2. Academic Validation
  3. Chick early amniotic fluid component improves heart function and protects against inflammation after myocardial infarction in mice

Chick early amniotic fluid component improves heart function and protects against inflammation after myocardial infarction in mice

  • Front Cardiovasc Med. 2022 Nov 16;9:1042852. doi: 10.3389/fcvm.2022.1042852.
Juan Wang 1 2,  Xiejiu Chen 3,  Lihong Zhang 4,  Yufan Zheng 3,  Jin Qian 5 6,  Ning Sun 7,  Xiaolei Ding 1 2,  Baiping Cui 1 2 3
Affiliations

Affiliations

  • 1 School of Medicine, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), Shanghai University, Nantong, China.
  • 2 Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai, China.
  • 3 State Key Laboratory of Medical Neurobiology, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
  • 4 Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
  • 5 Zhejiang HygeianCells BioMedical Co., Ltd., Hangzhou, China.
  • 6 Stem Cell Application Research Center, Hangzhou Branch of Yangtze Delta Region Institute of Tsinghua University, Hangzhou, China.
  • 7 Wuxi School of Medicine, Jiangnan University, Wuxi, China.
PMID: 36465449 DOI: 10.3389/fcvm.2022.1042852
Abstract

Myocardial infarction (MI) is the major cause of mortality around the world. We recently demonstrated that chick early amniotic fluid (ceAF) can effectively rescue ischemic heart injury, indicating that it has a therapeutic function in MI. However, its functional components and the underlying mechanisms remain to be clarified. Here, we demonstrated that a fraction of ceAF, peak 8 (P8), had a protective effect on acute MI. P8 significantly decreased cardiomyocyte cross-sectional areas and cardiomyocyte Apoptosis in MI mice. Using a human embryonic stem cell-derived cardiomyocyte model, which was subjected to hypoxia and reoxygenation, mimicking MI state, we found that P8 treatment reduced Apoptosis and reversed myocardial contractility. Mechanistically, P8 improved cardiac function by inhibiting NF-κB signaling and downregulating inflammatory cytokine expression. Using mass spectrometry, we identified that guanosine and deoxynucleoside were the main functional components of P8 that suppressed the inflammatory response in human embryonic stem cell-derived cardiomyocytes. Collectively, our data suggest that specific components from ceAF are promising therapeutic agents for ischemic heart injury and could be a potential supplement to current medications for MI.

Keywords

amniotic fluid; hESC-derived cardiomyocytes; immune cells; inflammation; myocardial infarction.

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