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Protection of adipose-derived mesenchymal stromal cells during acute lung injury requires autophagy maintained by

Yue Hu1, Jing Shao2, Lanying Shen3

  • 1Key Laboratory of Respiratory Disease of Zhejiang Province, Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, 310009, Hangzhou, Zhejiang, China. huyue88@zju.edu.cn.

Cell Death Discovery
|December 5, 2022
PubMed

Insights

Adipose-derived mesenchymal stem cells (ADSCs) alleviate acute lung injury (ALI) by regulating autophagy. This study reveals that mammalian target of rapamycin (mTOR)-mediated autophagy is crucial for ADSC

Area of Science:

  • Immunology and Regenerative Medicine
  • Cellular and Molecular Biology

Background:

  • Mesenchymal stem cells show therapeutic potential for acute lung injury (ALI).
  • The molecular mechanisms underlying stem cell therapy for ALI are not fully understood.
  • Autophagy's role in stem cell-mediated ALI treatment requires further investigation.

Purpose of the Study:

  • To investigate the therapeutic effects of adipose-derived mesenchymal stem cells (ADSCs) on lipopolysaccharide (LPS)-induced ALI.
  • To elucidate the role of autophagy in ADSC-mediated anti-inflammatory functions in ALI.
  • To determine the involvement of the mammalian target of rapamycin (mTOR) pathway in ADSC therapy for ALI.

Main Methods:

  • Isolation and characterization of ADSCs using alizarin red staining, oil red staining, and flow cytometry.
  • Assessment of lung injury and inflammation via Evans blue, wet/dry weight ratio, and H&E staining.
  • Detection of inflammatory cytokines (IFN-γ, IL-2, TNF-α) using ELISA.
  • Evaluation of autophagy using an mRFP-GFP-LC3 system, Western blotting, and electron microscopy.

Main Results:

  • ADSCs significantly alleviated inflammatory responses and tissue damage in LPS-induced ALI.
  • Autophagy was identified as a key mechanism maintaining the therapeutic efficacy of ADSCs in vivo.
  • In vitro, ADSCs utilized autophagy to exert anti-inflammatory effects on alveolar epithelial cells.
  • mTOR was confirmed as a critical regulator of autophagy in this context.

Conclusions:

  • ADSC treatment effectively reduces inflammation and damage in ALI models.
  • The therapeutic benefits of ADSCs in ALI are critically dependent on mTOR-mediated autophagy.
  • Targeting mTOR-mediated autophagy presents a potential therapeutic strategy for improving ADSC efficacy in ALI treatment.

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