Regulation of Myocardial Contractility and Cell Size by Distinct PI3K-PTEN Signaling Pathways

نویسندگان

  • Michael A. Crackower
  • Gavin Y. Oudit
  • Ivona Kozieradzki
  • Renu Sarao
  • Hui Sun
  • Takehiko Sasaki
  • Emilio Hirsch
  • Akira Suzuki
  • Tetsuo Shioi
  • Junko Irie-Sasaki
  • Rajan Sah
  • Hai-Ying M. Cheng
  • Vitalyi O. Rybin
  • Giuseppe Lembo
  • Luigi Fratta
  • Antonio J. Oliveira-dos-Santos
  • Jeffery L. Benovic
  • C.Ronald Kahn
  • Seigo Izumo
  • Susan F. Steinberg
  • Matthias P. Wymann
  • Peter H. Backx
  • Josef M. Penninger
چکیده

The PTEN/PI3K signaling pathway regulates a vast array of fundamental cellular responses. We show that cardiomyocyte-specific inactivation of tumor suppressor PTEN results in hypertrophy, and unexpectedly, a dramatic decrease in cardiac contractility. Analysis of double-mutant mice revealed that the cardiac hypertrophy and the contractility defects could be genetically uncoupled. PI3Kalpha mediates the alteration in cell size while PI3Kgamma acts as a negative regulator of cardiac contractility. Mechanistically, PI3Kgamma inhibits cAMP production and hypercontractility can be reverted by blocking cAMP function. These data show that PTEN has an important in vivo role in cardiomyocyte hypertrophy and GPCR signaling and identify a function for the PTEN-PI3Kgamma pathway in the modulation of heart muscle contractility.

برای دانلود رایگان 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

Mission Impossible: IGF-1 and PTEN Specifically “Akt”ing on Cardiac L-Type Ca Channels

The complex functional properties of cardiomyocytes are precisely regulated, oftentimes with millisecond precision. There are a multitude of signaling cascades and associated molecules that participate in this regulation. Insulin-like growth factor-1 (IGF-1), IGF receptors, phosphoinositides, phosphatidylinositol 3-kinase (PI3K), Akt or phosphokinase B (PKB), L-type Ca channels (LTCC), and intr...

متن کامل

Anti-cancer properties of Escherichia coli Nissle 1917 against HT-29 colon cancer cells through regulation of Bax/Bcl-xL and AKT/PTEN signaling pathways

Objective(s): Chemotherapies used to treat colon cancer might often fail due to the emergence of chemoresistance and side effects. Escherichia coli Nissle 1917 (EcN) is a beneficial probiotic, whose molecular mechanisms in the prevention of colon cancer are yet to be fully understood. The present study assessed the anti-cancer effects of EcN treatments in human colorec...

متن کامل

Mission impossible: IGF-1 and PTEN specifically "Akt"ing on cardiac L-type Ca2+ channels.

The complex functional properties of cardiomyocytes are precisely regulated, oftentimes with millisecond precision. There are a multitude of signaling cascades and associated molecules that participate in this regulation. Insulin-like growth factor-1 (IGF-1), IGF receptors, phosphoinositides, phosphatidylinositol 3-kinase (PI3K), Akt or phosphokinase B (PKB), L-type Ca channels (LTCC), and intr...

متن کامل

Cardiac regulation by phosphoinositide 3-kinases and PTEN.

The diverse effects mediated by PI3K/PTEN (phosphoinositide 3-kinase/phosphatase and tensin homologue deleted on chromosome 10) signalling in the heart clearly support an important biological and pathophysiological role for this signalling cascade. PI3Ks are a family of evolutionarily conserved lipid kinases that mediate many cellular responses to physiological and pathophysiological stimuli. C...

متن کامل

AKT family and miRNAs expression in IL-2-induced CD4+T cells

Objective(s): Study of non-coding RNAs is considerable to elucidate principal biological questions or design new therapeutic strategies. miRNAs are a group of non-coding RNAs that their functions in PI3K/AKT signaling and apoptosis pathways after T cell activation is not entirely clear. Herein, miRNAs expression and their putative targets in the mentioned pathways were studied in the activated ...

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

عنوان ژورنال:
  • Cell

دوره 110  شماره 

صفحات  -

تاریخ انتشار 2002