Qinghua Pu

Summary

Affiliation: University of Tennessee
Country: USA

Publications

  1. pmc Chronic insulin treatment suppresses PTP1B function, induces increased PDGF signaling, and amplifies neointima formation in the balloon-injured rat artery
    Qinghua Pu
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA
    Am J Physiol Heart Circ Physiol 296:H132-9. 2009
  2. pmc Chronic insulin treatment amplifies PDGF-induced motility in differentiated aortic smooth muscle cells by suppressing the expression and function of PTP1B
    Daming Zhuang
    Dept of Physiology, Univ of Tennessee, Memphis, TN 38163, USA
    Am J Physiol Heart Circ Physiol 295:H163-73. 2008
  3. pmc Suppression of PKG by PDGF or nitric oxide in differentiated aortic smooth muscle cells: obligatory role of protein tyrosine phosphatase 1B
    Daming Zhuang
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA
    Am J Physiol Heart Circ Physiol 300:H57-63. 2011
  4. ncbi request reprint Counter-regulatory function of protein tyrosine phosphatase 1B in platelet-derived growth factor- or fibroblast growth factor-induced motility and proliferation of cultured smooth muscle cells and in neointima formation
    Yingzi Chang
    Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
    Arterioscler Thromb Vasc Biol 26:501-7. 2006
  5. pmc Mechanisms related to NO-induced motility in differentiated rat aortic smooth muscle cells
    Qinghua Pu
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA
    Am J Physiol Heart Circ Physiol 300:H101-8. 2011

Collaborators

Detail Information

Publications5

  1. pmc Chronic insulin treatment suppresses PTP1B function, induces increased PDGF signaling, and amplifies neointima formation in the balloon-injured rat artery
    Qinghua Pu
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA
    Am J Physiol Heart Circ Physiol 296:H132-9. 2009
    ..These observations support the hypothesis that hyperinsulinemia induces the suppression of PTP1B function, leading to enhanced PDGFR signaling and neointimal hyperplasia...
  2. pmc Chronic insulin treatment amplifies PDGF-induced motility in differentiated aortic smooth muscle cells by suppressing the expression and function of PTP1B
    Daming Zhuang
    Dept of Physiology, Univ of Tennessee, Memphis, TN 38163, USA
    Am J Physiol Heart Circ Physiol 295:H163-73. 2008
    ..These observations uncover novel mechanisms that explain how insulin amplifies the motogenic capacity of the pivotal growth factor PDGF...
  3. pmc Suppression of PKG by PDGF or nitric oxide in differentiated aortic smooth muscle cells: obligatory role of protein tyrosine phosphatase 1B
    Daming Zhuang
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA
    Am J Physiol Heart Circ Physiol 300:H57-63. 2011
    ..We conclude that the upregulation of PTP1B by PDGF or NO is both necessary and sufficient to induce the downregulation of PKG via an effect on PKG mRNA levels...
  4. ncbi request reprint Counter-regulatory function of protein tyrosine phosphatase 1B in platelet-derived growth factor- or fibroblast growth factor-induced motility and proliferation of cultured smooth muscle cells and in neointima formation
    Yingzi Chang
    Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
    Arterioscler Thromb Vasc Biol 26:501-7. 2006
    ..The current study was designed to test the hypothesis that PTP1B attenuates PDGF- or FGF-induced motility and proliferation of cultured cells, as well as neointima formation in injured rat carotid arteries...
  5. pmc Mechanisms related to NO-induced motility in differentiated rat aortic smooth muscle cells
    Qinghua Pu
    Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA
    Am J Physiol Heart Circ Physiol 300:H101-8. 2011
    ..These results support the hypothesis that the comotogenic effect of insulin and NO occurs via an ANG II-mediated effect involving the suppression of PTP1B and upregulation of PI3K-δ and SHP2...