Dynamic Balance of pSTAT1 and pSTAT3 in C57BL/6 Mice Infected with Lethal Or Nonlethal Plasmodium yoelii

Shi, Xibao; Li, Qin; Liu, Guangjie; Shu, Zhao; Peng, Nanzheng; Chen, Xiaoping

doi:10.1038/cmi.2008.42

Cited by 19 publications

(24 citation statements)

References 34 publications

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“…JAK/STAT3 pathway is involved in cancer [52], immune response [53], ischemia [54], [55] and cellular stress [55], [56]. STAT3 has dual effects on cell survival, as STAT3 can act in deleterious or beneficial roles in cell survival.…”

Section: Discussionmentioning

confidence: 99%

STAT3 Regulates MMP3 in Heme-Induced Endothelial Cell Apoptosis

et al. 2013

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BackgroundWe have previously reported that free Heme generated during experimental cerebral malaria (ECM) in mice, is central to the pathogenesis of fatal ECM. Heme-induced up-regulation of STAT3 and CXCL10 promotes whereas up-regulation of HO-1 prevents brain tissue damage in ECM. We have previously demonstrated that Heme is involved in the induction of apoptosis in vascular endothelial cells. In the present study, we further tested the hypothesis that Heme reduces blood-brain barrier integrity during ECM by induction of apoptosis of brain vascular endothelial cells through STAT3 and its target gene matrix metalloproteinase three (MMP3) signaling.MethodsGenes associated with the JAK/STAT3 signaling pathway induced upon stimulation by Heme treatment, were assessed using real time RT2 Profile PCR arrays. A human MMP3 promoter was cloned into a luciferase reporter plasmid, pMMP3, and its activity was examined following exposure to Heme treatment by a luciferase reporter gene assay. In order to determine whether activated nuclear protein STAT3 binds to the MMP3 promoter and regulates MMP3 gene, we conducted a ChIP analysis using Heme-treated and untreated human brain microvascular endothelial cells (HBVEC), and determined mRNA and protein expression levels of MMP3 using qRT-PCR and Western blot. Apoptosis in HBVEC treated with Heme was evaluated by MTT and TUNEL assay.ResultsThe results show that (1) Heme activates a variety of JAK/STAT3 downstream pathways in HBVEC. STAT3 targeted genes such as MMP3 and C/EBPb (Apoptosis-related genes), are up regulated in HBVEC treated with Heme. (2) Heme-induced HBVEC apoptosis via activation of STAT3 as well as its downstream signaling molecule MMP3 and upregulation of CXCL10 and HO-1 expressions. (3) Phosphorylated STAT3 binds to the MMP3 promoter in HBVEC cells, STAT3 transcribed MMP3 and induced MMP3 protein expression in HBVEC cells.ConclusionsActivated STAT3 binds to the MMP3 promoter region and regulates MMP3 in Heme-induced endothelial cell apoptosis.

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Section: Discussionmentioning

confidence: 99%

STAT3 Regulates MMP3 in Heme-Induced Endothelial Cell Apoptosis

et al. 2013

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“…MARC-145 cells grown in 24-well plates were transfected in triplicate with the pcDNA3.1-FLAG (control vector) or pcDNA3.1-FLAG-nsp11 (1000 ng) or pcDNA3.1-FLAG-nsp11H129A (1000 ng), and 24 h later, transfected cells were mock-transfected or transfected with Poly(I:C) (1000 ng/well) by using Lipofectamine2000 for 6 h and lysed in lysing buffer (1% Nonidet P-40, 0.1% sodium deoxycholate, 0.1% SDS, 50 mM Tris-HCl, pH 7.4, 150 mM NaCl, 2 mM EDTA, 2 mM Na 3 VO 4 , 2 mM NaF and a protease inhibitor cocktail). The detailed procedure for immunoblots has been described (Shi et al, 2008). Briefly, the total protein concentration was quantified with the Bradford protein assay (Biocolor Bioscience & Technology Company, Shanghai).…”

Section: Western Blotmentioning

confidence: 99%

Endoribonuclease activities of porcine reproductive and respiratory syndrome virus nsp11 was essential for nsp11 to inhibit IFN-β induction

Shi

Wang

et al. 2011

Molecular Immunology

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Previous studies have shown that PRRSV nsp11, which was an endoribonuclease, was an interferon antagonist, however, the mechanism that nsp11 inhibited IFN-β production was unclear. To explore whether the endoribonuclease was required for nsp11 to disrupt the IFN-β production, substitutions of the presumed catalytic histidine and lysine residues of nsp11 were introduced into plasmid pcDNA 3.1-FLAG. The results showed that mutation that inactivated endoribonuclease made nsp11 lose its ability to inhibit Poly(I:C)-induced IFN-β promoter activity. In conclusion, our present work indicated that the endoribonuclease activity of nsp11 was essential for nsp11 to inhibit the IFN-β induction.

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“…or treated with Poly(I:C) for 6 h and lysed in lysing buffer (1% Nonidet P-40, 0.1% sodium deoxycholate, 0.1% SDS, 50 mM Tris-HCl pH 7.4, 150 mM NaCl, 2 mM EDTA, 2 mM Na3VO4, 2 mM NaF and a protease inhibitor cocktail). The detailed procedure for immunoblots has been described (Shi et al, 2008). Briefly, the total protein concentration was quantified with the Bradford protein assay (Biocolor Bioscience & Technology Company, Shanghai).…”

Section: Primermentioning

confidence: 99%

Porcine reproductive and respiratory syndrome virus (PRRSV) could be sensed by professional beta interferon-producing system and had mechanisms to inhibit this action in MARC-145 cells

et al. 2010

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Porcine reproductive and respiratory syndrome virus (PRRSV) causes an economically important disease in swine-producing area, and interferon beta (IFN-beta) is the first responder against the animal virus infection. However, whether PRRSV could induce the production of IFN-beta is controversial. In this paper, we first time found that PRRSV could phosphorylate IFN-regulatory factor 3 (IRF-3) and weakly activate the IFN-beta promoter in MARC-145 cells in early infection, but the activations of IRF-3 and IFN-beta promoter were rapidly inhibited in the following infection. Furthermore, which components or products of the invading PRRSV cause PRRSV to inhibit IFN-beta promoter activity attracted our attentions. The obtained results showed that PRRSV nsp1 could inhibit Poly(I:C)-induced IFN-beta promoter activity in MARC-145 cells by down-regulating the protein level of IRF-3 and inhibiting the phosphorylation of IRF-3. In conclusion, our results suggested that PRRSV could be sensed by professional IFN-beta-producing system and had mechanisms to inhibit this action in MARC-145 cells.

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Dynamic Balance of pSTAT1 and pSTAT3 in C57BL/6 Mice Infected with Lethal Or Nonlethal Plasmodium yoelii

Cited by 19 publications

References 34 publications

STAT3 Regulates MMP3 in Heme-Induced Endothelial Cell Apoptosis

STAT3 Regulates MMP3 in Heme-Induced Endothelial Cell Apoptosis

Endoribonuclease activities of porcine reproductive and respiratory syndrome virus nsp11 was essential for nsp11 to inhibit IFN-β induction

Porcine reproductive and respiratory syndrome virus (PRRSV) could be sensed by professional beta interferon-producing system and had mechanisms to inhibit this action in MARC-145 cells

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