Prostacyclin analogues inhibit fibroblast contraction of collagen gels through the cAMP-PKA pathway

نویسندگان

  • Koichiro Kamio
  • Xiangde Liu
  • Hisatoshi Sugiura
  • Shinsaku Togo
  • Tetsu Kobayashi
  • Shinsaku Kawasaki
  • Xing Q. Wang
  • Lijun Mao
  • Youngsoo Ahn
  • Cory Hogaboam
  • Myron L. Toews
  • Stephen I. Rennard
چکیده

Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, Nebraska Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan The Third Department of Internal Medicine, Mie University Graduate School of Medicine, Mie, Japan Department of Rheumatology, The Third Hospital of Peking University, Beijing, China Immunology Program, Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan Pharmacology, University of Nebraska Medical Center, Omaha, Nebraska

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

Prostacyclin analogs inhibit fibroblast contraction of collagen gels through the cAMP-PKA pathway.

Prostacyclin is an arachidonic acid metabolite that modulates vascular tone within the lung. The current study evaluated the hypothesis that prostacyclin can also modulate tissue remodeling by affecting fibroblast-mediated contraction of extracellular matrix. To accomplish this, fibroblasts were cultured in three-dimensional native type I collagen gels in the presence of prostacyclin analogs: c...

متن کامل

Prostaglandin E2 inhibits specific lung fibroblast functions via selective actions of PKA and Epac-1.

Via their capacities for proliferation and synthesis of matrix proteins such as collagen, fibroblasts are key effectors in the pathogenesis of fibrotic disorders such as idiopathic pulmonary fibrosis. Prostaglandin E(2) (PGE(2)) potently inhibits these functions in lung fibroblasts through receptor ligation and production of the second messenger cAMP, but the downstream pathways mediating such ...

متن کامل

Running title: PKA and Epac-1 in PGE2 inhibition of fibroblasts Prostaglandin E2 Inhibits Specific Lung Fibroblast Functions Via Selective Actions of PKA and Epac-1

Via their capacities for proliferation and synthesis of matrix proteins such as collagen, fibroblasts are key effectors in the pathogenesis of fibrotic disorders such as idiopathic pulmonary fibrosis. Prostaglandin E2 (PGE2) potently inhibits these functions in lung fibroblasts through receptor ligation and production of the second messenger cAMP, but the downstream pathways mediating such acti...

متن کامل

The PDE4 inhibitors roflumilast and rolipram augment PGE2 inhibition of TGF-β1 stimulated fibroblasts

Fibrotic diseases are characterized by the accumulation of extracellular matrix together with distortion and disruption of tissue architecture. Phosphodiesterase 4 (PDE4) inhibitors, by preventing the breakdown of cyclic AMP, can inhibit fibroblast functions and may be able to mitigate tissue remodeling. TGF-β1, a mediator of fibrosis, can potentially modulate cAMP by altering PGE2 metabolism. ...

متن کامل

PDE4 inhibitors roflumilast and rolipram augment PGE2 inhibition of TGF-{beta}1-stimulated fibroblasts.

Fibrotic diseases are characterized by the accumulation of extracellular matrix together with distortion and disruption of tissue architecture. Phosphodiesterase (PDE)4 inhibitors, by preventing the breakdown of cAMP, can inhibit fibroblast functions and may be able to mitigate tissue remodeling. Transforming growth factor (TGF)-beta1, a mediator of fibrosis, can potentially modulate cAMP by al...

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 2007