ArticleStem cells translational medicine2020
GARP is a key molecule for mesenchymal stromal cell responses to TGF-β and fundamental to control mitochondrial ROS levels.
Article in Stem cells translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- NLRP3 and AIM2 inflammasomes expression is modified by LPS and titanium ions increasing the release of active IL-1β in alveolar bone-derived MSCs.Stem cells translational medicine · 2024Article
- Investigation of the Effect of Curcumin on Protein Targets in NAFLD Using Bioinformatic Analysis.Nutrients · 2022Article
- GARP as a Therapeutic Target for the Modulation of Regulatory T Cells in Cancer and Autoimmunity.Frontiers in immunology · 2022Review
- Novel insights for improving the therapeutic safety and efficiency of mesenchymal stromal cells.World journal of stem cells · 2020Review
- Application of adipose-derived stem cells in photoaging: basic science and literature review.Stem cell research & therapy · 2020Review
- GARP promotes the proliferation and therapeutic resistance of bone sarcoma cancer cells through the activation of TGF-β.Cell death & disease · 2020Article
- GARP is a key molecule for mesenchymal stromal cell responses to TGF-β and fundamental to control mitochondrial ROS levels.Stem cells translational medicine · 2020Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multipotent mesenchymal stromal cells (MSCs) have emerged as a promising cell therapy in regenerative medicine and for autoimmune/inflammatory diseases. However, a main hurdle for MSCs-based therapies is the loss of their proliferative potential in vitro. Here we report that glycoprotein A repetitions predominant (GARP) is required for the proliferation and survival of adipose-derived MSCs (ASCs) via its regulation of transforming growth factor-β (TGF-β) activation. Silencing of GARP in human ASCs increased their activation of TGF-β which augmented the levels of mitochondrial reactive oxygen species (mtROS), resulting in DNA damage, a block in proliferation and apoptosis. Inhibition of TGF-β signaling reduced the levels of mtROS and DNA damage and restored the ability of GARP
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Registered trials
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