- adrenergic beta-2 receptor、beta-2 adrenoceptor、beta-2 receptor、beta2 adrenergic receptor、beta2 adrenoceptor、beta2 receptor
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/28 09:07:51」(JST)[Wiki en表示]
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- 1. β-2アドレナリン受容体機能不全および喘息の多型性 beta 2 adrenergic receptor dysfunction and polymorphism in asthma
- 2. 喘息の遺伝学 genetics of asthma
- 3. 昇圧剤および強心剤の使用 use of vasopressors and inotropes
- 4. 喘息におけるβ刺激剤：急性期投与および予防的使用 beta agonists in asthma acute administration and prophylactic use
- 5. 喘息におけるβ刺激剤：長期使用に関する議論 beta agonists in asthma controversy regarding chronic use
- A β1/2 adrenergic receptor-sensitive intracellular signaling pathway modulates CCL2 production in cultured spinal astrocytes.
- Morioka N, Abe H, Araki R, Matsumoto N, Zhang FF, Nakamura Y, Hisaoka-Nakashima K, Nakata Y.Author information Department of Pharmacology, Hiroshima University Graduate School of Biomedical and Health Sciences, Minami-ku, Hiroshima, Japan.AbstractThe phosphorylation of c-jun N-terminal kinase (JNK) and the subsequent production of C-C chemokine CCL2 (monocyte chemoattractant protein; MCP-1) in spinal astrocytes contribute to the initiation of neurological disorders including chronic pain. Astrocytes express neurotransmitter receptors which could be targeted to ameliorate neurological disorders. In the current study, the involvement of the β-adrenergic system in the regulation of JNK activity and CCL2 production after stimulation with tumor necrosis factor (TNF)-α, one of many initiators of neuroinflammation, was elucidated. Treatment of cultured spinal astrocytes with isoproterenol (a β-adrenergic receptor agonist; 1 µM) reduced both TNF-α-induced JNK1 phosphorylation, as observed by Western blotting, and the subsequent increase of both CCL2 mRNA expression and CCL2 production, which were measured by real time-PCR and ELISA, respectively. The effects of isoproterenol were completely blocked by pretreatment with either propranolol (a β-adrenoceptor antagonist) or H89 (a protein kinase A [PKA] inhibitor). The current study revealed that the regulation of glycogen synthase kinase-3β (GSK-3β) activity is a crucial factor in the inhibitory action of isoproterenol. The TNF-α-induced JNK1 phosphorylation was significantly blocked by treatment with GSK-3β inhibitors (either LiCl or TWS119), and stimulation of β-adrenergic receptors induced the inhibition of GSK-3β through the phosphorylation of Ser(9) . Moreover, treatment with isoproterenol markedly suppressed the TNF-α-induced increase of CCL2 mRNA expression and CCL2 production through a β-adrenergic receptor-PKA pathway mediated by GSK-3β regulation. Thus, activation of β1/2 adrenergic receptors expressed in spinal astrocytes could be a novel method of moderating neurological disorders with endogenous catecholamines or selective agonists.
- Journal of cellular physiology.J Cell Physiol.2014 Mar;229(3):323-32. doi: 10.1002/jcp.24452.
- The phosphorylation of c-jun N-terminal kinase (JNK) and the subsequent production of C-C chemokine CCL2 (monocyte chemoattractant protein; MCP-1) in spinal astrocytes contribute to the initiation of neurological disorders including chronic pain. Astrocytes express neurotransmitter receptors which c
- PMID 24037783
- Adrenergic and glucocorticoid modulation of the sterile inflammatory response.
- Cox SS1, Speaker KJ1, Beninson LA1, Craig WC1, Paton MM1, Fleshner M2.Author information 1Department of Integrative Physiology, University of Colorado, Boulder, United States.2Department of Integrative Physiology, University of Colorado, Boulder, United States; Center for Neuroscience, University of Colorado, Boulder, United States. Electronic address: firstname.lastname@example.org.AbstractExposure to an intense, acute stressor, in the absence of a pathogen, alters immune function. Exposure to a single bout of inescapable tail shock increases plasma and tissue concentrations of cytokines, chemokines, and the danger associated molecular pattern (DAMP) Hsp72. Although previous studies have demonstrated that adrenergic receptor (ADR) and glucocorticoid receptor (GCR)-mediated pathways alter pathogen or microbial associated molecular pattern (MAMP)-evoked levels of cytokines, chemokines, and Hsp72, far fewer studies have tested the role of these receptors across multiple inflammatory proteins or tissues to elucidate the differences in magnitude of stress-evoked sterile inflammatory responses. The goals of the current study were to (1) compare the sterile inflammatory response in the circulation, liver, spleen, and subcutaneous (SQ) adipose tissue by measuring cytokine, chemokine, and DAMP (Hsp72) responses; and (2) to test the role of alpha-1 (α1), beta-1 (β1), beta-2 (β2), and beta-3 (β3) ADRs, as well as GCRs in signaling the sterile inflammatory response. The data presented indicate plasma and SQ adipose are significantly more stress responsive than the liver and spleen. Further, administration of ADR and GCR-specific antagonists revealed both similarities and differences in the signaling mechanisms of the sterile inflammatory response in the tissues studied. Finally, given the selective increase in the chemokine monocyte chemotactic protein-1 (MCP-1) in SQ tissue, it may be that SQ adipose is an important site of leukocyte migration, possibly in preparation for infection as a consequence of wounding. The current study helps further our understanding of the tissue-specific differences of the stress-induced sterile inflammatory response.
- Brain, behavior, and immunity.Brain Behav Immun.2014 Feb;36:183-92. doi: 10.1016/j.bbi.2013.11.018. Epub 2013 Dec 7.
- Exposure to an intense, acute stressor, in the absence of a pathogen, alters immune function. Exposure to a single bout of inescapable tail shock increases plasma and tissue concentrations of cytokines, chemokines, and the danger associated molecular pattern (DAMP) Hsp72. Although previous studies h
- PMID 24321216
- The role of monocytes in angiogenesis and atherosclerosis.
- Jaipersad AS1, Lip GY1, Silverman S2, Shantsila E3.Author information 1University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom.2Department of Vascular Surgery, City Hospital, Birmingham, United Kingdom.3University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom. Electronic address: email@example.com.AbstractNew vessel formation inside the arterial wall and atherosclerotic plaques plays a critical role in pathogenesis of heart attacks and strokes. The 2 known mechanisms resulting in the formation of new vessels within the plaque are local ischemia and inflammation. Blood monocytes play an important role in both processes. First, they express receptors for vascular endothelial growth factor and some of them may serve as circulating ancestors of endothelial cells. Second, monocytes are associated with inflammation by synthesis of inflammatory molecules following their activation (e.g., after stimulation of Toll-like receptors). Neovascularization is a reparative response to ischemia, and includes 3 processes: angiogenesis, arteriogenesis, and vasculogenesis. Angiogenesis, the formation of new capillary vessels is known to occur in response to a hypoxic environment. The interaction between leukocytes and vascular wall via overexpression of various molecules facilitates the migration of inflammatory cells into the plaque microenvironment. Monocytes are intimately involved in tissue damage and repair and an imbalance of these processes may have detrimental consequences for plaque development and stability. Importantly, monocytes are comprised of distinct subsets with different cell surface markers and functional characteristics and this heterogeneity may be relevant to angiogenic processes in atherosclerosis. The aim of this review article is to present an overview of the available evidence supporting a role for monocytes in angiogenesis and atherosclerosis.
- Journal of the American College of Cardiology.J Am Coll Cardiol.2014 Jan 7;63(1):1-11. doi: 10.1016/j.jacc.2013.09.019. Epub 2013 Oct 16.
- New vessel formation inside the arterial wall and atherosclerotic plaques plays a critical role in pathogenesis of heart attacks and strokes. The 2 known mechanisms resulting in the formation of new vessels within the plaque are local ischemia and inflammation. Blood monocytes play an important role
- PMID 24140662
- β(2)-Adrenergic and M(2)-muscarinic receptors decrease basal t-tubular L-type Ca2+ channel activity and suppress ventricular contractility in heart failure
- EUROPEAN JOURNAL OF PHARMACOLOGY 724, 122-131, 2014-02-05
- NAID 120005440173
- 4) 幼少期の高アンドロゲン環境とインスリン抵抗性からみたPCOSの病因および管理に関する検討(シンポジウム3:生殖「多嚢胞性卵巣症候群(PCOS)の病因・病態と管理」,第65回日本産科婦人科学会・学術講演会)
- 日本産科婦人科學會雜誌 65(12), 2721-2736, 2013-12-01
- NAID 110009685697
- 総説 : 自律神経と末梢前庭器 : 末梢前庭系における分子生物学的考察
- Equilibrium research 71(3), 200-206, 2012-06-01
- NAID 10030781927
- The beta-2 adrenergic receptor also known as ADRB2, is a beta-adrenergic receptor, and also denotes the human gene encoding it. Contents. 1 Gene; 2 Structure; 3 Mechanism; 4 Function. 4.1 Muscular system; 4.2 Circulatory system; 4.3 ...
|リンク元||「beta-2 receptor」「beta-2 adrenoceptor」「adrenergic beta-2 receptor」「β2アドレナリンレセプター」|
- beta-2 adrenergic receptor、beta-2 adrenoceptor、beta2 adrenergic receptor、beta2 adrenoceptor、beta2 receptor
- beta-2 adrenergic receptor、beta-2 receptor、beta2 adrenergic receptor、beta2 adrenoceptor、beta2 receptor
- beta-2 adrenergic receptor
- beta2 adrenergic receptor、beta-2 adrenergic receptor