ArticleActa pharmacologica Sinica2021
BMSC-derived exosomes ameliorate sulfur mustard-induced acute lung injury by regulating the GPRC5A-YAP axis.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- Stem Cell Extracellular Vesicles as Anti-SARS-CoV-2 Immunomodulatory Therapeutics: A Systematic Review of Clinical and Preclinical Studies.Stem cell reviews and reports · 2024Pooled it
- The efficacy of extracellular vesicles for acute lung injury in preclinical animal models: a meta-analysis.BMC pulmonary medicine · 2024Pooled it
- Tissue regeneration strategies based on mesenchymal stem cell-derived extracellular vesicles: from bench to bedside.Burns & trauma · 2026Review
- Beyond immunomodulation: mechanisms and synergistic strategies of mesenchymal stem cells in promoting alveolar epithelial and endothelial repair in ARDS.Frontiers in immunology · 2026Review
- Native and Engineered Extracellular Vesicles for the Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome.Small science · 2025Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Expressions of apoptotic protein and gene following sulfur mustard-induced acute pulmonary injuries in rats.Iranian journal of basic medical sciences · 2025Article
- The dual role of mesenchymal stem cells in apoptosis regulation.Cell death & disease · 2024Review
- Endothelium-Derived Engineered Extracellular Vesicles Protect the Pulmonary Endothelial Barrier in Acute Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Translational medicine for acute lung injury.Journal of translational medicine · 2024Review
- Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating Gprc5a signaling.Nature communications · 2023Article
- HMSCs exosome-derived miR-199a-5p attenuates sulfur mustard-associated oxidative stress via the CAV1/NRF2 signalling pathway.Journal of cellular and molecular medicine · 2023Article
- Could extracellular vesicles derived from mesenchymal stem cells be a potential therapy for acute pancreatitis-induced cardiac injury?World journal of stem cells · 2023Review
- The Immunomodulatory Role of Cell-Free Approaches in SARS-CoV-2-Induced Cytokine Storm-A Powerful Therapeutic Tool for COVID-19 Patients.Biomedicines · 2023Review
- Therapeutic Benefits of Stem Cells and Exosomes for Sulfur-Mustard-Induced Tissue Damage.International journal of molecular sciences · 2023Review
- MiR-146a-5p delivered by hucMSC extracellular vesicles modulates the inflammatory response to sulfur mustard-induced acute lung injury.Stem cell research & therapy · 2023Article
- Aspirin reverses inflammatory suppression of chondrogenesis by stabilizing YAP.Cell proliferation · 2023Article
- Extracellular vesicles in the pathogenesis and treatment of acute lung injury.Military Medical Research · 2022Review
- Review
- Molecular Insight into the Therapeutic Effects of Stem Cell-Derived Exosomes in Respiratory Diseases and the Potential for Pulmonary Delivery.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sulfur mustard (SM) is a highly toxic chemical warfare agent that causes acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). There are no effective therapeutic treatments or antidotes available currently to counteract its toxic effects. Our previous study shows that bone marrow-derived mesenchymal stromal cells (BMSCs) could exert therapeutic effects against SM-induced lung injury. In this study, we explored the therapeutic potential of BMSC-derived exosomes (BMSC-Exs) against ALI and the underlying mechanisms. ALI was induced in mice by injection of SM (30 mg/kg, sc) at their medial and dorsal surfaces. BMSC-Exs (20 μg/kg in 200 μL PBS, iv) were injected for a 5-day period after SM exposure. We showed that BMSC-Exs administration caused a protective effect against pulmonary edema. Using a lung epithelial cell barrier model, BMSC-Exs (10, 20, 40 μg) dose-dependently inhibited SM-induced cell apoptosis and promoted the recovery of epithelial barrier function by facilitating the expression and relocalization of junction proteins (E-cadherin, claudin-1, occludin, and ZO-1). We further demonstrated that BMSC-Exs protected against apoptosis and promoted the restoration of barrier function against SM through upregulating G protein-coupled receptor family C group 5 type A (GPRC5A), a retinoic acid target gene predominately expressed in the epithelial cells of the lung. Knockdown of GPRC5A reduced the antiapoptotic and barrier regeneration abilities of BMSC-Exs and diminished their therapeutic effects in vitro and in vivo. BMSC-Exs-caused upregulation of GPRC5A promoted the expression of Bcl-2 and junction proteins via regulating the YAP pathway. In summary, BMSC-Exs treatment exerts protective effects against SM-induced ALI by promoting alveolar epithelial barrier repair and may be an alternative approach to stem cell-based therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.