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Published on: June 21, 2013
Cardiac aquaporin expression in humans, rats, and mice
Tanya L Butler1, Carol G Au, Baoxue Yang
1Kids Heart Research, Children's Hospital at Westmead, Locked Bag 4001, Westmead, NSW 2145, Australia.
Insights
Aquaporin-1 (AQP-1) water channels play a role in heart water permeability, but their expression is not altered by osmotic or ischemic stress in myocardial edema. This research investigates aquaporins in cardiac function.
Area of Science:
- Cardiovascular Biology
- Molecular Physiology
- Water Transport Mechanisms
Background:
- Myocardial edema, linked to cardiac dysfunction, is a critical factor in ischemia-reperfusion injury and cardiopulmonary bypass outcomes.
- Aquaporins (AQPs) are integral membrane proteins facilitating water transport, and their role in cardiac edema requires investigation.
Purpose of the Study:
- To assess the expression of aquaporin water channels in the myocardium of humans, rats, and mice.
- To determine the functional significance of myocardial AQP expression on water permeability.
- To investigate AQP-1 and AQP-4 regulation under osmotic and ischemic stress.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) for transcript analysis.
- Western blot analysis for protein expression confirmation.
- Measurement of water permeability in plasma membrane vesicles from AQP knockout mice.
- Isolated rat heart perfusion model to assess stress responses.
Main Results:
- Multiple AQP transcripts (e.g., AQP-1, -4, -7, -11) were detected in the hearts of humans, rats, and mice.
- AQP-1 protein was confirmed in all species; AQP-4 protein was detected only in mice.
- Knockout of AQP-1, but not AQP-4 or AQP-8, significantly reduced myocardial water permeability.
- Neither osmotic nor ischemic stress altered AQP-1 or AQP-4 expression in isolated rat hearts.
Conclusions:
- Aquaporin-1 (AQP-1) likely plays a functional role in myocardial water transport.
- Early responses to osmotic and ischemic stress in the heart do not appear to involve transcriptional or posttranslational regulation of AQP-1.
- Further research is needed to fully elucidate the role of AQPs in cardiac edema and dysfunction.
Abstract:
Water accumulation in the heart is important in ischemia-reperfusion injury and operations performed by 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 AQP-1, -4, -6, -7, -8, and -11 transcripts in the mouse heart. AQP-1, -6, -7, and -11 mRNAs were found in the rat heart as well as low levels of AQP-4 and -9. Human hearts contained AQP-1, -3, -4, -5, -7, -9, -10, and -11 mRNAs. AQP-1 protein expression was confirmed by Western blot analysis in all three species. AQP-4 protein was detected in the mouse heart but not in the 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 wild-type versus various AQP knockout mice. Water permeability was reduced by AQP-1 knockout but not by AQP-4 or AQP-8 knockout. With the use of a model of isolated rat heart perfusion, it was found that osmotic and ischemic stresses are not associated with changes in AQP-1 or AQP-4 expression. These studies support a possible functional role of AQP-1 in myocardium but indicate that early adaptations to osmotic and ischemic stress do not involve transcriptional or posttranslational AQP-1 regulation.

