Paras Kumar Mishra, PhD

Associate Professor at University of Nebraska Medical Center


Curriculum vitae



Cellular and Integrative Physiology

University of Nebraska Medical Center



Intracellular matrix metalloproteinase‐9 mediates epigenetic modifications and autophagy to regulate differentiation in human cardiac stem cells


Journal article


S. Yadav, P. Mishra
Stem Cells, 2021

Semantic Scholar DOI PubMed
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APA   Click to copy
Yadav, S., & Mishra, P. (2021). Intracellular matrix metalloproteinase‐9 mediates epigenetic modifications and autophagy to regulate differentiation in human cardiac stem cells. Stem Cells.


Chicago/Turabian   Click to copy
Yadav, S., and P. Mishra. “Intracellular Matrix Metalloproteinase‐9 Mediates Epigenetic Modifications and Autophagy to Regulate Differentiation in Human Cardiac Stem Cells.” Stem Cells (2021).


MLA   Click to copy
Yadav, S., and P. Mishra. “Intracellular Matrix Metalloproteinase‐9 Mediates Epigenetic Modifications and Autophagy to Regulate Differentiation in Human Cardiac Stem Cells.” Stem Cells, 2021.


BibTeX   Click to copy

@article{s2021a,
  title = {Intracellular matrix metalloproteinase‐9 mediates epigenetic modifications and autophagy to regulate differentiation in human cardiac stem cells},
  year = {2021},
  journal = {Stem Cells},
  author = {Yadav, S. and Mishra, P.}
}

Abstract

Epigenetic reprogramming and autophagy have critical roles in differentiation of stem cells. However, very little is known about how epigenetic modifications are mediated and how they contribute to autophagy and differentiation in human cardiac stem cells (hCSCs). Previously, we have reported that intracellular matrix metalloproteinase‐9 (MMP9), a collagenase, mediates cell death in hCSCs. Here, we investigated whether intracellular MMP9 mediates epigenetic modifications and autophagy in hCSCs. We created MMP9KO hCSCs and treated them with 5‐azacytidine, an inhibitor of DNA methylation, and bafilomycin A1, an inhibitor of autophagosome degradation, and evaluated epigenetic modifications, autophagic flux, and differentiation. Our results showed compromised epigenetic modifications, reduced autophagy, and impaired differentiation in MMP9KO hCSCs. Remarkably, paracrine MMP9 supplementation restored epigenetic modifications but further reduced autophagy in MMP9KO hCSCs. We conclude that intracellular MMP9 is a critical mediator of epigenetic modifications and autophagy in hCSCs. Furthermore, the endocrine and paracrine effects of MMP9 vary for regulating autophagy in hCSCs. These novel roles of MMP9 are valuable for stem cell therapy.


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