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1 Kids Heart Research, The Children's Hospital at Westmead, Sydney, New South Wales, Australia; Neurogenetics Research Unit and Institute for Neuromuscular Research, The Children's Hospital at Westmead, Sydney, New South Wales, Australia; Discipline of Pediatrics and Child Health, Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia
2 Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, United States
3 Kids Heart Research, The Children's Hospital at Westmead, Sydney, New South Wales, Australia; Neurogenetics Research Unit and Institute for Neuromuscular Research, The Children's Hospital at Westmead, Sydney, New South Wales, Australia
4 Muscle Development Unit, Children's Medical Research Institute, Sydney, New South Wales, Australia
5 Neurogenetics Research Unit and Institute for Neuromuscular Research, The Children's Hospital at Westmead, Sydney, New South Wales, Australia; Discipline of Pediatrics and Child Health, Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia
* To whom correspondence should be addressed. E-mail: davidw{at}chw.edu.au.
Water accumulation in the heart is important in ischemia/reperfusion injury and operations performed using cardiopulmonary bypass, with cardiac dysfunction associated with myocardial edema being the principal determinant of clinical outcome. As an initial step in determining the role of aquaporin (AQP) water channels in myocardial edema, we have assessed the myocardial expression of AQPs in humans, rats and mice. RT-PCR revealed expression of AQP1, 4, 6, 7, 8 and 11 transcripts in mouse heart. AQP1, 6, 7 and 11 mRNAs were found in rat heart, as well as low levels of AQP4 and 9. Human heart contained AQP1, 3, 4, 5, 7, 9, 10 and 11 mRNAs. AQP1 protein expression was confirmed by Western blot analysis in all three species. AQP4 protein was detected in mouse, but not rat or human heart. To determine the potential functional consequences of myocardial AQP expression, water permeability was measured in plasma membrane vesicles from myocardial cells of wildtype vs. various AQP knockout mice. Water permeability was reduced by AQP1 knockout, but not by AQP4 or AQP8 knockout. Using a model of isolated rat heart perfusion, it was found that osmotic and ischemic stresses are not associated with changes in AQP1 or AQP4 expression. These studies support a possible functional role of AQP1 in myocardium, but indicate that early adaptations to osmotic and ischemic stress do not involve transcriptional or post-translational AQP1 regulation.
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