Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPARγ and CD36

Mu, Qiong; Wang, Likun; Hang, Hang; Liu, Chun‐Feng; Wu, Guofeng

doi:10.1016/j.neulet.2017.04.038

Cited by 13 publications

(12 citation statements)

References 23 publications

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“…When inhibiting ROS with NAC, CO could no longer increase phosphorylated AMPK (Figure 2a,b). The class B scavenger receptor CD36 is involved in hematoma resolution after hemorrhagic stroke (Fang et al, 2014;Flores et al, 2016;Mu et al, 2017). The exact mechanisms of how CD36 is regulated after hemorrhage are unclear.…”

Section: Microglia Exposed To Blood Show Elevated Expression Of Ho-1mentioning

confidence: 99%

“…The exact mechanisms of how the HO-1-CO axis modulates microglial phagocytosis of erythrocytes after brain hemorrhage remains poorly understood. The class B scavenger receptor CD36 facilitates recognition and phagocytosis of apoptotic cells (Fadok, Warner, Bratton, & Henson, 1998) of the innate immune system and determines hematoma resolution after hemorrhagic stroke (Fang et al, 2014;Flores et al, 2016;Mu, Wang, Hang, Liu, & Wu, 2017). The mechanisms how CD36 might be regulated via the HO-1/CO axis have not been studied.…”

Section: Introductionmentioning

confidence: 99%

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Carbon monoxide controls microglial erythrophagocytosis by regulating CD36 surface expression to reduce the severity of hemorrhagic injury

Kaiser

Selzner

Weber

et al. 2020

Glia

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Microglial erythrophagocytosis is crucial in injury response to hemorrhagic stroke. We hypothesized that regulation of microglial erythrophagocytosis via HO‐1/CO depends on a pathway involving reactive oxygen species (ROS) and CD36 surface‐expression. The microglial BV‐2 cell line and primary microglia (PMG) were incubated +/−blood and +/−CO‐exposure. PMG isolated from tissue‐specific HO‐1‐deficient (LyzM‐Cre‐Hmox1 fl/fl) and CD36 −/− mice or siRNA against AMPK (AMP‐activated protein kinase) were used to test our hypothesis. In a murine subarachnoid hemorrhage (SAH) model, we compared neuronal injury in wild‐type and CD36 −/− mice. Readouts included vasospasm, microglia activation, neuronal apoptosis, and spatial memory. We observed increased microglial HO‐1‐expression after blood‐exposure. A burst in ROS‐production was seen after CO‐exposure, which led to increased amounts of phosphorylated AMPK with subsequently enhanced CD36 surface‐expression. Naïve PMG from LyzM‐Cre‐Hmox1 fl/fl mice showed reduced ROS‐production and CD36 surface‐expression and failed to respond to CO with increased CD36 surface‐expression. Lack of HO‐1 and CD36 resulted in reduced erythrophagocytosis that could not be rescued with CO. Erythrophagocytosis was enhanced in BV‐2 cells in the presence of exogenous CO, which was abolished in cells treated with siRNA to AMPK. CD36 −/− mice subjected to SAH showed enhanced neuronal cell death, which resulted in impaired spatial memory function. We demonstrate that microglial phagocytic function partly depends on a pathway involving HO‐1 with changes in ROS‐production, phosphorylated AMPK, and surface expression of CD36. CD36 was identified as a crucial component in blood clearance after hemorrhage that ultimately determines neuronal outcome. These results demand further investigations studying the potential neuroprotective properties of CO.

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Section: Microglia Exposed To Blood Show Elevated Expression Of Ho-1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Carbon monoxide controls microglial erythrophagocytosis by regulating CD36 surface expression to reduce the severity of hemorrhagic injury

Kaiser

Selzner

Weber

et al. 2020

Glia

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“…These results indicated that NMDA-induced neurotoxicity was associated with the increase in COX-2 protein expression, and increased PPARc activity could downregulate COX-2 protein expression in neurons with NMDA-induced neurotoxicity (Figure 4). ROSI exerted neuroprotective effect through reducing the COX-2 expression surrounding the infarcted site of the ischemic hemisphere [16][17][18]. Du et al [19] found that PPAR-c-mediated inhibition of COX-2 expression can protect hippocampal neurons from damage.…”

Section: Upregulation Of Ppar-c Inhibits Nmda-induced Neurotoxicity Tmentioning

confidence: 99%

Upregulation of PPAR-gamma activity inhibits cyclooxygenase 2 expression in cortical neurons with N-methyl-d-aspartic acid induced excitatory neurotoxicity

Weng

Chen

et al. 2019

Biotechnology & Biotechnological Equipment

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This study aimed to investigate the effect of upregulated peroxisome proliferator-activated receptor-gamma (PPAR-c) activity on cyclooxygenase 2 (COX-2) expression and N-methyl-Daspartic acid (NMDA)-induced excitatory neurotoxicity in primary cultured cortical neurons. Rat cortical neurons were cultured for 8 days in vitro, and divided into control, NMDA, MK-801 (selective NMDA antagonist), rosiglitazone (ROSI, PPAR-c agonist), GW9662 (PPAR-c antagonist), NS398 (selective COX-2 antagonist) and NS398 þ ROSI groups. Two hours after treatment in each group, cell viability, intracellular Ca 2þ concentrations, PPAR-c and COX-2 protein expression were detected by CCK-8 assay, flow cytometry and western blot assay, respectively. The results showed that compared with the control group, 100 lmol/L of NMDA significantly decreased the neuronal cell viability, increased Ca 2þ concentrations, which also increased the COX-2 protein expression and decreased PPAR-c expression in neurons. Compared with the NMDA group, the cell viability was increased, Ca 2þ concentrations and COX-2 protein expression were significantly decreased, PPAR-c expression was significantly increased in the MK-801, ROSI, NS398 and ROSI þ NS398 groups (both P < 0.01). This finding suggested that upregulation of PPAR-c activity can inhibit COX-2 expression, decrease Ca 2þ concentrations in primary cultured cortical neurons, and protect neurons against NMDA-induced excitatory neurotoxicity.

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“…Rosiglitazone (RSG) is an antidiabetic agent that belongs to the thiazolidinediones, and is a nuclear hormone receptor peroxisome proliferator gamma (PPARγ) agonist . These receptors express most abundantly in fat tissue where they assume the main role in metabolism of lipid and adipogenesis . Through actuating nuclear receptors PPARγ, RSG can control the glucose production and transportation, and furthermore direct the translation of the insulin response genes.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 These receptors express most abundantly in fat tissue where they assume the main role in metabolism of lipid and adipogenesis. 8,9 Through actuating nuclear receptors PPARγ, RSG can control the glucose production and transportation, and furthermore direct the translation of the insulin response genes. It likewise assumes basic role in adipogenesis, antiproliferative, anti-inflammatory, hepatoprotective, nephroprotective, and cardio protective.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of rosiglitazone, a peroxisome proliferator gamma agonist on adriamycin‐induced cardio toxicity via suppressing oxidative stress and apoptosis

Zhang

et al. 2019

IUBMB Life

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We investigated the rosiglitazone (RSG) effect on adriamycin (ADM)‐induced cardio toxicity in experimental animals. Forty adult Wistar male rats were separated into four groups as follows: normal control; RSG (10 mg/kg)‐treated; ADM (10 mg/kg)‐administered; and ADM (10 mg/kg) + RSG (10 mg/kg)‐treated. Serum lipid level, different biochemical biomarkers, histological analysis, and nuclear factor erythroid 2‐related factor/heme oxygenase‐1 (Nrf2/HO‐1), Caspase 3, B‐cell lymphoma 2 (Bcl‐2), and Bax gene expression were assessed in serum and cardiac tissue samples. Our results show that RSG treatment in ADM‐administered animals significantly diminished low‐density lipoprotein cholesterol, triglyceride, and total cholesterol, and increases high‐density lipoprotein cholesterol (HDL‐c) in comparison with the ADM group. RSG treatment reduced the effect of ADM administration on cardiac dysfunction markers such as cardiac troponin T Creatine Kinase‐MB, aspartate aminotransferase, and lactate dehydrogenase, showing the amelioration of cardio toxicity in ADM‐administered rats. Additionally, RSG treatment significantly decreased the level of malondialdehyde and nitric oxide in cardiovascular tissue. RSG‐treated rats in combination with ADM likewise showed a significant increase in reduced glutathione, superoxide dismutase, catalase content, and the activity of glutathione peroxidase (GPx) as compared with ADM group. Moreover, RSG treatment in ADM rats significantly increased an Nrf2 and HO‐1 expression in comparison with ADM group. While in apoptosis parameters, RSG treatment in ADM rats significantly diminished a cleaved caspase‐3 and Bax expression as well as expanded Bcl‐2 expression when contrasted with ADM group of rats. In conclusion, RSG is capable of protecting heart toxicity in ADM‐treated animals through defensive effects on oxidative stress and biochemical markers.

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Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPARγ and CD36

Cited by 13 publications

References 23 publications

Carbon monoxide controls microglial erythrophagocytosis by regulating CD36 surface expression to reduce the severity of hemorrhagic injury

Carbon monoxide controls microglial erythrophagocytosis by regulating CD36 surface expression to reduce the severity of hemorrhagic injury

Upregulation of PPAR-gamma activity inhibits cyclooxygenase 2 expression in cortical neurons with N-methyl-d-aspartic acid induced excitatory neurotoxicity

Ameliorative effect of rosiglitazone, a peroxisome proliferator gamma agonist on adriamycin‐induced cardio toxicity via suppressing oxidative stress and apoptosis

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