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Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Intravenous acellular human amniotic fluid prevents ischemic cardiac remodeling
Grace Mitchell1,2, Hadi Javan1,2, Ian Nickel1,2
1Division of Cardiothoracic Surgery, University of Utah School of Medicine, University of Utah, Helix Tower, Level 4 North, 30 N Mario Capecchi Dr., Salt Lake City, UT, 84112, USA.
Acellular human amniotic fluid (hAF) significantly reduces heart damage and fibrosis after injury in rats. This cardioprotective effect is linked to enhanced cellular tolerance to stress, suggesting hAF as a potential therapeutic adjunct.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Immunology
Background:
- Amniotic products are known for their immunomodulatory and tissue repair capabilities.
- Cardiac remodeling after injury contributes to heart failure.
- Investigating novel therapeutic agents for cardioprotection is crucial.
Purpose of the Study:
- To evaluate the impact of acellular human amniotic fluid (hAF) on cardiac remodeling post-myocardial infarction.
- To explore the cellular mechanisms underlying hAF's cardioprotective effects.
Main Methods:
- Acellular hAF was prepared from donated amniotic fluid.
- hAF was administered intravenously to rats following coronary ligation (myocardial infarction model).
- In vitro studies assessed H9C2 cell response to hypoxic stress with and without hAF.
Main Results:
- hAF treatment led to a nearly sixfold reduction in infarct size and fibrosis in rats.
- hAF-treated H9C2 cells exhibited improved viability and mitochondrial stability under hypoxia.
- Apoptosis was significantly reduced in hAF-exposed cells during hypoxic conditions.
Conclusions:
- A single dose of acellular hAF provides significant functional cardioprotection in a rat model of cardiac injury.
- The cardioprotective mechanism involves enhanced cellular tolerance to hypoxic stress, mediated by proteins within hAF.
- Acellular hAF presents a promising, readily available adjunct therapy for cardioprotection.
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