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Updated: Oct 11, 2025

Improving the Accuracy of Flow Cytometric Assessment of Mitochondrial Membrane Potential in Hematopoietic Stem and Progenitor Cells Through the Inhibition of Efflux Pumps
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Improving the Accuracy of Flow Cytometric Assessment of Mitochondrial Membrane Potential in Hematopoietic Stem and Progenitor Cells Through the Inhibition of Efflux Pumps

Published on: July 30, 2019

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RIPK1 Coordinates Bone Marrow Mesenchymal Stem Cell Survival by Maintaining Mitochondrial Homeostasis via p53

Qing Tian1, Chen Cao2, Weijian Qiu1

  • 1Department of Orthopaedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Stem Cells International
|November 29, 2021
PubMed

Insights

Receptor-interacting protein kinase 1 (RIPK1) is crucial for bone marrow mesenchymal stem cell (MSC) survival. Its absence impairs MSC proliferation, differentiation, and migration, leading to cell death via mitochondrial dysfunction and the p53-PUMA pathway.

Area of Science:

  • Cell Biology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Mesenchymal stem cells (MSCs) are vital for bone marrow microenvironment homeostasis.
  • The molecular mechanisms governing MSC survival are not fully understood.
  • Receptor-interacting protein kinase 1 (RIPK1) is implicated in programmed cell death and tissue homeostasis.

Purpose of the Study:

  • To investigate the role of RIPK1 in bone marrow MSCs.
  • To elucidate the molecular mechanisms underlying RIPK1's function in MSCs.

Main Methods:

  • RIPK1 knockdown in bone marrow MSCs.
  • Assessment of MSC proliferation, differentiation, and migration.
  • Analysis of mitochondrial permeability transition pore (mPTP) opening and mitochondrial DNA (mtDNA) damage.
  • Investigation of apoptosis and necroptosis.
  • Evaluation of the p53-PUMA signaling pathway.

Main Results:

  • RIPK1 knockdown suppressed proliferation, differentiation, and migration of bone marrow MSCs.
  • RIPK1 deficiency led to mPTP opening, mtDNA damage, and mitochondrial dysfunction.
  • Mitochondrial dysfunction induced apoptosis and necroptosis in MSCs.
  • The p53-PUMA axis was identified as a key pathway in RIPK1-deficient MSCs.

Conclusions:

  • RIPK1 is indispensable for the survival of bone marrow MSCs.
  • RIPK1 regulates MSC function through mitochondrial integrity and the p53-PUMA pathway.
  • Understanding RIPK1's role provides insights into bone marrow microenvironment homeostasis.

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