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- 1. 心臓の虚血性再潅流障害 ischemic reperfusion injury of the heart
- 2. 慢性関節リウマチにおける滑膜異常 synovial pathology in rheumatoid arthritis
- 3. ステロイド抵抗性喘息 glucocorticoid resistant asthma
- 4. 虚血プレコンディショニングの定義および病因 definition and pathogenesis of ischemic preconditioning
- 5. 免疫系に対するステロイドの影響 glucocorticoid effects on the immune system
- The Ang-(1-7)/Mas-1 axis attenuates the expression and signalling of TGF-β1 induced by AngII in mouse skeletal muscle.
- Morales MG1, Abrigo J1, Meneses C1, Simon F, Cisternas F1, Rivera JC1, Vazquez Y1, Cabello-Verrugio C1.Author information 1*Laboratorio de Biología y Fisiopatología Molecular, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas & Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.AbstractAngII (angiotensin II) induces pathological conditions such as fibrosis in skeletal muscle. In this process, AngII increases ROS (reactive oxygen species) and induces a biphasic phosphorylation of p38 MAPK (mitogen-activated protein kinase). In addition, AngII stimulates the expression and production of TGF (transforming growth factor)-β1 via a mechanism dependent on ROS production mediated by NADPH oxidase (NOX) and p38 MAPK activation. In the present study, we investigated whether Ang-(1-7) [angiotensin-(1-7)], through the Mas-1 receptor, can counteract the signalling induced by AngII in mouse skeletal muscle and cause a decrease in the expression and further activity of TGF-β1 in skeletal muscle cells. Our results show that Ang-(1-7) decreased the expression of TGF-β1 induced by AngII in a dose-dependent manner. In addition, we observed that Ang-(1-7) prevented the increase in TGF-β1 expression induced by AngII, ROS production dependent on NOX and the early phase of p38 MAPK phosphorylation. Interestingly, Ang-(1-7) also prevented the late phase of p38 MAPK phosphorylation, Smad-2 phosphorylation and Smad-4 nuclear translocation, an increase in transcriptional activity, as determined using the p3TP-lux reporter, and fibronectin levels, all of which are dependent on the TGF-β1 levels induced by AngII. We also demonstrated that Ang-(1-7) prevented the increase in TGF-β1, fibronectin and collagen content in the diaphragm of mice infused with AngII. All of these effects were reversed by the administration of A779, indicating the participation of Mas-1. In conclusion, our findings support the hypothesis that Ang-(1-7) decreases the expression and further biological activity of TGF-β1 induced by AngII in vitro and in vivo.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul 1;127(4):251-64. doi: 10.1042/CS20130585.
- AngII (angiotensin II) induces pathological conditions such as fibrosis in skeletal muscle. In this process, AngII increases ROS (reactive oxygen species) and induces a biphasic phosphorylation of p38 MAPK (mitogen-activated protein kinase). In addition, AngII stimulates the expression and productio
- PMID 24588264
- Structure- and ligand-based drug design of novel p38-alpha MAPK inhibitors in the fight against the Alzheimer's disease.
- Pinsetta FR1, Taft CA, de Paula da Silva CH.Author information 1a Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo , Av. do Café, s/n - Monte Alegre, Ribeirão Preto , SP 14040-903 , Brazil .AbstractAlzheimer's disease (AD) is characterized microscopically by the presence of amyloid plaques, which are accumulations of beta-amyloid protein inter-neurons, and neurofibrillary tangles formed predominantly by highly phosphorylated forms of the microtubule-associated protein, tau, which form tangled masses that consume neuronal cell body, possibly leading to neuronal dysfunction and ultimately death. p38α mitogen-activated protein kinase (MAPK) has been implicated in both events associated with AD, tau phosphorylation and inflammation. p38α MAPK pathway is activated by a dual phosphorylation at Thr180 and Tyr182 residues. Drug design of p38α MAPK inhibitors is mainly focused on small molecules that compete for Adenosine triphosphate in the catalytic site. Here, we used different approaches of structure- and ligand-based drug design and medicinal chemistry strategies based on a selected p38α MAPK structure deposited in the Protein Data Bank in complex with inhibitor, as well as others reported in literature. As a result of the virtual screening experiments performed here, as well as molecular dynamics, molecular interaction fields studies, shape and electrostatic similarities, activity and toxicity predictions, and pharmacokinetic and physicochemical properties, we have selected 13 compounds that meet the criteria of low or no toxicity potential, good pharmacotherapeutic profile, predicted activities, and calculated values comparable with those obtained for the reference compounds, while maintaining the main interactions observed for the most potent inhibitors.
- Journal of biomolecular structure & dynamics.J Biomol Struct Dyn.2014 Jul;32(7):1047-63. doi: 10.1080/07391102.2013.803441. Epub 2013 Jun 28.
- Alzheimer's disease (AD) is characterized microscopically by the presence of amyloid plaques, which are accumulations of beta-amyloid protein inter-neurons, and neurofibrillary tangles formed predominantly by highly phosphorylated forms of the microtubule-associated protein, tau, which form tangled
- PMID 23805842
- Long-term blue light exposure induces RGC-5 cell death in vitro: involvement of mitochondria-dependent apoptosis, oxidative stress, and MAPK signaling pathways.
- Huang C1, Zhang P, Wang W, Xu Y, Wang M, Chen X, Dong X.Author information 1Department of Ophthalmology, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing, 100191, China, email@example.com.AbstractThe mechanism of blue light-induced retinal ganglion cell (RGC) injury is poorly understood. In this study, we established a patented light-emitting diode-based system to study the effects of long-term blue light exposure under culture conditions on RGC-5 cells. Long-term blue light exposure significantly reduced cell viability in a time-dependent manner and induced apoptosis and necrosis in RGC-5 cells. Long-term blue light exposure marked an increase in the expression of Bax and active Caspase-3 (p17), which was accompanied by Bcl-2 down-regulation, and displayed features of the mitochondria-dependent apoptosis pathway. Blue light exposure also increased the generation of reactive oxygen species (ROS), and was a strong inducer of ROS-sensitive protein nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Moreover, blue light exposure constitutively activated p38 mitogen-activated protein kinases and c-Jun NH2-terminal kinase (JNK), as well as induced the phosphorylation of extracellular signal-regulated kinase in the early phase, in blue light-exposed RGC-5 cells. The protein expression of c-jun and c-fos was further enhanced after RGC-5 cells were exposed to blue light. Taken together, these findings indicated that blue light induced RGC-5 cell line death in dependence upon exposure duration. The potential mechanisms for this phenomenon might be via activated mitochondria-dependent apoptosis, increased ROS production and protein expressions of Nrf2 and HO-1, and activated JNK/p38 MAPK signaling pathways.
- Apoptosis : an international journal on programmed cell death.Apoptosis.2014 Jun;19(6):922-32. doi: 10.1007/s10495-014-0983-2.
- The mechanism of blue light-induced retinal ganglion cell (RGC) injury is poorly understood. In this study, we established a patented light-emitting diode-based system to study the effects of long-term blue light exposure under culture conditions on RGC-5 cells. Long-term blue light exposure signifi
- PMID 24682673
- The potent activity of sulfated polysaccharide, ascophyllan, isolated from Ascophyllum nodosum to induce nitric oxide and cytokine production from mouse macrophage RAW264.7 cells: Comparison between ascophyllan and fucoidan.
- Jiang Zedong,Okimura Takasi,Yamaguchi Kenichi,Oda Tatsuya
- Nitric Oxide : Biology and Chemistry / official journal of the Nitric Oxide Society 25(4), 407-415, 2011-11-30
- … Analysis using mitogen-activated protein (MAP) kinase inhibitors and western blot analysis suggested that c-Jun N-terminal kinase (JNK) and p38 MAP kinase are mainly involved in ascophyllan-induced NO production. …
- NAID 120003550949
- Involvement of MAPKs in ICAM-1 Expression in Glomerular Endothelial Cells in Diabetic Nephropathy
- Watanabe Naomi,Shikata Kenichi,Shikata Yasushi,Sarai Kei,Omori Kazuyoshi,Kodera Ryo,Sato Chikage,Wada Jun,Makino Hirofumi
- Acta Medica Okayama 65(4), 247-257, 2011-08
- … The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. …
- NAID 80021895207
- High-dose tobramycin inhibits lipopolysaccharide-induced MUC5AC production in human lung epithelial cells.
- Nakamura Shigeki,Yanagihara Katsunori,Araki Nobuko,Yamada Koichi,Morinaga Yoshitomo,Izumikawa Koichi,Seki Masafumi,Kakeya Hiroshi,Yamamoto Yoshihiro,Kamihira Shimeru,Kohno Shigeru
- European journal of pharmacology 659(1), 67-71, 2011-05-20
- … We demonstrate that high-dose tobramycin decreases MUC5AC gene expression and protein production in NCI-H292 cell stimulated with lipopolysaccharide of P. … MUC5AC protein of NCI-H292 cell stimulated by lipopolysaccharide was analyzed by an enzyme-linked immunosorbent assay and MUC5AC expression at the mRNA level was analyzed by RT-PCR. …
- NAID 120003220709
- Evidence is beginning to accumulate that p38 mitogen activated protein kinase (p38 MAPK) signaling pathway plays an important role in the regulation of cellular ... 1. Introduction Autoimmune diseases develop when immunological ...
- Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK14 is one of the four p38 MAPKs which play an important role in the cascades of cellular responses evoked by ...
|リンク元||「p38 mitogen-activated protein kinase」「p38マイトジェン活性化プロテインキナーゼ」「p38 MAPK」「p38 MAP kinase」「MAPキナーゼp38」|
- p38 mitogen-activated protein kinase、p38 MAP kinase、p38 MAPK、mitogen-activated protein kinase p38
- mitogen-activated protein kinase p38、p38 MAP kinase、p38 mitogen-activated protein kinase、p38 protein kinase
- mitogen-activated protein kinase p38、p38 MAPK、p38 mitogen-activated protein kinase、p38 protein kinase
- p38 mitogen-activated protein kinase、mitogen-activated protein kinase p38