Literature DB >> 1328657

Molecular regulation of cardiac myocyte adaptations to chronic hypoxia.

K A Webster1, N H Bishopric.   

Abstract

The effects of chronic hypoxia on isolated neonatal rat cardiac myocytes were investigated in a model system of myocardial hypoxia. Spontaneously beating myocardiocytes were cultured for up to one week inside an environmental chamber at an oxygen tension of between 4 and 8 mmHg. In order to stimulate a chronic reduced flow condition fresh hypoxic culture medium was replenished frequently to eliminate or minimize contributions of extracellular metabolite build-up, pH changes, or energy depletion. Under these conditions contractions became progressively impaired and irregular compared with aerobic cultures and beating frequency decreased to about 50% of control over 3 days. Reduced contractility was paralleled by a progressive decrease in the basal intracellular level of cAMP. Both of these effects could be reversed by introducing isoproterenol. Visualization of calcium fluxes using the fluorescent calcium chelator Indo-1 demonstrated that the slower contractions were associated with a pronounced decrease in the rate of calcium efflux during muscle relaxation. Changes in the expression of cAMP dependent genes was apparent in the hypoxic cells and the chronic administration of cAMP elevating drugs was toxic specifically to cells under hypoxia. We propose that cAMP may regulate some short and long-term adaptations of cardiac myocytes to chronic hypoxia.

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Year:  1992        PMID: 1328657     DOI: 10.1016/0022-2828(92)93388-z

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  7 in total

Review 1.  The role of Bcl-2 family member BNIP3 in cell death and disease: NIPping at the heels of cell death.

Authors:  T R Burton; S B Gibson
Journal:  Cell Death Differ       Date:  2009-01-09       Impact factor: 15.828

2.  Hypoxia-activated apoptosis of cardiac myocytes requires reoxygenation or a pH shift and is independent of p53.

Authors:  K A Webster; D J Discher; S Kaiser; O Hernandez; B Sato; N H Bishopric
Journal:  J Clin Invest       Date:  1999-08       Impact factor: 14.808

3.  Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress.

Authors:  Christopher J Dougherty; Lori A Kubasiak; Howard Prentice; Peter Andreka; Nanette H Bishopric; Keith A Webster
Journal:  Biochem J       Date:  2002-03-15       Impact factor: 3.857

4.  Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3.

Authors:  Lori A Kubasiak; Olga M Hernandez; Nanette H Bishopric; Keith A Webster
Journal:  Proc Natl Acad Sci U S A       Date:  2002-09-11       Impact factor: 11.205

5.  Early fetal hypoxia leads to growth restriction and myocardial thinning.

Authors:  Margie Ream; Alisa M Ray; Rashmi Chandra; Dona M Chikaraishi
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2008-05-28       Impact factor: 3.619

Review 6.  Rethinking Heart Failure.

Authors:  Hauke Fürstenwerth
Journal:  Cardiol Res       Date:  2012-11-20

7.  Cardiac adaptation to high altitude in the plateau pika (Ochotona curzoniae).

Authors:  Aurélien Pichon; Bai Zhenzhong; Dominique Marchant; Guoen Jin; Nicolas Voituron; Yun Haixia; Fabrice Favret; Jean-Paul Richalet; Ri-Li Ge
Journal:  Physiol Rep       Date:  2013-07-18
  7 in total

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