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fibrinogen-like protein 2 deficiency inhibits virus-induced fulminant hepatitis through abrogating inflammatory macrophage activation

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World Journal of Gastroenterology 2022年第4期28卷 479-496页

作者： Fang Xiao Hong-Wu Wang Jun-Jian Hu Ran Tao Xin-Xin Weng Peng Wang Di Wu Xiao-Jing Wang Wei-Ming Yan Dong Xi Xiao-Ping Luo Xiao-Yang Wan Qin Ning Department of Infectious Disease Tongji Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030Hubei ProvinceChina Department of Infectious Disease The First Affiliated Hospital of Guangxi Medical UniversityNanning 530000Guangxi ProvinceChina Department of Pediatrics Tongji HospitalWuhan 430030Hubei ProvinceChina

BACKGROUND Heterogeneous macrophages play an important role in multiple liver diseases,including viral fulminant hepatitis(VFH).fibrinogen-like protein 2(FGL2)is expressed on macrophages and regulates VFH pathogenesis;however,the underlying mechanism remains *** To explore how FGL2 regulates macrophage function and subsequent liver injury during *** Murine hepatitis virus strain 3(MHV-3)was used to induce VFH in FGL2-deficient(Fgl2-/-)and wild-type(WT)*** dynamic constitution of hepatic macrophages was *** transfer of Fgl2-/-or WT bone marrowderived macrophages(BMDMs)into WT recipients with macrophages depleted prior to infection was carried out and the consequent degree of liver damage was *** signaling cascades that may be regulated by FGL2 were detected in *** Following MHV-3 infection,hepatic macrophages were largely replenished by proinflammatory monocyte-derived macrophages(MoMFs),which expressed high levels of *** Fgl2-/-mice,the number of infiltrating inflammatory MoMFs was reduced compared with that in WT mice after viral *** depletion ameliorated liver damage in WT mice and further alleviated liver damage in Fgl2-/-*** transfer of Fgl2-/-BMDMs into macrophage-removed recipients significantly reduced the degree of liver *** of monocyte infiltration also significantly ameliorated liver ***,Fgl2 deletion impaired macrophage phagocytosis and the antigen presentation potential and attenuated the proinflammatory *** the molecular level,FGL2 deficiency impaired IRF3,IRF7,and p38 phosphorylation,along with NF-κB activation in BMDMs in response to viral *** Infiltrated MoMFs represent a major source of hepatic inflammation during VFH progression,and FGL2 expression on MoMFs maintains the proinflammatory phenotype via p38-dependent positive feedback,contributing to VFH pathogenesis.

关键词： Viral fulminant hepatitis fibrinogen-like protein 2 Proinflammatory macrophages Infiltrating macrophages P38

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fibrinogen-like protein 2 expression correlates with microthrombosis in rats with type 2 diabetic nephropathy

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The Journal of Biomedical Research 2011年第2期25卷 120-127页

作者： Guanhua Su Kun Liu Yan Wang Jue Wang Xiaowei Li Wenzhu Li Yuhua Liao Zhaohui Wang Department of Cardiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 Hubei China Division of Chines Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei China

fibrinogen-like protein 2 （fgl2）, a novel prothrombinase, is involved in microthrombosis. We examined fgl2 expression in the glomerular and tubulointerstitial capillaries and its correlation with microthromsis in rats with streptozocin-induced type 2 diabetic nephropathy. Our RT-PCR and immunoblotting analysis showed that fgl2 mRNA and protein levels were increased in microvascular endothelial cells of the glomeruli and renal interstitia at week 19 and became significantly elevated with the development of diabetic nephropathy （P 〈 0.01）. Fgl2 was not or only weakly expressed in the renal tissues of normal rats. Furthermore, a direct significant correlation （r = 0.543, P 〈 0.01） was found between fgl2 expression and microthrombotic capillaries in the renal tissues. Enzyme linked immunosorbent assays （ELISA） additionally showed that circulating TNF-α levels in rats with type 2 diabetes were significantly elevated and closely correlated with fgl2 expression （r = 0.871, P 〈 0.01）. Our results suggest that fgl2 may activate renal microthrombosis, thus contributing to glomerular hypertension and renal ischemia.

关键词： fibrinogen-like protein 2 microthrombosis type 2 diabetes diabetic nephropathy tumor necrosis factor-α

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Expression and Significance of fgl2 Prothrombinase in Cardiac Microvascular Endothelial Cells of Rats with Type 2 Diabetes

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第5期30卷 575-581页

作者：丁艳萍刘坤汪艳苏冠华邓荷萍曾秋棠廖玉华王朝晖 Department of Cardiology Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Ultrasonic Medicine Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

Microthrombosis may be involved in the pathogenesis of cardiac microangiopathy due to *** studies have shown that fibrinogen-like protein 2 (fgl2) plays a pivotal role in microthrombosis in viral hepatitis, acute vascular xenograft rejection and cytokine-induced fetal loss *** current study was designed to examine the expression of fgl2 in microvascular endothelial cells and investigate the effects of microthrombi due to fgl2 on cardiac function and structure in rats with type 2 *** induction of type 2 diabetes, 24 rats were observed ***2 expression and related cardiac microthrombosis were *** or circulating TNF-α was *** flow (CF) per min was calculated as an index of cardiac *** function and morphology were *** was found that Fgl2 was highly expressed in cardiac microvascular endothelial cells of rats with type 2 diabetes, which was promoted by local or circulating TNF-α.The Fgl2 expression was associated with cardiac hyaline *** parallel with the fgl2 expression, CF per min, cardiac diastolic or systolic function and cardiac morphology were aggravated to some *** was concluded that in rats with type 2 diabetes, microthrombosis due to fgl2 contributes to the impairment of cardiac diastolic or systolic function and morphological changes.

关键词： fibrinogen-like protein 2 type 2 diabetes ischemic heart disease microangiopathy tumor necrosis factor-α cardiac function

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Roles of Regulatory T Cells in Pathogenesis of Endometriosis

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Reproductive and Developmental Medicine 2019年第2期3卷 117-123页

作者： Xin-Xin Hou Xiao-Qiu Wang Da-Jin Li Laboratory for Reproductive Immunology Key Laboratory of Reproduction Regulation of NPFPCSIPPRShanghaiChina Laboratory for Reproductive Immunology Shanghai Key Laboratory of Female Reproductive Endocrine Related DiseasesHospital and Institute of Obstetrics and GynecologyIRDFudan University Shanghai Medical CollegeShanghaiChina

Numerous studies have shown aberrant immune cell function in endometriosis,including T cells,B cells,natural killer cells,and macrophages(MΦ).These alterations are thought to be induced by various mechanisms that promote the *** T cells(Tregs)may account for a decreased ability of newly recruited leukocytes to initiate effective immune responses against viable endometrial fragments,permitting their *** differentiate during the development of endometriosis,which confer immunosuppression or play other roles in disease *** this review,we provide an overview of the regulation and roles of Tregs in *** data provide further scientific evidence for the altered immune response in endometriosis,which could be a potential target in the treatment of *** review could create new diagnostic strategies and effective immune-targeted therapies for this highly prevalent *** progress in the field indicates that these goals may be achieved in the future.

关键词： Endometrial Stromal Cells Endometriosis fibrinogen-like protein 2 Regulatory T Cells

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