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Apoptotic vesicle-mediated senolytics requires mechanical loading.

Zhulin Xue1,2, Yexiang Jiang2, Bowen Meng2

  • 1Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing 100081, China.

Theranostics
|September 6, 2024
PubMed
Summary
This summary is machine-generated.

Mechanical unloading reduces apoptotic vesicles (apoVs) by down-regulating Piezo1. Infusing apoVs rescues this effect, maintaining apoptotic homeostasis and eliminating senescent cells.

Keywords:
apoptosisapoptotic vesiclesmechanical unloadingmesenchymal stem cellssenescent cells

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Area of Science:

  • Mechanobiology
  • Cellular Biology
  • Biomedical Engineering

Background:

  • Mechanical force is vital for extracellular vesicle (EV) functions, including biogenesis and release.
  • The specific impact of mechanical force on apoptotic vesicle (apoV) production remains largely unexplored.
  • Understanding this relationship is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the role of mechanical unloading in regulating apoV production and its consequences.
  • To determine the therapeutic potential of apoVs in counteracting mechanical unloading-induced cellular dysfunction.
  • To elucidate the underlying molecular mechanisms involving Piezo1 and calcium signaling.

Main Methods:

  • Utilized a hindlimb unloading (HU) mouse model to simulate mechanical unloading and analyzed bone marrow EVs.
  • Assessed cellular apoptosis resistance and aging phenotypes using HU mice and a cell microgravity model.
  • Employed microcomputed tomography, histochemistry, immunohistochemistry, and histomorphometry to evaluate apoV therapeutic effects.
  • Conducted gain and loss-of-function studies using siRNA and chemical treatments.

Main Results:

  • Mechanical unloading led to cellular apoptotic resistance and aging phenotypes, reducing circulating apoVs.
  • Down-regulated Piezo1 expression and reduced calcium influx were identified as key mechanisms.
  • Systemic infusion of apoVs rescued Piezo1 expression and calcium influx, mitigating unloading-induced effects.
  • ApoV treatment reversed cellular apoptotic resistance and senescent cell accumulation in HU mice.

Conclusions:

  • Mechanical force is essential for maintaining apoptotic homeostasis and clearing senescent cells.
  • Mesenchymal stem cell-derived apoVs show significant therapeutic potential.
  • Systemic apoV infusion can effectively rescue apoptotic resistance and eliminate senescent cells in conditions of mechanical unloading.