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Cited by 25Mesenchymal stem cell researchRespiratory Support and MechanismsMitochondrial Function and Pathology

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MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS

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Wang, Jinlong, Meng, Shanshan, Chen, Yixuan, Wang, Haofei, Hu, Wenhan, Liu, Shuai, Huang, Lili, Xu, Jingyuan, Li, Qing, Wu, Xiaojing, Huang, Wei, Huang, Yingzi·2025·Redox Report
DOI 10.1080/13510002.2025.2474897PMC PMC11912292
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Abstract

Background Mesenchymal stem cells (MSCs) are a potential therapy for acute respiratory distress syndrome (ARDS), but their mechanisms in repairing mitochondrial damage in ARDS endothelial cells remain unclear.Methods We first examined MSCs’ mitochondrial transfer ability and mechanisms to mouse pulmonary microvascular endothelial cells (MPMECs) in ARDS. Then, we investigated how MSC-mediated mitochondrial transfer affects the repair of endothelial damage. Finally, we elucidated the mechanisms by which MSC-mediated mitochondrial transfer promotes vascular regeneration.Results Compared to mitochondrial-damaged MSCs, normal MSCs showed a significantly higher mitochondrial transfer rate to MPMECs, with increases of 41.68% in vitro (P < 0.0001) and 10.50% in vivo (P = 0.0005). Furthermore, MSC-mediated mitochondrial transfer significantly reduced reactive oxygen species (P < 0.05) and promoted proliferation (P < 0.0001) in MPMECs. Finally, MSC-mediated mitochondrial transfer significantly increased the activity of the tricarboxylic acid (TCA) cycle (MD of CS mRNA: 23.76, P = 0.032), and further enhanced fatty acid synthesis (MD of FAS mRNA: 6.67, P = 0.0001), leading to a 6.7-fold increase in vascular endothelial growth factor release from MPMECs and promoted vascular regeneration in ARDS.Conclusion MSC-mediated mitochondrial transfer to MPMECs activates the TCA cycle and fatty acid synthesis, promoting endothelial proliferation and pro-angiogenic factor release, thereby enhancing vascular regeneration in ARDS.

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Figures

Figure 1. MSCs Mitigate Endothelial Injury in ARDS through Mitochondrial Transfer. (A) Representative flow cytometry histogram showing mitoTracker labeled mitochondrial transfer from MSCs to MPMECs (N = 3). Gray histogram, negative control. (B) Representative flow cytometry images and quantitative analysis of MSC-derived mitochondrial transfer to MPMECs (N = 4). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. (C) Representative immunofluorescence images and HALO quantitative analysis of mouse lung tissue showing MSC-derived mitochondrial transfer to MPMECs (N = 3). Green signal, CD31-positive MPMECs; red signal, mitochondria derived from MSCs; blue signal, nuclei; scale bar, 50 μm. (D) Representative flow cytometry images and quantitative analysis of single-cell suspension from mouse lung tissue showing MSC-derived mitochondrial transfer to MPMECs (N = 3). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. (E) Representative Western Blot images and quantitative analysis of mitochondrial complex I expression in ARDS mouse lung tissue under different conditions (N = 4). (F) Representative Western Blot images and quantitative analysis of mitochondrial complex I expression in MPMECs treated with different conditions (N = 5). (G) Flow cytometry analysis of average ROS fluorescence intensity in MPMECs treated with different conditions (N = 4). (H) Flow cytometry analysis of apoptosis rate in MPMECs treated with different conditions (N = 5). (I) Representative H&E staining images and quantitative analysis using lung injury score of lung tissues from ARDS mouse treated with MSCs or rotenone-treated MSCs (N = 7); scale bar, 100 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 1. MSCs Mitigate Endothelial Injury in ARDS through Mitochondrial Transfer. (A) Representative flow cytometry histogram showing mitoTracker labeled mitochondrial transfer from MSCs to MPMECs (N = 3). Gray histogram, negative control. (B) Representative flow cytometry images and quantitative analysis of MSC-derived mitochondrial transfer to MPMECs (N = 4). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. (C) Representative immunofluorescence images and HALO quantitative analysis of mouse lung tissue showing MSC-derived mitochondrial transfer to MPMECs (N = 3). Green signal, CD31-positive MPMECs; red signal, mitochondria derived from MSCs; blue signal, nuclei; scale bar, 50 μm. (D) Representative flow cytometry images and quantitative analysis of single-cell suspension from mouse lung tissue showing MSC-derived mitochondrial transfer to MPMECs (N = 3). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. (E) Representative Western Blot images and quantitative analysis of mitochondrial complex I expression in ARDS mouse lung tissue under different conditions (N = 4). (F) Representative Western Blot images and quantitative analysis of mitochondrial complex I expression in MPMECs treated with different conditions (N = 5). (G) Flow cytometry analysis of average ROS fluorescence intensity in MPMECs treated with different conditions (N = 4). (H) Flow cytometry analysis of apoptosis rate in MPMECs treated with different conditions (N = 5). (I) Representative H&E staining images and quantitative analysis using lung injury score of lung tissues from ARDS mouse treated with MSCs or rotenone-treated MSCs (N = 7); scale bar, 100 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 2. MSCs Promote Endothelial Cell Proliferation and Vascular Regeneration in ARDS through Mitochondrial Transfer. (A) Quantitative flow cytometry analysis of CFSE mean fluorescence intensity in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (B) Relative expression of cell proliferation marker Ki67 mRNA in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (C) Quantitative flow cytometry analysis of CFSE mean fluorescence intensity in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 5). (D) Relative expression of Ki67 mRNA in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). (E) Relative expression of Ki67 mRNA in ARDS mouse lung tissue under different conditions (N = 4). (F-G) Relative expression of HGF mRNA (F) and VEGF mRNA (G) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 12). (H-I) Relative expression of HGF mRNA (H) and VEGF mRNA (I) in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 12). (J-K) Relative expression of HGF mRNA (J) and VEGF mRNA (K) in ARDS mouse lung tissue under different conditions (N = 4). (L-M) ELISA quantitative analysis of HGF (L) and VEGF (M) in cell culture supernatants of mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 12). (N-O) Representative immunohistochemical images (N) and HALO quantitative analysis (O) of lung vasculature in ARDS mice under different conditions (N = 4). Brown signal, endothelial cells; blue signal, nuclei; scale bar, 20 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 2. MSCs Promote Endothelial Cell Proliferation and Vascular Regeneration in ARDS through Mitochondrial Transfer. (A) Quantitative flow cytometry analysis of CFSE mean fluorescence intensity in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (B) Relative expression of cell proliferation marker Ki67 mRNA in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (C) Quantitative flow cytometry analysis of CFSE mean fluorescence intensity in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 5). (D) Relative expression of Ki67 mRNA in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). (E) Relative expression of Ki67 mRNA in ARDS mouse lung tissue under different conditions (N = 4). (F-G) Relative expression of HGF mRNA (F) and VEGF mRNA (G) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 12). (H-I) Relative expression of HGF mRNA (H) and VEGF mRNA (I) in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 12). (J-K) Relative expression of HGF mRNA (J) and VEGF mRNA (K) in ARDS mouse lung tissue under different conditions (N = 4). (L-M) ELISA quantitative analysis of HGF (L) and VEGF (M) in cell culture supernatants of mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 12). (N-O) Representative immunohistochemical images (N) and HALO quantitative analysis (O) of lung vasculature in ARDS mice under different conditions (N = 4). Brown signal, endothelial cells; blue signal, nuclei; scale bar, 20 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 3. MSCs Transfer Mitochondria to MPMECs via TNTs. (A) Representative confocal microscopy image showing mitochondrial transfer from MSCs to MPMECs via TNTs (N = 3). Red signal, MSCs; green signal, MPMECs; enlarged section, TNT; scale bar, 10 μm. (B) Flow cytometry quantification of mitochondrial transfer rate from MSCs to MPMECs in co-culture systems with different concentrations of Cytochalasin B (N = 4). (C) Quantitative flow cytometry analysis of ROS in MPMECs treated with different conditions (N = 5). (D) Quantitative flow cytometry analysis of apoptosis in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 3). (E-F) Relative expression of Mfn1 mRNA (E) and Mfn2 mRNA (F) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (G) Relative expression of Miro1 mRNA in MSCs co-cultured with MPMECs under different conditions (N = 3). (H-I) Relative expression of Miro1 mRNA (H) and Miro1 protein (I) in negative control MSCs and Miro1 knockdown MSCs (N = 3). (J) Representative flow cytometry images and quantitative analysis of mitochondrial transfer rate from negative control MSCs or Miro1 knockdown MSCs to mitochondrial damaged MPMECs (N = 4). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 3. MSCs Transfer Mitochondria to MPMECs via TNTs. (A) Representative confocal microscopy image showing mitochondrial transfer from MSCs to MPMECs via TNTs (N = 3). Red signal, MSCs; green signal, MPMECs; enlarged section, TNT; scale bar, 10 μm. (B) Flow cytometry quantification of mitochondrial transfer rate from MSCs to MPMECs in co-culture systems with different concentrations of Cytochalasin B (N = 4). (C) Quantitative flow cytometry analysis of ROS in MPMECs treated with different conditions (N = 5). (D) Quantitative flow cytometry analysis of apoptosis in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 3). (E-F) Relative expression of Mfn1 mRNA (E) and Mfn2 mRNA (F) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (G) Relative expression of Miro1 mRNA in MSCs co-cultured with MPMECs under different conditions (N = 3). (H-I) Relative expression of Miro1 mRNA (H) and Miro1 protein (I) in negative control MSCs and Miro1 knockdown MSCs (N = 3). (J) Representative flow cytometry images and quantitative analysis of mitochondrial transfer rate from negative control MSCs or Miro1 knockdown MSCs to mitochondrial damaged MPMECs (N = 4). CD31, marker for MPMECs; mitoTracker, marker for MSC-derived mitochondria. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 4. MPMECs Accept Mitochondria from MSCs through Dynamin-Dependent Clathrin-Mediated Endocytosis. (A) Representative fluorescence microscopy image showing mitochondrial transfer from MSCs to mitochondrial damaged MPMECs cultured in Transwell chambers for isolation (N = 3). Red signal, mitochondria of MPMECs; green signal, mitochondria from MSCs; scale bar, 10 μm. (B) Flow cytometry quantification of mitochondrial transfer rate from MSCs to mitochondrial damaged MPMECs cultured in Transwell chambers for isolation under different conditions (N = 5). (C) Quantitative flow cytometry analysis of ROS in MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). (D) Quantitative flow cytometry analysis of apoptosis in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 5). (E-F) Relative expression of Mfn1 mRNA (E) and Mfn2 mRNA (F) in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 4. MPMECs Accept Mitochondria from MSCs through Dynamin-Dependent Clathrin-Mediated Endocytosis. (A) Representative fluorescence microscopy image showing mitochondrial transfer from MSCs to mitochondrial damaged MPMECs cultured in Transwell chambers for isolation (N = 3). Red signal, mitochondria of MPMECs; green signal, mitochondria from MSCs; scale bar, 10 μm. (B) Flow cytometry quantification of mitochondrial transfer rate from MSCs to mitochondrial damaged MPMECs cultured in Transwell chambers for isolation under different conditions (N = 5). (C) Quantitative flow cytometry analysis of ROS in MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). (D) Quantitative flow cytometry analysis of apoptosis in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 5). (E-F) Relative expression of Mfn1 mRNA (E) and Mfn2 mRNA (F) in mitochondrial damaged MPMECs, or cultured with MSCs in Transwell chambers for isolation under different conditions (N = 4). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 5. MSCs Transfer Mitochondria to MPMECs Promoting Fatty Acid Synthesis and Vascular Regeneration. (A) Quantitative analysis of ATP in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (B-D) Relative expression of key fatty acid synthesis enzyme FAS mRNA (B), ACC mRNA (C), ACLY mRNA (D) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (E-G) Relative expression of key fatty acid synthesis enzyme FAS mRNA (E), ACC mRNA (F), ACLY mRNA (G) in lung tissues of ARDS mice, or treated with MSCs under different conditions (N = 4). (H) Representative immunofluorescence images of FAS in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 3). Red signal, FAS; blue signal, nuclei; scale bar, 20 μm. (I-J) Relative expression of VEGF mRNA (I) and HGF mRNA (J) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (K-L) ELISA quantitative analysis of VEGF (K) and HGF (L) in cell culture supernatants of mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 5. MSCs Transfer Mitochondria to MPMECs Promoting Fatty Acid Synthesis and Vascular Regeneration. (A) Quantitative analysis of ATP in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). (B-D) Relative expression of key fatty acid synthesis enzyme FAS mRNA (B), ACC mRNA (C), ACLY mRNA (D) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (E-G) Relative expression of key fatty acid synthesis enzyme FAS mRNA (E), ACC mRNA (F), ACLY mRNA (G) in lung tissues of ARDS mice, or treated with MSCs under different conditions (N = 4). (H) Representative immunofluorescence images of FAS in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 3). Red signal, FAS; blue signal, nuclei; scale bar, 20 μm. (I-J) Relative expression of VEGF mRNA (I) and HGF mRNA (J) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (K-L) ELISA quantitative analysis of VEGF (K) and HGF (L) in cell culture supernatants of mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 5). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 6. MSCs Transfer Mitochondria to MPMECs Stimulating the TCA Cycle and Activating Citrate-Dependent Fatty Acid Synthesis. (A-C) Relative expression of the key TCA cycle enzyme CS mRNA (A), IDH mRNA (B) and OGDH mRNA (C) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (D) Relative expression of CS mRNA in mitochondrial damaged MPMECs, or co-cultured with MSCs with or without Devimistat (N = 4). (E-G) Relative expression of key fatty acid synthesis enzyme FAS mRNA (E), ACC mRNA (F) and ACLY mRNA (G) in mitochondrial damaged MPMECs, or co-cultured with MSCs with or without Devimistat (N = 4). (H) Representative immunofluorescence images of FAS in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 3). Red signal, FAS; blue signal, nuclei. (I-K) Relative expression of key fatty acid synthesis enzyme FAS mRNA (I), ACC mRNA (J) and ACLY mRNA (K) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 6. MSCs Transfer Mitochondria to MPMECs Stimulating the TCA Cycle and Activating Citrate-Dependent Fatty Acid Synthesis. (A-C) Relative expression of the key TCA cycle enzyme CS mRNA (A), IDH mRNA (B) and OGDH mRNA (C) in mitochondrial damaged MPMECs, or co-cultured with MSCs under different conditions (N = 4). (D) Relative expression of CS mRNA in mitochondrial damaged MPMECs, or co-cultured with MSCs with or without Devimistat (N = 4). (E-G) Relative expression of key fatty acid synthesis enzyme FAS mRNA (E), ACC mRNA (F) and ACLY mRNA (G) in mitochondrial damaged MPMECs, or co-cultured with MSCs with or without Devimistat (N = 4). (H) Representative immunofluorescence images of FAS in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 3). Red signal, FAS; blue signal, nuclei. (I-K) Relative expression of key fatty acid synthesis enzyme FAS mRNA (I), ACC mRNA (J) and ACLY mRNA (K) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 7. Citrate Restores the Vascular Regenerative Function of Mitochondrially Damaged MSCs. (A-C) Relative expression of key fatty acid synthesis enzyme FAS mRNA (A), ACC mRNA (B) and ACLY mRNA (C) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (D-E) Relative expression of VEGF mRNA (D) and HGF mRNA (E) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (F-G) ELISA quantitative analysis of VEGF (F) and HGF (G) in cell culture supernatants of mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (H) Representative images of H&E staining (top row) and endothelial cell immunohistochemical analysis (bottom row) of lung tissue in ARDS mice, or treated with MSCs under different conditions (N = 3). The brown signal indicates endothelial cells; the blue signal indicates nuclei; scale bar, 20 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 7. Citrate Restores the Vascular Regenerative Function of Mitochondrially Damaged MSCs. (A-C) Relative expression of key fatty acid synthesis enzyme FAS mRNA (A), ACC mRNA (B) and ACLY mRNA (C) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (D-E) Relative expression of VEGF mRNA (D) and HGF mRNA (E) in mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (F-G) ELISA quantitative analysis of VEGF (F) and HGF (G) in cell culture supernatants of mitochondrial damaged MPMECs co-cultured with MSCs under different conditions (N = 4). (H) Representative images of H&E staining (top row) and endothelial cell immunohistochemical analysis (bottom row) of lung tissue in ARDS mice, or treated with MSCs under different conditions (N = 3). The brown signal indicates endothelial cells; the blue signal indicates nuclei; scale bar, 20 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central
Figure 8. MSCs Alleviate LPS-Induced Lung Injury. (A–B) Representative H&E-stained images (A) and quantitative analysis of lung injury score (B) of lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). Scale bar, 50 μm. (C) Representative immunohistochemical images of endothelial cell adhesion protein Occludin in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). Brown signal, Occludin-positive signal; blue signal, nuclei; scale bar, 50 μm. (D) HALO quantitative analysis of Occludin immunohistochemistry in lung tissues from normal mice, ARDS, and ARDS treated with MSCs (N = 3). (E-F) ELISA quantitative analysis of iNOS (E) and eNOS (F) expression in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs. (G) The LWW/BW ratio from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). (H) Evans blue content in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.
Figure 8. MSCs Alleviate LPS-Induced Lung Injury. (A–B) Representative H&E-stained images (A) and quantitative analysis of lung injury score (B) of lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). Scale bar, 50 μm. (C) Representative immunohistochemical images of endothelial cell adhesion protein Occludin in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). Brown signal, Occludin-positive signal; blue signal, nuclei; scale bar, 50 μm. (D) HALO quantitative analysis of Occludin immunohistochemistry in lung tissues from normal mice, ARDS, and ARDS treated with MSCs (N = 3). (E-F) ELISA quantitative analysis of iNOS (E) and eNOS (F) expression in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs. (G) The LWW/BW ratio from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs (N = 3). (H) Evans blue content in lung tissues from normal mice, sham-operated, ARDS, ARDS treated with MSCs, and sham-operated mice treated with MSCs. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Each dot represents an independent experiment. Error bars indicate mean ± SD.CC BY-NC · PubMed Central

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Metadata

Authors
Wang, J., Meng, S., Chen, Y., Wang, H., Hu, W., Liu, S., Huang, L., Xu, J., Li, Q., Wu, X., Huang, W., & Huang, Y.
Affiliations
Zhongda Hospital Southeast University (CN)
Corresponding author
Huang, Yingzi
ORCID
Venue
Redox Report
Publisher
Informa UK Limited
Published
2025-03-13
Volume
30
Issue
1
Pages
2474897-2474897
ISSN
  • 1351-0002 (ISSN-L)
  • 1743-2928
DOI
10.1080/13510002.2025.2474897
PMC
PMC11912292
OpenAlex
W4408464831
Cited by
25
References
6
Citations by year
2026: 14 · 2025: 11
FWCI
16.16
Type
journal article
Language
en
Open access
Licence
Locations
  • Redox Report (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Key R&D Program of China (2022YFC2304600)
  • National Natural Science Foundation of China (82272235, 82102300, 82272211, 82302470)
  • Science Foundation of the Commission of Health of Jiangsu Province (ZDB2020009)
  • Jiangsu Province Key research and development Program (Social Development) Special Project (BE2021734)
  • China Postdoctoral Science Foundation (2022M710685)
  • Special fund project for health science and technology development of Nanjing Municipal Health Commission (YKK21265)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
mesenchymal stem cells, mitochondrial transfer, acute respiratory distress syndrome, endothelial cells, vascular regeneration, metabolic reprogramming, TCA cycle, fatty acid synthesis, reactive oxygen species, endothelial cell proliferation, vascular endothelial growth factor, angiogenesis, mitochondrial damage
MeSH terms
Animals, Cells, Cultured, Humans, Male, Mice, Inbred C57BL, Mitochondria, Regeneration, Respiratory Distress Syndrome, Reactive Oxygen Species, Endothelial Cells, Cell Proliferation, Mice, Mesenchymal Stem Cells

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