Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathways

  • 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

Research output: Contribution to journalArticlepeer-review

545 Scopus citations

Abstract

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. PI3Kα mediates the alteration in cell size while PI3Kγ acts as a negative regulator of cardiac contractility. Mechanistically, PI3Kγ 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-PI3Kγ pathway in the modulation of heart muscle contractility.

Original languageEnglish
Pages (from-to)737-749
Number of pages13
JournalCell
Volume110
Issue number6
DOIs
StatePublished - Sep 20 2002

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