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

Yong Sook Kim, Hyang Hee Cho, Dong Im Cho, Hye yun Jeong, Soo yeon Lim, Ju Hee Jun, Mi Ra Kim, Bo Gyeong Kang, Meeyoung Cho, Hye jin Kang, Wan Seok Kang, Goo Taeg Oh, Youngkeun Ahn

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2 Scopus citations


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.

Original languageEnglish
Article number307
JournalCell Death and Disease
Issue number4
StatePublished - Apr 2021

Bibliographical note

Funding Information:
This work was supported by the National Research Foundation of Korea (2019R1A2C3003547, 2019R1A2C2010884, and 2019R1A4A1028534), a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and funded by the Ministry of Health and Welfare, Republic of Korea (HI18C1352). The authors declare no competing financial interests.

Publisher Copyright:
© 2021, The Author(s).


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