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| 1 | Role of HSP-90 for increased nNOS-mediated vasodilation in mesenteric arteries in portal hypertension显示文摘AIM:To explore the role of heat shock protein-90 (HSP-90) for nitrergic vasorelaxation in the splanchnic circulation in rats with and without portal hypertension. METHODS: Neuronal nitric oxide synthase (nNOS) and HSP-90 were analyzed by immunofluorescence, western blotting and co-immunoprecipitation in the mesenteric vasculature and isolated nerves of portal-vein-ligated (PVL) rats and sham operated rats. In vitro perfused de-endothelialized mesenteric arterial vasculature was preconstricted with norepinephrine (EC80) and tested for nNOS-mediated vasorelaxation by periarterial nerve stimulation (PNS, 2-12 Hz, 45V) before and after incubation with geldanamycin (specific inhibitor of HSP-90 signalling, 3 μg/mL) or L-NAME (non-specific NOSblocker, 10-4 mol/L). RESULTS: nNOS and HSP-90 expression was significantly increased in mesenteric nerves from PVL as compared to sham rats. Moreover, nNOS and HSP-90 were visualized in mesenteric nerves by immunofluorescence and immunoprecipitation of nNOS co-immunoprecitated HSP-90 in sham and PVL rats. PNS induced a frequencydependent vasorelaxation which was more pronounced in PVL as compared to sham rats. L-NAME and geldanamycin markedly reduced nNOS-mediated vasorelaxation abrogating differences between the study groups. The effect of L-NAME and geldanamycin on nNOS-mediated vasorelaxation was significantly greater in PVL than in sham animals. However, no difference in magnitude of effect between L-NAME and geldanamycin was noted. CONCLUSION: HSP-90 acts as a signalling mediator of nNOS-dependent nerve mediated vascular responses in mesenteric arteries, and the increased nitrergic vasorelaxation observed in portal hypertension is mediated largely by HSP-90. | Lukas Moleda Lars Jurzik Matthias Froh Erwin Gbele Claus Hellerbrand Rainer H Straub Jürgen Schlmerich Reiner Wiest | 2010 | World Journal of Gastroenterology2010，16，15： | 4 |
| 2 | 水基清洗技术——航空航天零件工业绿色清洗技术介绍(二) | 易举 孙卓 Rainer Straub | 2009 | 国防制造技术2009，0，6： | 2 |
| 3 | Neuroendocrine immune mechanisms in rheumatic diseases显示文摘 | Johannes W.J Bijlsma Rainer H Straub Alfonse T Masi Robert G Lahita Maurizio Cutolo | 2002 | Trends in Immunology2002，，2： | 1 |
| 4 | Stimulation of TNF receptor type 2 expands regulatory T cells and ameliorates established collagen-induced arthritis in mice显示文摘Tumor necrosis factor(TNF)and its receptors TNF receptor type 1(TNFR1)and type 2(TNFR2)have a central role in chronic inflammatory diseases.While TNFR1 mainly confers inflammation,activation of TNFR2 elicits not only pro-inflammatory but also anti-inflammatory effects.In this study,we wanted to investigate the anti-inflammatory therapeutic potential of selective activation of TNFR2 in mice with established collageninduced arthritis.Mice with established arthritis induced by immunization with bovine collagen type II were treated with six injections of the TNFR2-specific agonist TNCscTNF80,given every second day.Two days after treatment cessation,the cell compositions of bone marrow,spleen and lymph nodes were analyzed.Mice were visually scored until day 30 after the start of therapy and the degree of joint inflammation was determined by histology.Treatment with TNCscTNF80 increased arthritis-induced myelopoiesis.Little effect was seen on the infiltration rate of inflammatory immature myeloid cells and on the reduction of lymphoid cells in secondary lymphoid organs.Upon treatment,frequency of regulatory T(Treg)cells in the CD4+T-cell population was increased in both spleen and inguinal lymph nodes.In addition,the expression of TNFR2 on Treg cells was enhanced.The clinical score started to improve 1 week after cessation treatment and remained lower 30 days after initiation of therapy.The histological score also revealed amelioration of joint inflammation in TNCscTNF80-treated versus control mice.Activation of TNFR2 might provide a suitable therapeutic strategy in autoimmune arthritis by increasing the numbers of regulatory cell types,in particular Treg cells,and by attenuation of arthritis. | Vanessa Lamontain Tobias Schmid Dorothea Weber-Steffens David Zeller Zsuzsa Jenei-Lanzl Harald Wajant Rainer H Straub Daniela N Männel | 2019 | Cellular & Molecular Immunology2019，16，1： | 1 |
| 5 | How psychological stress via hormones and nerve fibers may exacerbate rheumatoid arthritis显示文摘 | Rainer H Straub Firdaus and apoptosis Arthritis S Dhabhar Johannes W J Bijlsma | 2005 | Arthritis Rheum2005，52，1： | 1 |
| 6 | Sympathetic neurotran- smitters in joint inflammation显示文摘 | Rainer H Straub Peter Hirle | 2005 | Rheum Dis Clin North Am2005，31，1： | 1 |
| 7 | Cortisol‐mediated adhesion of synovial fibroblasts is dependent on the degradation of anandamide and activation of the endocannabinoid system显示文摘 | Torsten Lowin Wentao Zhu Katja Dettmer‐Wilde Rainer H. Straub | 2012 | Arthritis & Rheumatism2012，，12： | 1 |
| 8 | How psychological stress via hormones and nerve fibers may exacerbate rheumatoid arthritis显示文摘 | Rainer H Straub FS Dhabhar JW | 2005 | Arthritis & Rheumatism2005，52，： | 1 |
| 9 | Dialogue between the CNS and the immunesystem in lymphoid organs 显示文摘 | Rainer H Straub W | 1998 | lmmunol Today1998，19，9： | 1 |
| 10 | Restoring the balance of the autonomic nervous system as an innovative approach to the treatment of rheumatoid arthritis显示文摘 | Frieda A Koopman Susanne P Stoof Rainer H Straub | 2011 | Mol Med2011，17，910： | 1 |
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