho M.Kang H.-J.Kang W.S.Oh G.T.Ahn Y.
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2021
Journal Title
Cell Death and Disease
ISSN
2041-4889JCR Link
Citation
Cell Death and Disease vol. 12, no. 4
Publisher
Springer Nature
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Resistin-like alpha (Retnla) is a member of the resistin family and known to modulate fibrosis and inflammation. Here, we investigated the role of Retnla in the cardiac injury model. Myocardial infarction (MI) was induced in wild type (WT), Retnla knockout (KO), and Retnla transgenic (TG) mice. Cardiac function was assessed by echocardiography and was significantly preserved in the KO mice, while worsened in the TG group. Angiogenesis was substantially increased in the KO mice, and cardiomyocyte apoptosis was markedly suppressed in the KO mice. By Retnla treatment, the expression of p21 and the ratio of Bax to Bcl2 were increased in cardiomyocytes, while decreased in cardiac fibroblasts. Interestingly, the numbers of cardiac macrophages and unsorted bone marrow cells (UBCs) were higher in the KO mice than in the WT mice. Besides, phosphorylated histone H3(+) cells were more frequent in bone marrow of KO mice. Moreover, adiponectin in UBCs was notably higher in the KO mice compared with WT mice. In an adoptive transfer study, UBCs were isolated from KO mice to transplant to the WT infarcted heart. Cardiac function was better in the KO-UBCs transplanted group in the WT-UBCs transplanted group. Taken together, proliferative and adiponectin-rich bone marrow niche was associated with substantial cardiac recovery by suppression of cardiac apoptosis and proliferation of cardiac fibroblast. © 2021, The Author(s).
DOI
10.1038/s41419-021-03593-z
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자연과학대학 > 생명과학전공 > Journal papers
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