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We are analyzing https://link.springer.com/article/10.1007/s00109-016-1468-2.

Title:
Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α | Journal of Molecular Medicine
Description:
Abstract The insulin-sensitive glucose transporter 4 (GLUT4) is a predominant facilitative glucose transporter in vascular smooth muscle cells (VSMCs) and is significantly upregulated in rabbit neointima. This study investigated the role of GLUT4 in VSMC proliferation, the cellular mechanism underlying PDGF-BB-stimulated GLUT4 translocation, and effects of SM22α, an actin-binding protein, on this process. Chronic treatment of VSMCs with PDGF-BB significantly elevated GLUT4 expression and glucose uptake. PDGF-BB-induced VSMC proliferation was dependent on GLUT4-mediated glucose uptake. Meanwhile, the response of GLUT4 to insulin decreased in PDGF-BB-stimulated VSMCs. PDGF-BB-induced GLUT4 translocation partially rescued glucose utilization in insulin-resistant cells. Immunofluorescence and western blot analysis revealed that PDGF-BB induced GLUT4 translocation in an actin dynamics-dependent manner. SM22α disruption facilitated GLUT4 translocation and glucose uptake by promoting actin dynamics and cortical actin polymerization. Similar results were observed in VSMCs of SM22α āˆ’/āˆ’ mice. The in vivo experiments showed that the glucose level in the neointima induced by ligation was significantly increased in SM22α āˆ’/āˆ’ mice, accompanied by increased neointimal thickness, compared with those in wild-type mice. These findings suggest that GLUT4-mediated glucose uptake is involved in VSMC proliferation, and provide a novel link between SM22α and glucose utilization in PDGF-BB-triggered proliferation. Key Messages • GLUT4-mediated glucose uptake is required for the VSMC proliferation. • PDGF-BB-induced GLUT4 translocation partially rescues glucose uptake in insulin resistance. • SM22α disruption enhances PDGF-BB-induced GLUT4 translocation. • Glucose level in injured vascular tissue is positively correlated with neointimal hyperplasia.
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Keywords {šŸ”}

article, pubmed, google, scholar, cas, glucose, glut, muscle, smooth, vascular, translocation, cell, cells, zhang, actin, smα, uptake, proliferation, biol, central, han, insulin, diabetes, growth, access, liu, xie, dong, mol, plateletderived, physiol, res, privacy, cookies, content, journal, zhao, chen, lin, miao, shu, vsmcs, vsmc, protein, mice, factor, kinase, analysis, publish, search,

Topics {āœ’ļø}

pdgf-bb-induced vsmc proliferation ya-nan shuĀ &Ā mei han platelet-derived growth factor pdgf-bb-stimulated vsmcs month download article/chapter pdgf-bb-triggered proliferation insulin-independent glut4 translocation glut4-mediated glucose uptake agonist-induced vascular reactivity insulin-regulatable glucose transporter actin dynamics-dependent manner smooth muscle cells 25-kda actin-binding protein pdgf-bb represses skeletal muscle cells catecholamine-induced proliferation cortical actin polymerization wild-type mice increase glut4 translocation promoting actin dynamics influence cell growth full article pdf insulin-resistant cells actin-binding protein golden retriever model related subjects insulin receptor substrates increases myocardial damage pin lv privacy choices/manage cookies injured vascular tissue molecular medicine aims ya-juan yin pi3kgamma-akt-as160 attenuates glucose intolerance article zhao glut4 translocation protein-dye binding author information authors li-hua dong sm22α āˆ’/āˆ’ mice mouse carotid artery glucose utilization improves insulin resistance glucose uptake actin remodeling insulin signaling sm22alpha transcription occurs xiao-li xie article journal

Schema {šŸ—ŗļø}

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         headline:Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α
         description:The insulin-sensitive glucose transporter 4 (GLUT4) is a predominant facilitative glucose transporter in vascular smooth muscle cells (VSMCs) and is significantly upregulated in rabbit neointima. This study investigated the role of GLUT4 in VSMC proliferation, the cellular mechanism underlying PDGF-BB-stimulated GLUT4 translocation, and effects of SM22α, an actin-binding protein, on this process. Chronic treatment of VSMCs with PDGF-BB significantly elevated GLUT4 expression and glucose uptake. PDGF-BB-induced VSMC proliferation was dependent on GLUT4-mediated glucose uptake. Meanwhile, the response of GLUT4 to insulin decreased in PDGF-BB-stimulated VSMCs. PDGF-BB-induced GLUT4 translocation partially rescued glucose utilization in insulin-resistant cells. Immunofluorescence and western blot analysis revealed that PDGF-BB induced GLUT4 translocation in an actin dynamics-dependent manner. SM22α disruption facilitated GLUT4 translocation and glucose uptake by promoting actin dynamics and cortical actin polymerization. Similar results were observed in VSMCs of SM22α āˆ’/āˆ’ mice. The in vivo experiments showed that the glucose level in the neointima induced by ligation was significantly increased in SM22α āˆ’/āˆ’ mice, accompanied by increased neointimal thickness, compared with those in wild-type mice. These findings suggest that GLUT4-mediated glucose uptake is involved in VSMC proliferation, and provide a novel link between SM22α and glucose utilization in PDGF-BB-triggered proliferation. • GLUT4-mediated glucose uptake is required for the VSMC proliferation. • PDGF-BB-induced GLUT4 translocation partially rescues glucose uptake in insulin resistance. • SM22α disruption enhances PDGF-BB-induced GLUT4 translocation. • Glucose level in injured vascular tissue is positively correlated with neointimal hyperplasia.
         datePublished:2016-09-08T00:00:00Z
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            Glucose uptake
            Proliferation
            SM22α
            VSMCs
            Molecular Medicine
            Human Genetics
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      headline:Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α
      description:The insulin-sensitive glucose transporter 4 (GLUT4) is a predominant facilitative glucose transporter in vascular smooth muscle cells (VSMCs) and is significantly upregulated in rabbit neointima. This study investigated the role of GLUT4 in VSMC proliferation, the cellular mechanism underlying PDGF-BB-stimulated GLUT4 translocation, and effects of SM22α, an actin-binding protein, on this process. Chronic treatment of VSMCs with PDGF-BB significantly elevated GLUT4 expression and glucose uptake. PDGF-BB-induced VSMC proliferation was dependent on GLUT4-mediated glucose uptake. Meanwhile, the response of GLUT4 to insulin decreased in PDGF-BB-stimulated VSMCs. PDGF-BB-induced GLUT4 translocation partially rescued glucose utilization in insulin-resistant cells. Immunofluorescence and western blot analysis revealed that PDGF-BB induced GLUT4 translocation in an actin dynamics-dependent manner. SM22α disruption facilitated GLUT4 translocation and glucose uptake by promoting actin dynamics and cortical actin polymerization. Similar results were observed in VSMCs of SM22α āˆ’/āˆ’ mice. The in vivo experiments showed that the glucose level in the neointima induced by ligation was significantly increased in SM22α āˆ’/āˆ’ mice, accompanied by increased neointimal thickness, compared with those in wild-type mice. These findings suggest that GLUT4-mediated glucose uptake is involved in VSMC proliferation, and provide a novel link between SM22α and glucose utilization in PDGF-BB-triggered proliferation. • GLUT4-mediated glucose uptake is required for the VSMC proliferation. • PDGF-BB-induced GLUT4 translocation partially rescues glucose uptake in insulin resistance. • SM22α disruption enhances PDGF-BB-induced GLUT4 translocation. • Glucose level in injured vascular tissue is positively correlated with neointimal hyperplasia.
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      dateModified:2016-09-08T00:00:00Z
      pageStart:181
      pageEnd:192
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         GLUT4
         Glucose uptake
         Proliferation
         SM22α
         VSMCs
         Molecular Medicine
         Human Genetics
         Internal Medicine
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      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
      name:Key Laboratory of Medical Biotechnology of Hebei Province, Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, People’s Republic of China
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