Synergistic Role of Protein Phosphatase Inhibitor 1 and SERCA2a in the Acquisition of the Contractile Phenotype of Arterial Smooth Muscle Cells

نویسندگان

  • Larissa Lipskaia
  • Regis Bobe
  • Jiqiu Chen
  • Irene C Turnbull
  • Jose J. Lopez
  • Elise Merlet
  • Dongtaq Jeong
  • Ioannis Karakikes
  • Alexandra S. Ross
  • Lifan Liang
  • Nathalie Mougenot
  • Fabrice Atassi
  • Anne-Marie Lompré
  • Sima T. Tarzami
  • Jason C. Kovacic
  • Evangelia Kranias
  • Roger J. Hajjar
  • Lahouaria Hadri
چکیده

Cardiovascular Research Center. Mount Sinai School of Medicine, New York, NY; Inserm UMRS 956, Université Pierre et Marie Curie-Paris 6, Paris, France; LIA/Transatlantic Cardiovascular Research Center Université Pierre et Marie Curie/Mount Sinai School of Medicine, New York, NY; INSERM U770, University Paris Sud, Le Kremlin-Bicêtre, France; PECMV-Université Pierre et Marie Curie-Paris, Paris, France; University of Cincinnati, Cincinnati, OH

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Synergistic role of protein phosphatase inhibitor 1 and sarco/endoplasmic reticulum Ca2+ -ATPase in the acquisition of the contractile phenotype of arterial smooth muscle cells.

BACKGROUND Phenotypic modulation or switching of vascular smooth muscle cells from a contractile/quiescent to a proliferative/synthetic phenotype plays a key role in vascular proliferative disorders such as atherosclerosis and restenosis. Although several calcium handling proteins that control differentiation of smooth muscle cells have been identified, the role of protein phosphatase inhibitor...

متن کامل

The role of autophagy in advanced glycation end product-induced proliferation and migration in rat vascular smooth muscle cells

Objective(s): To investigate the role of autophagy in advanced glycation end products (AGEs)-induced proliferation and migration in rat vascular smooth muscle cells (VSMCs).Materials and Methods: After culture, VSMCs were treated with 0, 1, 10, and 100 μg/ml concentrations of AGEs. Autophagy specific protein light chain 3 (LC3)-I/II was determined by western blotting, autophagosomes were observ...

متن کامل

A Decoy Peptide Targeted to Protein Phosphatase 1 Attenuates Degradation of SERCA2a in Vascular Smooth Muscle Cells

Neointimal growth in the injured vasculature is largely facilitated by the proliferation of vascular smooth muscle cells (VSMC), which associates with reduced sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2a) activity. The gene transfer-mediated restoration of the SERCA2a level thus attenuates neointimal growth and VSMC proliferation. We previously reported that a peptide targeted to protein ph...

متن کامل

Effect of Oxidized Low Density Lipoprotein on the Expression of Runx2 and SPARC Genes in Vascular Smooth Muscle Cells

Background: Vascular calcification is an important stage in atherosclerosis. During this stage, vascular smooth muscle cells (VSMC) synthesize many osteogenic factors such as osteonectin (encoded by SPARC). Oxidative stress plays a critical role in atherosclerosis progression, and its accumulation in the vascular wall stimulates the development of atherosclerosis and vascular calcification. The...

متن کامل

Inactivation of serum response factor contributes to decrease vascular muscular tone and arterial stiffness in mice.

RATIONALE Vascular smooth muscle (SM) cell phenotypic modulation plays an important role in arterial stiffening associated with aging. Serum response factor (SRF) is a major transcription factor regulating SM genes involved in maintenance of the contractile state of vascular SM cells. OBJECTIVE We investigated whether SRF and its target genes regulate intrinsic SM tone and thereby arterial st...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2013