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JAK-STAT pathway in carcinogenesis:Is it relevant to cholangiocarcinoma progression?

World Journal of Gastroenterology 2007年第48期13卷 6478-6491页

作者： Olga V Smirnova Tatiana Yu Ostroukhova Roman L Bogorad Laboratory of Endocrinology Biological Faculty M.V. Lomonosov Moscow State University Inserm U845 Paris France Université Paris Descartes Faculté de Médecine René Descartes Centre de Recherche Croissance et Signalisation Equipe PRL GH and tumours Site Necker Paris F-75015 France

The features of JAK-STAT signaling in liver cells are discussed in the current review. The role of this signaling cascade in carcinogenesis is accentuated. The possible involvement of this pathway and alteration of its elements are compared for normal cholangiocytes, cholangiocarcinoma predisposition and development. Prolactin and interleukin-6 are described in detail as the best studied examples. In addition, the non-classical nuclear translocation of cytokine receptors is discussed in terms of its possible implication to cholangiocarcinoma development.

关键词： Cholangiocarcinoma Janus tyrosine Kinases signal transducers and activators of transcription Prolactin Interleukin-6 Cytokine receptors Receptor tyrosine kinases

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Activation of JAK-STAT pathway is required for platelet-derived growth factor-induced proliferation of pancreatic stellate cells

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World Journal of Gastroenterology 2005年第22期11卷 3385-3391页

作者： Atsushi Masamune Masahiro Satoh Kazuhiro Kikuta Noriaki Suzuki Tooru Shimosegawa Division of Gastroenterology Tohoku University Graduate School of Medicine Sendai Japan

AM: To clarify the role of Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway in platelet-derived growth factor (PDGF) induced proliferation in activated pancreatic stellate cells (PSCs). METHODS: PSCs were isolated from rat pancreas tissue, and used in their culture-activated, myofibroblast-like phenotype. STAT-specific binding activity was assessed by electrophoretic mobility shift assay. Activation of Src, JAK2, STAT1, STAT3, and ERK was determined by Western blotting using anti-phosphospecific antibodies. Cell proliferation was assessed by measuring the incorporation of 5-bromo-2'-deoxyuridine. RESULTS: PDGF-BB induced STAT-specific binding activity, and activation of Src, JAK2, STAT1, STAB, and ERK. Ethanol and acetaldehyde at clinically relevant concentrations decreased basal activation of JAK2 and STAT3. PDGF-induced activation of STAT1 and STAT3 was inhibited by a Src inhibitor PP1 and a JAK2 inhibitor AG490, whereas PDGF-induced activation of ERK was inhibited by PP1, and not by AG490. PDGF-induced proliferation was inhibited by PP1 and AG490 as well as by STAT3 antisense oligonucleotide. CONCLUSION: PDGF-BB activated JAK2-STAT pathway via Src-dependent mechanism. Activation of 3AK2-STAT3 pathway, in addition to ERK, may play a role in PDGF-induced proliferation of PSCs.

关键词： Pancreatitis Pancreatic fibrosis Pancreatic stellate cells Platelet-derived growth factor Janus kinase signal transducers and activators of transcription

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Electroacupuncture targeting the immune system to alleviate sepsis

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Acupuncture and Herbal Medicine 2024年第1期4卷 56-67页

作者： Mengyue Fang Yuye Lan Man Li Chennan Li Bin Xu Yan Ma Sulukkana Noiprasert Xianghong Jing Lingling Yu Tongji Hospital Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina School of Basic Medicine Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Key Laboratory of Integrated Acupuncture and Medicine Research of Ministry of Education Nanjing University of Chinese MedicineNanjingChina Wuhan No.1 Hospital Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina School of Integrative Medicine Mae Fah Luang UniversityChiangraiThailand Institute of Acupuncture and Moxibustion China Academy of Chinese Medical SciencesBeijingChina Institute of Integrated Traditional Chinese and Western Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

Sepsis is a life-threatening inflammatory syndrome with high morbidity and mortality ***,options for sepsis are still limited to general treatment in intensive care units(ICUs),and effective therapies that improve sepsis survival are *** disturbances play a vital role in the pathology of sepsis and are associated with protracted inflammation,susceptibility to infections,and ***,many investigators have focused on the potential benefits of immunomodulation therapy for ***(EA)has been practiced in clinics for many years and has shown advantages in treating infectious *** the last few decades,our understanding of the efficacy and mechanisms of EA in sepsis has undergone considerable *** searched the literature regarding“CNKI,Wan Fang Data,VIP Database,PubMed,and Ingenta Connect”from 2010 to 2023,using the keywords“sepsis”“septic”and“electroacupuncture”and 336 sources were ***,we included 82 studies that targeted the immune system to determine EA’s anti-inflammatory and immunomodulatory effects on *** this review,we found that EA has clinical benefits in relieving septic inflammation,improving immune function,and attenuating related multi-organ injury through several mechanisms,such as activation of the cholinergic anti-inflammatory pathway(CAP),vagaladrenal axis,inhibition of the nuclear factor Kappa-B(NF-κB)signaling pathway,signal transducers and activators of transcription(STAT)signaling pathway,and improvement of immune cell ***,EA may be a promising complementary therapy for sepsis *** also expect these data will contribute to further studies on EA in sepsis.

关键词： Cholinergic anti-inflammatory pathway Electroacupuncture Nuclear factor Kappa-B Sepsis signal transducers and activators of transcription Vagal-adrenal axis

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IL-6 Family of Cytokines Mediates Isoproterenolinduced Delayed STAT3 Activation in Mouse Heart

IL-6 Family of Cytokines Mediates Isoproterenolinduced Delay...

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2002全国青年药理学英文学术会议

作者： YIN Feng, ZHANG You-yi, HAN Qi-de(Institute of Vascular Medicine, Peking University Third Hospital,Peking University Institute of Cardiovascular Science, 100083 Beijing)

AIM: To elucidate the molecular mechanism of Isoproterenol-induced hypertrophic response, we examined the role of Isoproterenol in activation of signal transducers and activators of transcription (STAT) in mouse heart. METHODS: Male, 8-week-old Balb/c mice were treated with Isoproterenol (15 mg/kg body weight) or vehicle by intraperitoneal injection. Mice were killed at various time points, and extracts from left ventricles were used to detect tyrosine phosphorylation of STAT3 by Western Blot analysis. RT-PCR analysis was performed to determine the expression of IL-6 family cytokines mRNA in

关键词： Isoproterenol signal transducers and activators of transcription Interleukin-6 Myocardium

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