The Experts below are selected from a list of 113181 Experts worldwide ranked by ideXlab platform
Daochun Wang - One of the best experts on this subject based on the ideXlab platform.
-
Rhein attenuates renal Inflammatory Injury of uric acid nephropathy via lincRNA-Cox2/miR-150-5p/STAT1 axis.
International immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on uric acid nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with uric acid (UA) to induce Inflammatory Injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and Inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and Inflammatory Injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal Inflammatory Injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
-
rhein attenuates renal Inflammatory Injury of uric acid nephropathy via lincrna cox2 mir 150 5p stat1 axis
International Immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on uric acid nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with uric acid (UA) to induce Inflammatory Injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and Inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and Inflammatory Injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal Inflammatory Injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
Qingwu Yang - One of the best experts on this subject based on the ideXlab platform.
-
heme activates tlr4 mediated Inflammatory Injury via myd88 trif signaling pathway in intracerebral hemorrhage
Journal of Neuroinflammation, 2012Co-Authors: Qi Zhong, Yu Zhou, Fenglin Lv, Jingqi Li, Jingzhou Wang, Bingyin Su, Qingwu YangAbstract:Inflammatory Injury plays a critical role in intracerebral hemorrhage (ICH)-induced neurological deficits; however, the signaling pathways are not apparent by which the upstream cellular events trigger innate immune and Inflammatory responses that contribute to neurological impairments. Toll-like receptor 4 (TLR4) plays a role in Inflammatory damage caused by brain disorders. In this study, we investigate the role of TLR4 signaling in ICH-induced inflammation. In the ICH model, a significant upregulation of TLR4 expression in reactive microglia has been demonstrated using real-time RT-PCR. Activation of microglia was detected by immunohistochemistry, cytokines were measured by ELISA, MyD88, TRIF and NF-κB were measured by Western blot and EMSA, animal behavior was evaluated by animal behavioristics. Compared to WT mice, TLR4−/− mice had restrained ICH-induced brain damage showing in reduced cerebral edema and lower neurological deficit scores. Quantification of cytokines including IL-6, TNF-α and IL-1β and assessment of macrophage infiltration in perihematoma tissues from TLR4−/−, MyD88−/− and TRIF−/− mice showed attenuated Inflammatory damage after ICH. TLR4−/− mice also exhibited reduced MyD88 and TRIF expression which was accompanied by decreased NF-κB activity. This suggests that after ICH both MyD88 and TRIF pathways might be involved in TLR4-mediated Inflammatory Injury possibly via NF-κB activation. Exogenous hemin administration significantly increased TLR4 expression and microglial activation in cultures and also exacerbated brain Injury in WT mice but not in TLR4−/− mice. Anti-TLR4 antibody administration suppressed hemin-induced microglial activation in cultures and in the mice model of ICH. Our findings suggest that heme potentiates microglial activation via TLR4, in turn inducing NF-κB activation via the MyD88/TRIF signaling pathway, and ultimately increasing cytokine expression and Inflammatory Injury in ICH. Targeting TLR4 signaling may be a promising therapeutic strategy for ICH.
-
Heme activates TLR4-mediated Inflammatory Injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage.
Journal of neuroinflammation, 2012Co-Authors: Sen Lin, Yu Zhou, Qi Zhong, Jingzhou Wang, Qing Yin, Qingwu YangAbstract:Inflammatory Injury plays a critical role in intracerebral hemorrhage (ICH)-induced neurological deficits; however, the signaling pathways are not apparent by which the upstream cellular events trigger innate immune and Inflammatory responses that contribute to neurological impairments. Toll-like receptor 4 (TLR4) plays a role in Inflammatory damage caused by brain disorders. In this study, we investigate the role of TLR4 signaling in ICH-induced inflammation. In the ICH model, a significant upregulation of TLR4 expression in reactive microglia has been demonstrated using real-time RT-PCR. Activation of microglia was detected by immunohistochemistry, cytokines were measured by ELISA, MyD88, TRIF and NF-κB were measured by Western blot and EMSA, animal behavior was evaluated by animal behavioristics. Compared to WT mice, TLR4−/− mice had restrained ICH-induced brain damage showing in reduced cerebral edema and lower neurological deficit scores. Quantification of cytokines including IL-6, TNF-α and IL-1β and assessment of macrophage infiltration in perihematoma tissues from TLR4−/−, MyD88−/− and TRIF−/− mice showed attenuated Inflammatory damage after ICH. TLR4−/− mice also exhibited reduced MyD88 and TRIF expression which was accompanied by decreased NF-κB activity. This suggests that after ICH both MyD88 and TRIF pathways might be involved in TLR4-mediated Inflammatory Injury possibly via NF-κB activation. Exogenous hemin administration significantly increased TLR4 expression and microglial activation in cultures and also exacerbated brain Injury in WT mice but not in TLR4−/− mice. Anti-TLR4 antibody administration suppressed hemin-induced microglial activation in cultures and in the mice model of ICH. Our findings suggest that heme potentiates microglial activation via TLR4, in turn inducing NF-κB activation via the MyD88/TRIF signaling pathway, and ultimately increasing cytokine expression and Inflammatory Injury in ICH. Targeting TLR4 signaling may be a promising therapeutic strategy for ICH.
Long Shuang Huang - One of the best experts on this subject based on the ideXlab platform.
-
The angiocrine Rspondin3 instructs interstitial macrophage transition via metabolic–epigenetic reprogramming and resolves Inflammatory Injury
Nature immunology, 2020Co-Authors: Bisheng Zhou, Lissette Magana, Zhigang Hong, Long Shuang Huang, Sreeparna Chakraborty, Yoshikazu Tsukasaki, Cary Huang, Li Wang, Balaji B. GaneshAbstract:Macrophages demonstrate remarkable plasticity that is essential for host defense and tissue repair. The tissue niche imprints macrophage identity, phenotype and function. The role of vascular endothelial signals in tailoring the phenotype and function of tissue macrophages remains unknown. The lung is a highly vascularized organ and replete with a large population of resident macrophages. We found that, in response to Inflammatory Injury, lung endothelial cells release the Wnt signaling modulator Rspondin3, which activates β-catenin signaling in lung interstitial macrophages and increases mitochondrial respiration by glutaminolysis. The generated tricarboxylic acid cycle intermediate α-ketoglutarate, in turn, serves as the cofactor for the epigenetic regulator TET2 to catalyze DNA hydroxymethylation. Notably, endothelial-specific deletion of Rspondin3 prevented the formation of anti-Inflammatory interstitial macrophages in endotoxemic mice and induced unchecked severe Inflammatory Injury. Thus, the angiocrine-metabolic-epigenetic signaling axis specified by the endothelium is essential for reprogramming interstitial macrophages and dampening Inflammatory Injury.
-
The angiocrine Rspondin3 instructs interstitial macrophage transition via metabolic–epigenetic reprogramming and resolves Inflammatory Injury
Nature Immunology, 2020Co-Authors: Bisheng Zhou, Lissette Magana, Zhigang Hong, Long Shuang Huang, Sreeparna Chakraborty, Yoshikazu Tsukasaki, Cary Huang, Li Wang, Balaji Ganesh, Xiaopei GaoAbstract:Macrophages demonstrate remarkable plasticity that is essential for host defense and tissue repair. The tissue niche imprints macrophage identity, phenotype and function. The role of vascular endothelial signals in tailoring the phenotype and function of tissue macrophages remains unknown. The lung is a highly vascularized organ and replete with a large population of resident macrophages. We found that, in response to Inflammatory Injury, lung endothelial cells release the Wnt signaling modulator Rspondin3, which activates β-catenin signaling in lung interstitial macrophages and increases mitochondrial respiration by glutaminolysis. The generated tricarboxylic acid cycle intermediate α-ketoglutarate, in turn, serves as the cofactor for the epigenetic regulator TET2 to catalyze DNA hydroxymethylation. Notably, endothelial-specific deletion of Rspondin3 prevented the formation of anti-Inflammatory interstitial macrophages in endotoxemic mice and induced unchecked severe Inflammatory Injury. Thus, the angiocrine–metabolic–epigenetic signaling axis specified by the endothelium is essential for reprogramming interstitial macrophages and dampening Inflammatory Injury. The angiocrine Rspondin3 is produced by endothelial cells (ECs) and controls growth and development. Malik and colleagues show that lung ECs produce Rspondin3 following Injury and specifically direct interstitial macrophages into an anti-Inflammatory and wound-healing program.
-
mtDNA Activates cGAS Signaling and Suppresses the YAP-Mediated Endothelial Cell Proliferation Program to Promote Inflammatory Injury.
Immunity, 2020Co-Authors: Long Shuang Huang, Zhigang Hong, Xiaopei Gao, Shiqin Xiong, Ming Zhong, Jalees Rehman, Asrar B. MalikAbstract:Cytosolic DNA acts as a universal danger-associated molecular pattern (DAMP) signal; however, the mechanisms of self-DNA release into the cytosol and its role in Inflammatory tissue Injury are not well understood. We found that the internalized bacterial endotoxin lipopolysaccharide (LPS) activated the pore-forming protein Gasdermin D, which formed mitochondrial pores and induced mitochondrial DNA (mtDNA) release into the cytosol of endothelial cells. mtDNA was recognized by the DNA sensor cGAS and generated the second messenger cGAMP, which suppressed endothelial cell proliferation by downregulating YAP1 signaling. This indicated that the surviving endothelial cells in the penumbrium of the Inflammatory Injury were compromised in their regenerative capacity. In an experimental model of Inflammatory lung Injury, deletion of cGas in mice restored endothelial regeneration. The results suggest that targeting the endothelial Gasdermin D activated cGAS-YAP signaling pathway could serve as a potential strategy for restoring endothelial function after Inflammatory Injury.
Xiaopei Gao - One of the best experts on this subject based on the ideXlab platform.
-
The angiocrine Rspondin3 instructs interstitial macrophage transition via metabolic–epigenetic reprogramming and resolves Inflammatory Injury
Nature Immunology, 2020Co-Authors: Bisheng Zhou, Lissette Magana, Zhigang Hong, Long Shuang Huang, Sreeparna Chakraborty, Yoshikazu Tsukasaki, Cary Huang, Li Wang, Balaji Ganesh, Xiaopei GaoAbstract:Macrophages demonstrate remarkable plasticity that is essential for host defense and tissue repair. The tissue niche imprints macrophage identity, phenotype and function. The role of vascular endothelial signals in tailoring the phenotype and function of tissue macrophages remains unknown. The lung is a highly vascularized organ and replete with a large population of resident macrophages. We found that, in response to Inflammatory Injury, lung endothelial cells release the Wnt signaling modulator Rspondin3, which activates β-catenin signaling in lung interstitial macrophages and increases mitochondrial respiration by glutaminolysis. The generated tricarboxylic acid cycle intermediate α-ketoglutarate, in turn, serves as the cofactor for the epigenetic regulator TET2 to catalyze DNA hydroxymethylation. Notably, endothelial-specific deletion of Rspondin3 prevented the formation of anti-Inflammatory interstitial macrophages in endotoxemic mice and induced unchecked severe Inflammatory Injury. Thus, the angiocrine–metabolic–epigenetic signaling axis specified by the endothelium is essential for reprogramming interstitial macrophages and dampening Inflammatory Injury. The angiocrine Rspondin3 is produced by endothelial cells (ECs) and controls growth and development. Malik and colleagues show that lung ECs produce Rspondin3 following Injury and specifically direct interstitial macrophages into an anti-Inflammatory and wound-healing program.
-
mtDNA Activates cGAS Signaling and Suppresses the YAP-Mediated Endothelial Cell Proliferation Program to Promote Inflammatory Injury.
Immunity, 2020Co-Authors: Long Shuang Huang, Zhigang Hong, Xiaopei Gao, Shiqin Xiong, Ming Zhong, Jalees Rehman, Asrar B. MalikAbstract:Cytosolic DNA acts as a universal danger-associated molecular pattern (DAMP) signal; however, the mechanisms of self-DNA release into the cytosol and its role in Inflammatory tissue Injury are not well understood. We found that the internalized bacterial endotoxin lipopolysaccharide (LPS) activated the pore-forming protein Gasdermin D, which formed mitochondrial pores and induced mitochondrial DNA (mtDNA) release into the cytosol of endothelial cells. mtDNA was recognized by the DNA sensor cGAS and generated the second messenger cGAMP, which suppressed endothelial cell proliferation by downregulating YAP1 signaling. This indicated that the surviving endothelial cells in the penumbrium of the Inflammatory Injury were compromised in their regenerative capacity. In an experimental model of Inflammatory lung Injury, deletion of cGas in mice restored endothelial regeneration. The results suggest that targeting the endothelial Gasdermin D activated cGAS-YAP signaling pathway could serve as a potential strategy for restoring endothelial function after Inflammatory Injury.
Mei-hua Wan - One of the best experts on this subject based on the ideXlab platform.
-
Effect of Sheng-jiang powder on multiple-organ Inflammatory Injury in acute pancreatitis in rats fed a high-fat diet.
World journal of gastroenterology, 2019Co-Authors: Yi-fan Miao, Yu-mei Zhang, Lv Zhu, Huan Chen, Ling Yuan, Hong-xin Kang, Hong-yu Ren, Mei-hua WanAbstract:Background Obesity worsens Inflammatory organ Injury in acute pancreatitis (AP), but there is no effective preventive strategy. Sheng-jiang powder (SJP) has been shown to alleviate multiple-organ Inflammatory Injury in rats with high-fat diet-induced obesity. Hence, SJP is supposed to have an effect on multiple-organ Inflammatory Injury in AP in rats fed a high-fat diet. Aim To explore how obesity may contribute to aggravating Inflammatory organ Injury in AP in rats and observe the effect of SJP on multiple-organ Inflammatory Injury in AP in rats fed a high-fat diet. Methods Rats were randomly assigned to a control group (CG), an obese group (OG), and an SJP treatment group (SG), with eight rats per group. The rats in the OG and SG were fed a high-fat diet. From the third week, the rats in the SG were given oral doses of SJP (5 g/kg of body weight). After 12 wk, AP was induced in the three groups. Serum amylase level, body weight, Lee's index, serum biochemistry parameters, and serum Inflammatory cytokine and tissue cytokine levels were assessed, and the tissue histopathological scores were evaluated and compared. Results Compared with the CG, serum triglyceride, total cholesterol, interleukin-6, and interleukin-10 levels were significantly higher in the OG, and serum high-density lipoprotein cholesterol level was significantly lower in the OG. Moreover, enhanced oxidative damage was observed in the pancreas, heart, spleen, lung, intestine, liver, and kidney. Evidence of an imbalanced antioxidant defense system, especially in the pancreas, spleen, and intestine, was observed in the obese AP rats. Compared with the OG, serum high-density lipoprotein cholesterol, interleukin-10, and superoxide dismutase expression levels in the pancreas, spleen, and intestine were increased in the SG. Additionally, SJP intervention led to a decrease in the following parameters: body weight; Lee's index; serum triglyceride levels; serum total cholesterol levels; malondialdehyde expression levels in the pancreas, heart, spleen, lung, and liver; myeloperoxidase expression levels in the lung; and pathological scores in the liver. Conclusion Obesity may aggravate the Inflammatory reaction and pathological multiple-organ Injury in AP rats, and SJP may alleviate multiple-organ Inflammatory Injury in AP in rats fed a high-fat diet.
-
Sheng-jiang powder ameliorates obesity-induced pancreatic Inflammatory Injury via stimulating activation of the AMPK signalling pathway in rats
World Journal of Gastroenterology, 2018Co-Authors: Yi-fan Miao, Yu-mei Zhang, Lv Zhu, Huan Chen, Ling Yuan, Mei-hua WanAbstract:Sheng-jiang powder ameliorates obesity-induced pancreatic Inflammatory Injury via stimulating activation of the AMPK signalling pathway in rats