Targeting TRAF7 to Enhance Angiogenesis and Mitigate Ischemia-Induced Brain Damage: Insights from in Vivo and in Vitro Models

文献类型： 外文期刊

第一作者： Feng, Nianping

作者： Feng, Nianping;Wu, Yun;Li, Genjie;Li, Yushan;Guan, Yuexin;Xiao, Xingjun;Zheng, Haihong;Ji, Jingjing;Zhang, Zhuo

作者机构：

关键词： cerebral ischemic stroke; angiogenesis; TRAFA7; KLF4; VEGF

期刊名称：JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS （ 影响因子：3.2； 五年影响因子：2.2 ）

ISSN： 0393-974X

年卷期： 2024 年 38 卷 2 期

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收录情况： SCI

摘要： Background: Cerebral ischemic stroke (CIS) results from insufficient blood supply to the brain, leading to disabilities and even death. Currently, available CIS treatment primarily focuses on promoting angiogenesis. The tumor necrosis factor receptorassociated factor 7 (TRAF7) plays a pivotal role in various biological processes and has been associated with neuronal damage. However, its role in CIS remains uncertain. Therefore, this study aimed to investigate the role of TRAF7 in angiogenesis during Methods: A middle cerebral-arterial occlusion (MCAO) mice model with knocked-down TRAF7 was established to investigate its effects on neurological deficits, brain water content, and infarct volume. CD31/ki67 dual-immunofluorescent (IF) staining was performed to assess the impact of TRAF7 on angiogenesis in vivo. Furthermore, an Oxygen and Glucose Deprivation and Reoxygenation (OGD/R) cell model was constructed to mimic ischemia and explore the influence of the TRAF7/Krupple-like family of transcription factor 4 (KLF4) axis on cell migration and tube formation. Results: TRAF7 protein expression was found to be elevated in both the in vivo and in vitro ischemic models. Its silencing improved neurological function, reduced cerebral water content and infarct volume, and enhanced angiogenesis after CIS in vivo. Furthermore, its silencing promoted bEnd3 cell migration and tube formation following OGD/R injury. Moreover, it was observed that TRAF7 regulated expression levels of KLF4 and vascular endothelial growth factor (VEGF) in both in vivo and in vitro settings. Mechanistically, it was found that TRAF7 mediated bEnd3 cell migration and angiogenesis post-OGD/R injury by Conclusions: Our findings indicate that TRAF7 knockdown confers vascular protection against CIS, offering a novel perspective for CIS treatment.

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