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Your search keyword '"Luo, Qianqian"' showing total 14 results
Start Over Author "Luo, Qianqian" Publisher wiley
14 results on '"Luo, Qianqian"'

1. Outside Front Cover: Plasma Process. Polym. 3/2024

Author

Tan, Menghao, primary, Chen, Wei, additional, Li, Mengchao, additional, Luo, Qianqian, additional, Xiao, Yujun, additional, Liu, Fang, additional, Wang, Xingquan, additional, Gao, Zhiqiang, additional, Chang, Xiaopeng, additional, Gong, Teng, additional, Huang, Jun, additional, and Ostrikov, Kostya (Ken), additional

Published
2024
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7. Hypoxic preconditioning enhances the differentiation of bone marrow stromal cells into mature oligodendrocytes via the mTOR/HIF‐1α/VEGF pathway in traumatic brain injury

Author

Guo-Hua Wang, Jin Chen, Luo Qianqian, Lihua Shen, Xiaoyu Yuan, Deqiang Gan, Yechao Sun, and Lingzhi Ding

Subjects
Male, Vascular Endothelial Growth Factor A, Stromal cell, Mesenchymal Stem Cell Transplantation, 050105 experimental psychology, lcsh:RC321-571, Mice, 03 medical and health sciences, Behavioral Neuroscience, chemistry.chemical_compound, 0302 clinical medicine, oligodendrogenesis, Brain Injuries, Traumatic, VEGF Signaling Pathway, Animals, Medicine, 0501 psychology and cognitive sciences, Remyelination, Hypoxia, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Mechanistic target of rapamycin, PI3K/AKT/mTOR pathway, Original Research, biology, Vascular Endothelial Growth Factors, business.industry, TOR Serine-Threonine Kinases, traumatic brain injury, 05 social sciences, Cell Differentiation, Mesenchymal Stem Cells, Mice, Inbred C57BL, Vascular endothelial growth factor, Transplantation, Oligodendroglia, remyelination, medicine.anatomical_structure, chemistry, Cancer research, biology.protein, Rabbits, Bone marrow, business, hypoxic preconditioning, 030217 neurology & neurosurgery, bone marrow stromal cells
Abstract

Objective Traumatic brain injury (TBI) results not only in gray matter damage, but also in severe white matter injury (WMI). Previous findings support hypoxic preconditioning (HP) could augment the efficacy of bone marrow stromal cell (BMSC) transplantation in a TBI mouse model. However, whether HP‐treated BMSCs (H‐BMSCs) could overcome remyelination failure after WMI is unclear, and the molecular mechanisms remain to be explored. Here, we focused on the therapeutic benefits of H‐BMSC transplantation for treating WMI, as well as its underlying mechanisms. Methods In vitro, BMSCs were incubated at passage 4 in the hypoxic preconditioning (1.0% oxygen) for 8 hr. In vivo, a TBI mouse model was established, and DMEM cell culture medium (control), normal cultured BMSCs (N‐BMSCs), or H‐BMSCs were transplanted to mice 24 hr afterward. Neurobehavioral function, histopathological changes, and oligodendrogenesis were assessed for up to 35 days post‐TBI. Results Compared with the control group, improvement of cognitive functions and smaller lesion volumes was observed in the two BMSC‐transplanted groups, especially the H‐BMSC group. H‐BMSC transplantation resulted in a greater number of neural/glial antigen 2 (NG2)–positive and adenomatous polyposis coli (APC)–positive cells than N‐BMSC transplantation in both the corpus callosum and the striatum. In addition, we observed that the expression levels of hypoxia‐inducible factor‐1a (HIF‐1α), phosphorylated mechanistic target of rapamycin (p‐mTOR), and vascular endothelial growth factor (VEGF) were all increased in H‐BMSC–transplanted mice. Furthermore, the mTOR pathway inhibitor rapamycin attenuated the impact of HP both in vivo and in vitro. Conclusion The results provided mechanistic evidences suggesting that HP‐treated BMSCs promoted remyelination partly by modulating the pro‐survival mTOR/HIF‐1α/VEGF signaling pathway., The aim of the present study was to assess the effects of HP‐treated BMSCs (H‐BMSCs) on neuronal behavior and the differentiation of cells in the white matter area following TBI in mice. H‐BMSC transplantation not only ameliorated neurological deficits, but also enhanced axonal regeneration and remyelination in mice after TBI, which may involve the mTOR/HIF‐1α/VEGF pathway. This study provided novel biological and histopathological evidences for TBI treatment that H‐BMSC transplantation may serve as a promising therapeutic option for both gray matter and white matter.

Published
2020
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