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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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Oxidative Stress-induced Autophagy Compromises Stem Cell Viability.

Ravi Prakash1, Eram Fauzia2, Abu Junaid Siddiqui1

  • 1Laboratory for Stem Cell & Restorative Neurology, Department of Biotechnology, Era's Lucknow Medical College and Hospital, Era University, Lucknow, Uttar Pradesh, India.

Stem Cells (Dayton, Ohio)
|March 16, 2022
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Summary

Oxidative stress enhances autophagy in stem cells, impacting their survival. Inhibiting autophagy improves stem cell viability, offering strategies to enhance cell-based therapies for ischemic injuries.

Keywords:
Ambra1Beclin1H2O2O2•−autophagyhuman dental pulp stem cellhuman mesenchymal stem celloxygen-glucose deprivation

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Area of Science:

  • * Stem Cell Biology
  • * Regenerative Medicine
  • * Oxidative Stress Biology

Background:

  • * Stem cell therapies show promise for ischemic injuries like stroke.
  • * Critical challenge: ensuring transplanted cell survival in oxidative stress conditions.
  • * Investigating oxidative stress impact on human dental pulp stem cells (hDPSC) and human mesenchymal stem cells (hMSC).

Purpose of the Study:

  • * To determine how oxidative stress affects hDPSC and hMSC viability.
  • * To elucidate the role of autophagy and specific signaling pathways in this process.
  • * To identify potential strategies for improving cell survival post-transplantation.

Main Methods:

  • * Induced oxidative stress using oxygen-glucose deprivation (OGD).
  • * Analyzed autophagy markers (Ambra1, Beclin1) and reactive oxygen species (ROS) levels.
  • * Utilized ROS scavengers, pathway inhibitors (p38, Erk1/2), and autophagy inhibitors (3-MA).

Main Results:

  • * OGD-induced oxidative stress (O2•-, H2O2) enhanced autophagy in hDPSC and hMSC.
  • * Autophagy induction was mediated by ROS-p38-Erk1/2 signaling pathways.
  • * Inhibiting autophagy significantly improved hDPSC viability under oxidative stress.

Conclusions:

  • * Oxidative stress triggers autophagy in stem cells via ROS-dependent signaling.
  • * Autophagy plays a detrimental role in stem cell survival under stress.
  • * Targeting autophagy presents a viable strategy to enhance stem cell therapy efficacy.