Weipeng Hu

Peking University

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Feng Zheng

Second Affiliated Hospital of Fujian Medical University

Yu‐Shang Yang

West China Hospital of Sichuan University

Long-Qi Chen

Sichuan University

Zhigang Pan

Second Affiliated Hospital of Fujian Medical University

Yong Yuan

West China Hospital of Sichuan University

Xiumei Guo

Second Affiliated Hospital of Fujian Medical University

Xinyue Huang

University of Electronic Science and Technology of China

Yu Xiong

Second Affiliated Hospital of Fujian Medical University

Qi‐Xin Shang

West China Hospital of Sichuan University

Xiangrong Chen

Fujian Medical University

Cooperative Institutions

Fujian Medical University

127

Second Affiliated Hospital of Fujian Medical University

103

Sichuan University

West China Hospital of Sichuan University

Sun Yat-sen University

Zhejiang University

Peking University

Chinese Academy of Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

Capital Medical University

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Silencing of Mig-7 expression inhibits in-vitro invasiveness and vasculogenic mimicry of human glioma U87 Cells

Neuroreport (2019)

Zhigang Pan Qiangbin Zhu Wei You Canfang Shen Weipeng Hu

Gliomas are the most common malignant primary brain tumors with poor prognosis. The migration-inducing gene-7 (Mig-7) protein is a cysteine-rich protein. Vasculogenic mimicry can replace endothelium-dependent blood vessels and supply blood to tumors, thus promoting tumor invasion and metastasis. They have also been shown to play critical roles in the development and progression of various cancers. We attempted to explore the role of Mig-7 and vasculogenic mimicry in glioma progression. We demonstrated that Mig-7 and vasculogenic mimicry were not expressed in normal tissues. In glioma, Mig-7 expression was positively associated with vasculogenic mimicry formation, the expression of both increased with increasing glioma pathological grade. In-vitro, Mig-7 silencing may inhibit the in-vitro invasiveness and formation of vasculogenic mimicry in human glioma U87 cells by inhibiting the phosphatidylinositol 3-kinase/AKT/ matrix metalloproteinases 2 and matrix metalloproteinases 9 signaling pathway. The present study thus indicates a potential role for Mig-7 as a target in the treatment of glioma.

Vasculogenic mimicry

U87

10.1097/wnr.0000000000001317

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Citations (7)

Nodal skip metastasis may undermine the predictive power of topographic pN classification in esophageal squamous cell carcinoma

Surgery (2018)

Yu‐Shang Yang Weipeng Hu Wen‐Ping Wang Yong Yuan Long-Qi Chen

10.1016/j.surg.2018.04.023

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Citations (6)

Prognostic value of lymphovascular invasion in patients with esophageal squamous cell carcinoma

Annals of Translational Medicine (2019)

Yi‐Min Gu Yu‐Shang Yang Weipeng Hu Wen‐Ping Wang Yong Yuan

Whether lymphovascular invasion (LVI) in esophageal squamous cell carcinoma (ESCC) should be considered an independent prognostic factor for survival is controversial. The aim of this report was to investigate the prognostic value of LVI for patients with ESCC.Between October 2010 and July 2011, 152 ESCC patients were retrospectively reviewed. All of the patients underwent curative resection as their primary treatment. Clinicopathological features and overall survival (OS) rate were investigated. Kaplan-Meier curves were used to calculate the OS rate, and the prognostic factors were identified by Cox regression model.Positive LVI was found in 49 (32.2%) patients. Patients with negative LVI had a significantly better 5-year OS rate than those with positive LVI (52.9% vs. 28.8%; P=0.000). The age, T stage, N stage, tumor differentiation, and LVI were demonstrated to be significant prognostic factors for OS through univariate analyses. LVI was confirmed as an independent prognostic factor for OS through multivariate survival analyses. Subgroup analyses revealed that LVI was associated with a decreased OS in node-negative patients, and no significant difference was observed in node-positive cases.Our study highlighted that LVI is an independent prognostic factor in patients with resectable ESCC. LVI may facilitate the stratification of patients with poor survival.

Lymphovascular invasion

Univariate analysis

T-stage

10.21037/atm.2019.05.23

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Citations (13)

Meteorological Variation Is a Predisposing Factor for Aneurismal Subarachnoid Hemorrhage: A 5-Year Multicenter Study in Fuzhou, China

World Neurosurgery (2019)

Qing Huang Shaowei Lin Weipeng Hu Huangyuan Li Pei‐Sen Yao

10.1016/j.wneu.2019.08.048

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Citations (16)

Omega-3 polyunsaturated fatty acid supplementation attenuates microglial-induced inflammation by inhibiting the HMGB1/TLR4/NF-κB pathway following experimental traumatic brain injury

Journal of Neuroinflammation (2017)

Xiangrong Chen Shukai Wu Chunnuan Chen Baoyuan Xie Zhongning Fang

Microglial activation and the subsequent inflammatory response in the central nervous system play important roles in secondary damage after traumatic brain injury (TBI). High-mobility group box 1 (HMGB1) protein, an important mediator in late inflammatory responses, interacts with transmembrane receptor for advanced glycation end products (RAGE) and toll-like receptors (TLRs) to activate downstream signaling pathways, such as the nuclear factor (NF)-κB signaling pathway, leading to a cascade amplification of inflammatory responses, which are related to neuronal damage after TBI. Omega-3 polyunsaturated fatty acid (ω-3 PUFA) is a commonly used clinical immunonutrient, which has antioxidative and anti-inflammatory effects. However, the effects of ω-3 PUFA on HMGB1 expression and HMGB1-mediated activation of the TLR4/NF-κB signaling pathway are not clear. The Feeney DM TBI model was adopted to induce brain injury in rats. Modified neurological severity scores, brain water content, and Nissl staining were employed to determine the neuroprotective effects of ω-3 PUFA supplementation. Assessment of microglial activation in lesioned sites and protein markers for proinflammatory, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, interferon (IFN)-γ, and HMGB1 were used to evaluate neuroinflammatory responses and anti-inflammation effects of ω-3 PUFA supplementation. Immunofluorescent staining and western blot analysis were used to detect HMGB1 nuclear translocation, secretion, and HMGB1-mediated activation of the TLR4/NF-κB signaling pathway to evaluate the effects of ω-3 PUFA supplementation and gain further insight into the mechanisms underlying the development of the neuroinflammatory response after TBI. It was found that ω-3 PUFA supplementation inhibited TBI-induced microglial activation and expression of inflammatory factors (TNF-α, IL-1β, IL-6, and IFN-γ), reduced brain edema, decreased neuronal apoptosis, and improved neurological functions after TBI. We further demonstrated that ω-3 PUFA supplementation inhibited HMGB1 nuclear translocation and secretion and decreased expression of HMGB1 in neurons and microglia in the lesioned areas. Moreover, ω-3 PUFA supplementation inhibited microglial activation and the subsequent inflammatory response by regulating HMGB1 and the TLR4/NF-κB signaling pathway. The results of this study suggest that microglial activation and the subsequent neuroinflammatory response as well as the related HMGB1/TLR4/NF-κB signaling pathway play essential roles in secondary injury after TBI. Furthermore, ω-3 PUFA supplementation inhibited TBI-induced microglial activation and the subsequent inflammatory response by regulating HMGB1 nuclear translocation and secretion and also HMGB1-mediated activation of the TLR4/NF-κB signaling pathway, leading to neuroprotective effects.

HMGB1

Proinflammatory cytokine

RAGE

10.1186/s12974-017-0917-3

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Citations (206)

Analysis of the Causes and Experience in the Diagnosis and Treatment of Intravertebral Mobile Nerve Sheath Tumors—Case Report and Review of the Literature

World Neurosurgery (2020)

Wei You Weipeng Hu Fan Wang Zhigang Pan Qiangbin Zhu

Nerve sheath tumor

Cauda equina

10.1016/j.wneu.2020.07.166

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Citations (1)

ADAMTS13 inhibits oxidative stress and ameliorates progressive chronic kidney disease following ischaemia/reperfusion injury

Acta Physiologica (2020)

Suhan Zhou Jie Guo Liang Zhao Yixin Liao Qin Zhou

Reduced A Disintegrin And Metalloproteinase with a ThromboSpondin type 1 motif member 13 (ADAMTS13) levels are observed in kidney disease. We test whether recombinant human ADAMTS13 (rhADAMTS13) mitigates renal injury in chronic kidney disease (CKD) and the potential mechanisms.CKD was established 3 months after ischaemia/reperfusion (IR). ADAMTS13 and von Willebrand factor (vWF) levels, renal function and morphological changes were analysed. Afferent arteriolar responses to angiotensin II (Ang II) and acetylcholine (ACh) were measured. Oxidative stress-related molecules were detected.Higher vWF and lower ADAMTS13 levels were observed in CKD mice, which were markedly attenuated by rhADAMTS13. rhADAMTS13 alleviated renal dysfunction, as documented by decreased blood urea nitrogen (BUN), serum creatinine, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) levels in CKD mice. Moreover, rhADAMTS13 attenuated transforming growth factor (TGF)-β1/Smad3 activation. Plasma vWF: ADAMTS13 ratio showed positive correlations with malondialdehyde (MDA), hydrogen peroxide (H2 O2 ) and proteinuria, and correlated inversely with superoxide dismutase (SOD) and catalase (CAT). Finally, rhADAMTS13 inhibited reactive oxygen species (ROS) levels and improved microvascular functional disorders, accompanied by the inhibition of glycogen synthase kinase (GSK) 3β hyperactivity and upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) expression.Acute kidney injury (AKI) reduces the expression of ADAMTS13 that contributes to progressive CKD, microvascular dysfunction, oxidative stress, inhibition of Nrf2 activity and renal histopathological damage. All of which can be alleviated by administration of rhADAMTS13.

10.1111/apha.13586

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Citations (13)

Absence of hepatic segment of inferior vena cava with compensatory augmentation of azygos vein in patient under right upper lobectomy

Asian Journal of Surgery (2024)

Weipeng Hu Jue Li Guowei Che

Azygos vein

10.1016/j.asjsur.2024.06.126

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Citations (0)

Effect of magnesium sulfate on cerebral vasospasm in the treatment of aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis

Frontiers in Neurology (2023)

Hanlin Zheng Xiumei Guo Xinyue Huang Yu Xiong Wen Gao

The use of magnesium sulfate for treating aneurysmal subarachnoid hemorrhage (aSAH) has shown inconsistent results across studies. To assess the impact of magnesium sulfate on outcomes after aSAH, we conducted a systematic review and meta-analysis of relevant randomized controlled trials.PubMed, Embase, and the Cochrane Library were searched for relevant literature on magnesium sulfate for aSAH from database inception to March 20, 2023. The primary outcome was cerebral vasospasm (CV), and secondary outcomes included delayed cerebral ischemia (DCI), secondary cerebral infarction, rebleeding, neurological dysfunction, and mortality.Of the 558 identified studies, 16 comprising 3,503 patients were eligible and included in the analysis. Compared with control groups (saline or standard treatment), significant differences were reported in outcomes of CV [odds ratio (OR) = 0.61, p = 0.04, 95% confidence interval (CI) (0.37-0.99)], DCI [OR = 0.57, p = 0.01, 95% CI (0.37-0.88)], secondary cerebral infarction [OR = 0.49, p = 0.01, 95% CI (0.27-0.87)] and neurological dysfunction [OR = 0.55, p = 0.04, 95% CI (0.32-0.96)] after magnesium sulfate administration, with no significant differences detected in mortality [OR = 0.92, p = 0.47, 95% CI (0.73-1.15)] and rebleeding [OR = 0.68, p = 0.55, 95% CI (0.19-2.40)] between the two groups.The superiority of magnesium sulfate over standard treatments for CV, DCI, secondary cerebral infarction, and neurological dysfunction in patients with aSAH was demonstrated. Further randomized trials are warranted to validate these findings with increased sample sizes.

Cerebral Vasospasm

10.3389/fneur.2023.1249369

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Citations (0)

Fenofibrate improves vascular endothelial function and contractility in diabetic mice

Redox Biology (2018)

Nan Xu Qin Wang Shan Jiang Qijing Wang Weipeng Hu

Fenofibrate, a peroxisome proliferator-activated receptors α (PPARα) agonist, reduces vascular complications of diabetic patients but its protective mechanisms are not fully understood. Here we tested the hypothesis that fenofibrate improves vascular endothelial dysfunction by balancing endothelium-dependent relaxation and contractility of the aorta in diabetes mellitus (DM). In streptozotocin-induced diabetic mice, eight weeks of fenofibrate treatment (100 mg/Kg/d) improved endothelium dependent relaxation in the macro- and microvessels, increased nitric oxide (NO) levels, reduced renal damage markers and effects of the vasoconstrictor prostaglandin. Levels of superoxide dismutase and catalase were both reduced and hydrogen peroxide was increased in vehicle-treated DM, but these changes were reversed by fenofibrate treatment. Vasodilation of the aorta after fenofibrate treatment was reversed by PPARα or AMPKα inhibitors. Western blots showed that fenofibrate treatment elevated PPARα expression, induced liver kinase B1 (LKB1) translocation from the nucleus to the cytoplasm and activated AMP-activated protein kinase-α (AMPKα), thus activating endothelial NO synthase (eNOS). Also, fenofibrate treatment decreased NF-κB p65 and cyclooxygenase 2 proteins in aortas. Finally, incubation with indomethacin in vitro improved aortic contractility in diabetic mice. Overall, our results show that fenofibrate treatment in diabetic mice normalizes endothelial function by balancing vascular reactivity via increasing NO production and suppressing the vasoconstrictor prostaglandin, suggesting mechanism of action of fenofibrate in mediating diabetic vascular complications.

Fenofibrate

Endothelial Dysfunction

10.1016/j.redox.2018.09.024

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Citations (38)