Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse

Monica M. Montano, Candida L. Desjardins, Yong Qui Doughman, Yee Hsee Hsieh, Yanduan Hu, Heather M. Bensinger, Connie Chaudhary, Julian E. Stelzer, Thomas E. Dick, Brian D. Hoit, Margaret P. Chandler, Xin Yu, Michiko Watanabe

Research output: Contribution to journalArticle

Abstract

AimsThe transcription factor hexamethylene-bis-acetamide-inducible protein 1 (HEXIM1) regulates myocardial vascularization and growth during cardiogenesis. Our aim was to determine whether HEXIM1 also has a beneficial role in modulating vascularization, myocardial growth, and function within the adult heart.Methods and resultsTo achieve our objective, we created and investigated a mouse line wherein HEXIM1 was re-expressed in adult cardiomyocytes to levels found in the foetal heart. Our findings support a beneficial role for HEXIM1 through increased vascularization, myocardial growth, and increased ejection fraction within the adult heart. HEXIM1 re-expression induces angiogenesis, that is, essential for physiological hypertrophy and maintenance of cardiac function. The ability of HEXIM1 to co-ordinate processes associated with physiological hypertrophy may be attributed to HEXIM1 regulation of other transcription factors (HIF-1-, c-Myc, GATA4, and PPAR-) that, in turn, control many genes involved in myocardial vascularization, growth, and metabolism. Moreover, the mechanism for HEXIM1-induced physiological hypertrophy appears to be distinct from that involving the PI3K/AKT pathway.ConclusionHEXIM1 re-expression results in the induction of angiogenesis that allows for the co-ordination of tissue growth and angiogenesis during physiological hypertrophy.

Original languageEnglish (US)
Pages (from-to)74-82
Number of pages9
JournalCardiovascular Research
Volume99
Issue number1
DOIs
StatePublished - Jul 1 2013
Externally publishedYes

Fingerprint

Cardiomegaly
Hypertrophy
Growth
Transcription Factors
Physiologic Neovascularization
Fetal Heart
Peroxisome Proliferator-Activated Receptors
Phosphatidylinositol 3-Kinases
Cardiac Myocytes
Maintenance
Genes
Proteins

Keywords

  • Angiogenesis
  • HEXIM1
  • Hypertrophy

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Montano, M. M., Desjardins, C. L., Doughman, Y. Q., Hsieh, Y. H., Hu, Y., Bensinger, H. M., ... Watanabe, M. (2013). Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse. Cardiovascular Research, 99(1), 74-82. https://doi.org/10.1093/cvr/cvt086

Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse. / Montano, Monica M.; Desjardins, Candida L.; Doughman, Yong Qui; Hsieh, Yee Hsee; Hu, Yanduan; Bensinger, Heather M.; Chaudhary, Connie; Stelzer, Julian E.; Dick, Thomas E.; Hoit, Brian D.; Chandler, Margaret P.; Yu, Xin; Watanabe, Michiko.

In: Cardiovascular Research, Vol. 99, No. 1, 01.07.2013, p. 74-82.

Research output: Contribution to journalArticle

Montano, MM, Desjardins, CL, Doughman, YQ, Hsieh, YH, Hu, Y, Bensinger, HM, Chaudhary, C, Stelzer, JE, Dick, TE, Hoit, BD, Chandler, MP, Yu, X & Watanabe, M 2013, 'Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse', Cardiovascular Research, vol. 99, no. 1, pp. 74-82. https://doi.org/10.1093/cvr/cvt086
Montano MM, Desjardins CL, Doughman YQ, Hsieh YH, Hu Y, Bensinger HM et al. Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse. Cardiovascular Research. 2013 Jul 1;99(1):74-82. https://doi.org/10.1093/cvr/cvt086
Montano, Monica M. ; Desjardins, Candida L. ; Doughman, Yong Qui ; Hsieh, Yee Hsee ; Hu, Yanduan ; Bensinger, Heather M. ; Chaudhary, Connie ; Stelzer, Julian E. ; Dick, Thomas E. ; Hoit, Brian D. ; Chandler, Margaret P. ; Yu, Xin ; Watanabe, Michiko. / Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse. In: Cardiovascular Research. 2013 ; Vol. 99, No. 1. pp. 74-82.
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