Profilin 2 and Endothelial Exosomal Profilin 2 Promote Angiogenesis and Myocardial Infarction Repair in Mice

Cardiovascular diseases (CVD) are the leading cause of death worldwide, wherein myocardial infarction (MI) is the most dangerous one. Promoting angiogenesis is a prospective strategy to alleviate MI. Our previous study indicated that profilin 2 (PFN2) may be a novel target associated with angiogenes...

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Published inFrontiers in cardiovascular medicine Vol. 9; p. 781753
Main Authors Li, Zhenkun, Huo, Xueyun, Chen, Keyan, Yang, Fenghua, Tan, Weijiang, Zhang, Qi, Yu, Haixu, Li, Changlong, Zhou, Deshan, Chen, Hao, Zhao, Baoquan, Wang, Yuan, Chen, Zhenwen, Du, Xiaoyan
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 11.04.2022
Subjects
angiogenesis
Cardiovascular Medicine
endothelial cells
exosomes
myocardial infarction
profilin 2
endothelial cells
profilin 2
angiogenesis
exosomes
myocardial infarction
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Summary:Cardiovascular diseases (CVD) are the leading cause of death worldwide, wherein myocardial infarction (MI) is the most dangerous one. Promoting angiogenesis is a prospective strategy to alleviate MI. Our previous study indicated that profilin 2 (PFN2) may be a novel target associated with angiogenesis. Further results showed higher levels of serum PFN2 and exosomal PFN2 in patients, mice, and pigs with MI. In this study, we explored whether PFN2 and endothelial cell (EC)-derived exosomal PFN2 could increase angiogenesis and be beneficial for the treatment of MI. Serum PFN2, exosomes, and exosomal PFN2 were elevated in rats with MI. PFN2 and exosomes from PFN2-overexpressing ECs (OE-exo) enhanced EC proliferation, migration, and tube formation ability. OE-exo also significantly increased the vessel number in zebrafish and protected the ECs from inflammatory injury. Moreover, OE-exo-treated mice with MI showed improvement in motor ability, ejection fraction, left ventricular shortening fraction, and left ventricular mass, as well as increased vessel numbers in the MI location, and decreased infarction volume. Mechanistically, PI3K might be the upstream regulator of PFN2, while ERK might be the downstream regulator in the PI3K-PFN2-ERK axis. Taken together, our findings demonstrate that PFN2 and exosomal PFN2 promote EC proliferation, migration, and tube formation through the PI3K-PFN2-ERK axis. Exosomal PFN2 may be a valuable target in the repair of MI injury via angiogenesis.
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Reviewed by: Jian Zhang, Nanjing Medical University, China; Jinxuan Zhao, Nanjing Drum Tower Hospital, China
These authors have contributed equally to this work
Edited by: Shijun Wang, Zhongshan Hospital, Fudan University, China
This article was submitted to Cardiovascular Metabolism, a section of the journal Frontiers in Cardiovascular Medicine
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2022.781753