Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction
Background: Cerebral infarction (CI) is a common and frequently occurring acute neurological disease in clinical practice, posing a severe threat to human health. CI results from various causes leading to local cerebral tissue ischemia and hypoxia due to vascular occlusion and impaired blood supply,...
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Elsevier
2025-06-01
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| Series: | IBRO Neuroscience Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2667242125000478 |
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| author | Bo Zhu Kun Guo Lei Zha Zhengli Di Hongwei Zhao Le Chang Naibing Gu |
| author_facet | Bo Zhu Kun Guo Lei Zha Zhengli Di Hongwei Zhao Le Chang Naibing Gu |
| author_sort | Bo Zhu |
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| description | Background: Cerebral infarction (CI) is a common and frequently occurring acute neurological disease in clinical practice, posing a severe threat to human health. CI results from various causes leading to local cerebral tissue ischemia and hypoxia due to vascular occlusion and impaired blood supply, which in turn leads to tissue necrosis and corresponding clinical manifestations of neurological deficits. However, to date, treatment options for cerebral infarction remain limited. Therefore, it is crucial to rapidly establish collateral circulation to compensate for the occluded vessels and restore blood flow perfusion. Objective: To assess the effect of bone marrow mesenchymal cells transfected with intelectin-1 (Itln-1) gene on the angiogenesis and apoptosis of CI. Method: Lentiviral-mediated transfection of the Itln-1 gene into bone marrow mesenchymal stem cells (BMSCs) was performed, followed by intravenous injection into rats with CI through the tail vein. The volume of the CI, capillary density, and apoptotic cells were detected. Results: With the increase of AKT and eNOS phosphorylation levels, BMSCs with overexpression Itln-1 gene could significantly promote angiogenesis and reduce the infarct volume in the ischemic penumbra. Meanwhile, the ratio of Bcl-2/Bax increased, and apoptotic cells decreased. Conclusion: The overexpression of Itln-1 can effectively promote CI angiogenesis and inhibit cell apoptosis than transplantation of Itln-1 gene or MSCS alone |
| format | Article |
| id | doaj-art-5bfa8a5172cb45bab269c2e57c22f35d |
| institution | OA Journals |
| issn | 2667-2421 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | IBRO Neuroscience Reports |
| spelling | doaj-art-5bfa8a5172cb45bab269c2e57c22f35d2025-08-20T02:06:19ZengElsevierIBRO Neuroscience Reports2667-24212025-06-011861962610.1016/j.ibneur.2025.03.012Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarctionBo Zhu0Kun Guo1Lei Zha2Zhengli Di3Hongwei Zhao4Le Chang5Naibing Gu6Department of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaDepartment of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaDepartment of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaDepartment of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaDepartment of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaDepartment of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaCorresponding author.; Department of Neurology, Xi’an Central Hospital, 161 Xiwu Road, Xi’an, Shaanxi 710003, ChinaBackground: Cerebral infarction (CI) is a common and frequently occurring acute neurological disease in clinical practice, posing a severe threat to human health. CI results from various causes leading to local cerebral tissue ischemia and hypoxia due to vascular occlusion and impaired blood supply, which in turn leads to tissue necrosis and corresponding clinical manifestations of neurological deficits. However, to date, treatment options for cerebral infarction remain limited. Therefore, it is crucial to rapidly establish collateral circulation to compensate for the occluded vessels and restore blood flow perfusion. Objective: To assess the effect of bone marrow mesenchymal cells transfected with intelectin-1 (Itln-1) gene on the angiogenesis and apoptosis of CI. Method: Lentiviral-mediated transfection of the Itln-1 gene into bone marrow mesenchymal stem cells (BMSCs) was performed, followed by intravenous injection into rats with CI through the tail vein. The volume of the CI, capillary density, and apoptotic cells were detected. Results: With the increase of AKT and eNOS phosphorylation levels, BMSCs with overexpression Itln-1 gene could significantly promote angiogenesis and reduce the infarct volume in the ischemic penumbra. Meanwhile, the ratio of Bcl-2/Bax increased, and apoptotic cells decreased. Conclusion: The overexpression of Itln-1 can effectively promote CI angiogenesis and inhibit cell apoptosis than transplantation of Itln-1 gene or MSCS alonehttp://www.sciencedirect.com/science/article/pii/S2667242125000478Intelectin-1BMSCsAngiogenesisApoptosisCI |
| spellingShingle | Bo Zhu Kun Guo Lei Zha Zhengli Di Hongwei Zhao Le Chang Naibing Gu Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction IBRO Neuroscience Reports Intelectin-1 BMSCs Angiogenesis Apoptosis CI |
| title | Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction |
| title_full | Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction |
| title_fullStr | Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction |
| title_full_unstemmed | Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction |
| title_short | Effect of BMSCs overexpressing intelectin-1 on angiogenesis in rats with cerebral infarction |
| title_sort | effect of bmscs overexpressing intelectin 1 on angiogenesis in rats with cerebral infarction |
| topic | Intelectin-1 BMSCs Angiogenesis Apoptosis CI |
| url | http://www.sciencedirect.com/science/article/pii/S2667242125000478 |
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