Protective Effects of Chicken Bone Marrow-Derived Mesenchymal Stem Cells on a Mouse Model of Acute Lung Injury

Abstract Objective: Mesenchymal stem cells (MSCs) were an emergent tool to prevent acute lung injury (ALI) and its complications. We attempted to isolate, culture, and characterize chicken bone marrow-derived mesenchymal stem cells (BM-MSCs), investigate whether BM-MSCs protect against lipopolysaccharide (LPS)-induced ALI, and explore the related mechanisms. Methods: Ninety-six male ICR (6 wks old) mice were divided into three groups: Con, LPS, and LPS + MSC. Mice in the LPS and Ex+LPS groups received 5 mg/kg LPS intratracheally to induce ALI. Histopathological micrographs showed morphological changes in the lung, heart, liver, kidney, and aorta. Lung permeability, bronchoalveolar lavage fluid (BALF) cell counts, oxidative stress parameters, and inflammatory cytokine levels in the BALF, plasma, and lung tissue were detected. Furthermore, gene expression levels for Toll-Like Receptor 4 (TRL4) and myeloid differentiation factor (Mdy88) were measured. Besides, a survival analysis was performed in sixty male ICR mice. Results: BM-MSCs administration significantly increased the survival rate and decreased the histopathological severity of LPS-induced lung, liver, kidney, and aortic injury. BM-MSC administration improved LPS-induced pulmonary inflammation, systemic inflammation, and oxidative stress injury. BM-MSC administration reduced the infiltration of neutrophils in lung, liver, kidney, and heart tissues. In addition, BM-MSC administration reduced TRL4 and Mdy88 mRNA expression in mice with ALI. Conclusions: Chicken BM-MSCs improved LPS-induced ALI and liver, kidney, heart, and aortic injury. Chicken BM-MSCs improved LPS-induced ALI, in part through TLR4/Myd88 signaling and inhibition of inflammation and oxidative stress injury. BM-MSCs improved LPS-induced pulmonary fibrosis via suppressing TGF-β and MMP-9. BM-MSCs reduced neutrophil content via suppressing CXCL-1, IL-8, and TNF-α.

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Chicken bone marrow mesenchymal stem cells improve lung and distal organ injury

Scientific Reports ◽

10.1038/s41598-021-97383-4 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Hexuan Niu ◽

Hanan Song ◽

Yuhan Guan ◽

Xianchun Zong ◽

Ruili Niu ◽

...

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Inflammatory Cytokine ◽

Organ Injury ◽

Stress Injury ◽

Chicken Bone ◽

Oxidative Stress Injury ◽

And Oxidative Stress

AbstractMesenchymal stem cells (MSCs) are associated with pulmonary protection and longevity. We separated chicken bone marrow-derived mesenchymal stem cells (BM-MSCs); investigated whether BM-MSCs can improve lipopolysaccharide (LPS)-induced lung and distal organ injury; and explored the underlying mechanisms. Ninety-six male ICR (6 weeks old) mice were randomly divided into three groups: Sham, LPS, and LPS + MSC groups. The mice were intratracheally injected with 5 mg/kg LPS to induce acute lung injury (ALI). The histopathological severity of injury to the lung, liver, kidney, heart, and aortic tissues was detected. Wet/dry ratio, protein concentrations in bronchoalveolar lavage fluid (BALF), BALF cell counts, inflammatory cytokine levels in serum, inflammatory cytokine gene expression, and oxidative stress-related indicators were detected. In addition, a survival analysis was performed in sixty male ICR mice (6 weeks old, 18–20 g). This study used chicken BM-MSCs, which are easier to obtain and more convenient than other animal or human MSCs, and have MSC-associated properties, such as a colony forming ability, multilineage differentiation potential, and certain phenotypes. BM-MSCs administration significantly improved the survival rate, systemic inflammation, and the histopathological severity of lung, liver, kidney, and aortic injury during ALI. BM-MSCs administration reduced the levels of inflammatory factors in BALF, the infiltration of neutrophils, and oxidative stress injury in lung tissue. In addition, BM-MSCs administration reduced TRL4 and Mdy88 mRNA expression during ALI. Chicken BM-MSCs serve as a potential alternative resource for stem cell therapy and exert a prominent effect on LPS-induced ALI and extrapulmonary injury, in part through TRL4/Mdy88 signaling and inhibition of neutrophil inflammation and oxidative stress injury.

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Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

Journal of Immunology Research ◽

10.1155/2021/2389029 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Haijun Zhao ◽

Yanhui He

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Endothelial Cells ◽

Inflammatory Response ◽

Protective Effects ◽

Stress Injury ◽

Oxidative Stress Injury ◽

Marrow Mesenchymal Stem Cells ◽

And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

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New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning

Journal of Cellular Biochemistry ◽

10.1002/jcb.29298 ◽

2019 ◽

Vol 120 (12) ◽

pp. 19902-19914 ◽

Cited By ~ 6

Author(s):

Fei Zhang ◽

Wuxun Peng ◽

Jian Zhang ◽

Wentao Dong ◽

Dajiang Yuan ◽

...

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Stress Injury ◽

Nrf2 Pathway ◽

Oxidative Stress Injury ◽

New Strategy ◽

Marrow Mesenchymal Stem Cells

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Exosomes Derived from miR-214-Enriched Bone Marrow-Derived Mesenchymal Stem Cells Regulate Oxidative Damage in Cardiac Stem Cells by Targeting CaMKII

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/4971261 ◽

2018 ◽

Vol 2018 ◽

pp. 1-21 ◽

Cited By ~ 22

Author(s):

Yan Wang ◽

Ranzun Zhao ◽

Debin Liu ◽

Wenwen Deng ◽

Guanxue Xu ◽

...

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Oxidative Damage ◽

Bioactive Molecules ◽

Cardiac Stem Cells ◽

Stress Injury ◽

Hypoxic Conditions ◽

Oxidative Stress Injury

Cardiac stem cells (CSCs) have emerged as one of the most promising stem cells for cardiac protection. Recently, exosomes from bone marrow-derived mesenchymal stem cells (BMSCs) have been found to facilitate cell proliferation and survival by transporting various bioactive molecules, including microRNAs (miRs). In this study, we found that BMSC-derived exosomes (BMSC-exos) significantly decreased apoptosis rates and reactive oxygen species (ROS) production in CSCs after oxidative stress injury. Moreover, a stronger effect was induced by exosomes collected from BMSCs cultured under hypoxic conditions (Hypoxic-exos) than those collected from BMSCs cultured under normal conditions (Nor-exos). We also observed greater miR-214 enrichment in Hypoxic-exos than in Nor-exos. In addition, a miR-214 inhibitor or mimics added to modulate miR-214 levels in BMSC-exos revealed that exosomes from miR-214-depleted BMSCs partially reversed the effects of hypoxia-induced exosomes on oxidative damage in CSCs. These data further confirmed that miR-214 is the main effector molecule in BMSC-exos that protects CSCs from oxidative damage. miR-214 mimic and inhibitor transfection assays verified that CaMKII is a target gene of miR-214 in CSCs, with exosome-pretreated CSCs exhibiting increased miR-214 levels but decreased CaMKII levels. Therefore, the miR-214/CaMKII axis regulates oxidative stress-related injury in CSCs, such as apoptosis, calcium homeostasis disequilibrium, and excessive ROS accumulation. Collectively, these findings suggest that BMSCs release miR-214-containing exosomes to suppress oxidative stress injury in CSCs through CaMKII silencing.

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