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6篇 您的检索式:作者名="Peter Tipping"
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1cytoplasmic domain of tissue factor promotes liver fibrosis in mice显示文摘AIM To evaluate the role of tissue factor(TF) and protease activated receptor(PAR)-2 in liver fibrosis.METHODS Using CCl4 administration for eight weeks, we induced hepatic fibrosis in wild-type C57BL/6 mice and in mice with deletion of the cytoplasmic signalling domain of TF(TF§CT/§CT), deletion of PAR-2(PAR-2-/-) and combined deletion of TF signalling domain and PAR-2(TF§CT/§CT/PAR-2-/-). Hepatic fibrosis area was assessed by quantitative imaging of picrosirius red staining. Hepatic collagen content was assessed by hydroxyproline levels. Hepatic stellate cells(αSMA positive) and hepatic macrophages(CD68 positive) were identified by immunohistochemistry. Hepatic gene expression was determined by PCR and liver TGFβ1 content by ELISA.RESULTS CCl4 treated mice with deletion of the PAR-2 gene(PAR-2-/-) and the cytoplasmic domain of TF(TF§CT/§CT) developed significantly less hepatic fibrosis, characterised by reduced liver fibrosis area and hydroxyproline content, compared to control wildtype mice treated with CCl4. The observed reduction in histological fibrosis was accompanied by a significant decrease in the hepatic content of TGFβ, the prototypic fibrogenic cytokine, as well as fewer activated hepatic stellate cells and hepatic macrophages. Deletion of the TF cytoplasmic signalling domain reduced hepatic fibrosis to levels similar to thoseobserved in mice lacking PAR-2 signalling but combined deletion provided no added protection against fibrosis indicating a lack of mutual modulating effects that have been observed in other contexts such as angiogenic responses.CONCLUSION Tissue factor cytoplasmic domain is involved in TF-PAR-2 signalling initiating hepatic fibrosis and is a potential therapeutic target, as its deletion would not impact coagulation.Virginia Knight Dinushka Lourensz Jorge Tchongue Jeanne Correia Peter Tipping William Sievert 2017World Journal of Gastroenterology2017,23,31:3
2Immune regulation by CD52-expressing CD4 T cells显示文摘由表示 CD52 CD4 T 房间的 T 房间规定看起来操作由二不同并且可能 synergistic 机制。第一由它从表示那然后绑在由损害 T 房间受体的 phosphorylation 稀释受动器 T 房间激活的酸绑定的像免疫球蛋白的 lectins-10 (Siglec-10 ) 受体联系了的禁止的 sialic 的 CD52 的高水平的 CD4 T 房间的房间表面的版本 lck 和 zap-70。第二机制看起来由由被导致他们的扩大的二原子价的 anti-CD52 抗体模仿的迄今为止未辩别出的内长的 ligand 的 CD52 分子的 crosslinkage。Ban-Hock Toh Tin Kyaw Peter Tipping Alex Bobik 2013Cellular & Molecular Immunology2013,10,5:2
3Cytotoxic and Proinflammatory CD8+ T Lymphocytes Promote Development of Vulnerable Atherosclerotic Plaques in ApoE-Deficient Mice显示文摘Tin Kyaw Amy Winship Christopher Tay Peter Kanellakis Hamid Hosseini Anh Cao Priscilla Li Peter Tipping Alex Bobik Ban-Hock Toh 2013Circulation2013,,9:1
4Continuous veno-venous hemofiltration with dialysis removes cytokines from the circulation of septic patients显示文摘RINALDO BELLOMO PETER TIPPING NEIL BOYCE 1993Critical Care Medicine1993,,4:1
5Immune modulation with interleukin-4 and interleukin-10 prvents crescent formation and glomerular injury in experiment glomerulonephritis显示文摘Peter G Tipping A Richard K 1997Eur J Imm1997,27,:1
6Protease-Activated Receptor-2 Augments Experimental Crescentic Glomerulonephritis显示文摘Leon Moussa Jim Apostolopoulos Piers Davenport Jorge Tchongue Peter G. Tipping 2007The American Journal of Pathology2007,,:1
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