Cardiac aquaporin expression in humans, rats, and mice

Butler, Tanya L.; Au, Carol G.; Yang, Baoxue; Egan, Jonathan R.; Tan, Yee Mun; Hardeman, Edna C.; North, Klaus; Winlaw, David S.

doi:10.1152/ajpheart.00090.2006

Cited by 89 publications

(113 citation statements)

References 56 publications

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“…Furthermore, there is species-specific distribution of AQP1 in myocardium. Rats express AQP1 in the cardiomyocytes, humans and mice in the endothelium (9). In consistence with these studies, our results from real-time PCR, western-blot, and immunohistochemical staining revealed the expression of AQP1 in the rat myocardium.…”

Section: Discussionsupporting

confidence: 82%

“…In consistence with these studies, our results from real-time PCR, western-blot, and immunohistochemical staining revealed the expression of AQP1 in the rat myocardium. Myocardial expression of AQP1 might be associated with water permeability since knockout of AQP1 reduced the water permeability in plasma membrane vesicles from myocardial cells (9). Anatomical and physiological factors can prevent the accumulation of excess interstitial fluid in normal hearts.…”

Section: Discussionmentioning

confidence: 99%

“…AQP2 was found to be absent in rat myocardium using both RNAse protein assay and RT-PCR (9,31). Analyses of rat heart samples using RT-PCR, northern, western, and RNAse protection assays all revealed that AQP3 is absent (9,31,32). Low levels of AQP4 were detected in rat myocardium by RT-PCR, while results from RNAse protection assay and western blot revealed that it is absent (9,31).…”

Section: Discussionmentioning

confidence: 99%

“…AQPs are a family of small hydrophobic integral membrane proteins and are constitutively expressed in the cell membranes in plants, animals, and humans (9). Since the discovery of the first AQP (AQP1, initially called CHIP 28) in 1993 (10), 13 AQPs have been found in mammals (AQP 0-12) (11).…”

Section: Introductionmentioning

confidence: 99%

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The expression profile of aquaporin 1 in rat myocardium after severe burns

Li¹,

Zha²,

Li³

et al. 2015

Turk J Med Sci

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Background/aim: To investigate the myocardial expression profile of aquaporin 1 (AQP1) in rats after severe burns.Materials and methods: Ninety healthy male adult Wistar rats were randomly assigned to the following treatments: sham operation (control group, n = 6), immediate fluid resuscitation treatment post scalding (IF group, n = 42), and delayed fluid resuscitation treatment after scalding (DF group, n = 42). At 3, 6, 12, 24, 48, 72, and 120 h after scalding, myocardial water contents were assayed and AQP1 expressions were detected by real-time polymerase chain reaction and western blot. The AQP levels in the myocardium at 12 h after scalding were assayed by gene microarrays.Results: Scald injuries resulted in significantly synchronized increases in the myocardial water contents and the myocardial mRNA and protein expression of AQP1, with a peak at 12 h after scalding. Rats receiving delayed fluid resuscitation treatment had more severe myocardial edema and significantly higher myocardial AQP1 expressions than the rats receiving immediate fluid resuscitation treatment. The mRNAs of 6 other AQPs (AQP2, 3, 4, 6, 7, and 12b) were found to be changed in the myocardium among rats with different treatments. Conclusion:AQP1 may play a functional role in the development of myocardial edema after scalding. Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The expression profile of aquaporin 1 in rat myocardium after severe burns

Li¹,

Zha²,

Li³

et al. 2015

Turk J Med Sci

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“…The mRNA expression of AQP -1, -3, -5, -7, -9, -10, and -11 was detected in human hearts, while AQP -1, -4, -6, -7, -8, and -11 were detected in hearts from mice and rats [3]. The protein expression of AQP6 was detected inside the myocytes in mice, while AQP4 was exclusively observed on the intercalated discs between cardiac myocytes [4].…”

Section: Editorial Textmentioning

confidence: 94%

On the Role of Aquaporins in Myocardial Injury

Ozu¹

2014

Biochem & Pharmacol

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The presence of aquaporins in the cardiovascular system has been well documented, however our knowledge about their role in myocardial pathophysiology is now being elucidated. A brief overview of the presence, function and regulation of aquaporins in myocardial injury is here presented. On the Role of Aquaporins in Myocardial InjuryMarcelo Ozu* Editorial TextCardiopulmonary bypass (CPB) renders the myocardium susceptible to water imbalance and subsequent Myocardial edema (ME) as a consequence of decreased cardiac energy supply [1]. Factors leading to ME include hemodilution, ischemia and reperfusion, as well as osmotic gradients arising from pathological changes of the physiological state.Several members of the aquaporin (AQP) family have been described in the myocardium [2]. The mRNA expression of AQP -1, -3, -5, -7, -9, -10, and -11 was detected in human hearts, while AQP -1, -4, -6, -7, -8, and -11 were detected in hearts from mice and rats [3]. The protein expression of AQP6 was detected inside the myocytes in mice, while AQP4 was exclusively observed on the intercalated discs between cardiac myocytes [4].Experiments with AQP1 knock-out mice showed microcardia, decreased myocyte dimensions and low blood pressure [5]. On the other hand, knock-out mice for AQP7 showed a conserved cardiac morphology, although low content of glycerol and ATP was observed [6].Nowadays, research is focused on the role that aquaporins play in myocardial injury. AQP -1, -4, and -6 seems to play different roles in myocardial infarction (MI) in mouse hearts. While the time dependent pattern of the observed up-regulated expression of AQP4 in MI coincides with that of ME and cardiac dysfunction, the expression of AQP1 and AQP6 persistently increase [4].One of the first reports of aquaporins in heart revealed that AQP1 colocalizes with Caveolin-3 at 20°C and 37°C in rats [7]. Interestingly, when rat cardiac myocytes were exposed to hypertonic media AQP1 was reversibly internalized [7]. In addition, a more recent report showed that AQP1 cosegragates with Caveolin-1 in mice [5]. Recent works demonstrated that the levels of AQP1 mRNA and protein increase 12 hours after global myocardial ischemia in goats following CPB [8]. Moreover, the treatment with HgCl2 reduced ME, indicating that AQP1 is involved in the development of edema [8]. Other works showed that AQP1 expression is inversely correlated with the protein expression of Connexin 43 in goats following CPB [9]. Altogether, these evidences suggest an important role of AQP1 in the regulation of Connexin 43 in the progression of ME, and a related localization of AQP1 and Caveolin-1.In mouse hearts AQP1 was shown to be localized at caveolae but also in endothelial cell membranes. Cardioplegia, ischemia and hypoxia decrease AQP1 mRNA as well as total protein expression and glycosylation [10]. In endothelium, AQP1 does not regulate the endothelium-derived hyperpolarizing factor (EDH (F)) or NOdependent relaxation, but its deletion increases prostanoids-dependent relaxation in resist...

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The involvement of AQP1 in heart oedema induced by global myocardial ischemia

Ding

Yan

Huang

et al. 2012

Cell Biochemistry & Function

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Aquaporin-1 (AQP1) is a member of aquaporin family that was previously proven to be involved in myocardial dysfunction; however, the role of AQP1 in myocardial stunning is less clear. To determine the change of AQP1 expression level in the heart and its effect on oedema after global myocardial ischemia, 40 adult goats underwent cardiopulmonary bypass (CPB) with an aortic cross-clamp time of 2 h and total bypass time of 6, 12, 24, 48 and 72 h followed by subsequent reperfusion. AQP1 function of eight goats was inhibited by HgCl(2) during the 24 h on CPB. All groups were compared with eight sham bypass control goats. Myocardial water content was measured, and the APQ1 mRNA and protein levels were detected by RT-PCR and immunoblotting, respectively. The results showed that the degree of myocardial oedema increased significantly at 6, 12, 24 and 48 h of reperfusion after CPB as compared with the control and recovered at 72 h of subsequent reperfusion. Expression levels of AQP1 mRNA and protein began to increase at 12 h and peaked at 24 h of CPB following reperfusion. Furthermore, myocardial oedema was reduced in the HgCl(2) group compared with the time-matched CPB and control groups. These data suggested that AQP1 expression increases in CPB and AQP1 plays an important role in myocardial oedema during CPB.

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Cardiac aquaporin expression in humans, rats, and mice

Cited by 89 publications

References 56 publications

The expression profile of aquaporin 1 in rat myocardium after severe burns

The expression profile of aquaporin 1 in rat myocardium after severe burns

On the Role of Aquaporins in Myocardial Injury

The involvement of AQP1 in heart oedema induced by global myocardial ischemia

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