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

Ding, Fang; Yan, Yingjie; Huang, Jianbin; Mei, Ju; Zhu, Jiaquan; Líu, Hao

doi:10.1002/cbf.2860

Cited by 14 publications

(15 citation statements)

References 14 publications

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“…Elevated AQP1 expression in choroid plexus epithelium after 24 h of systemic hyponatremia is thought to be partially responsible for brain edema and neuronal degeneration [21]. The increased expression of AQP1 plays an important role in myocardial edema during cardiopulmonary bypass [22]. On the other hand, inhibition of AQP1 level in human pulmonary microvascular endothelial cells with siRNA induced high permeability by decreasing the levels of VE-cadherin, epithelial Na + channel, and Na-K ATPase [23].…”

Section: Introductionmentioning

confidence: 97%

Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Jiang

Wang

Zheng

et al. 2015

Cardiovascular Pathology

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Section: Introductionmentioning

confidence: 97%

Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Jiang

Wang

Zheng

et al. 2015

Cardiovascular Pathology

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“…For example, AQP‐4 is involved in cerebral edema, and its deletion in mice reduces brain edema after acute water intoxication and ischemic stroke 35 . Myocardial edema was alleviated by inhibiting the function of AQP‐1 36 . HgCl 2 was known to inhibit AQP‐1 activity reversibly by covalent modification of cysteine 187 located outside the plasma membrane 24 .…”

Section: Discussionmentioning

confidence: 99%

Effects of Low‐Intensity Ultrasound on Gramicidin D‐Induced Erythrocyte Edema

Lim

Seo

Kim

et al. 2014

J of Ultrasound Medicine

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Objectives To determine whether low‐intensity ultrasound (US) can reduce red blood cell (RBC) edema and, if so, whether the US activity is associated with aquaporin 1 (AQP‐1), a water channel in the cell membrane. Methods Red blood cell edema was induced by gramicidin D treatment at 40 ng/mL for 20 minutes and evaluated by a hematocrit assay. Low‐intensity continuous wave US at 1 MHz was applied to RBCs for the last 10 minutes of gramicidin D treatment. To determine whether US activity was associated with AQP‐1, RBCs were treated with 40 μM mercuric chloride (HgCl2), an AQP‐1 inhibitor, for 20 minutes at the time of gramicidin D treatment. Posttreatment morphologic changes in RBCs were observed by actin staining with phalloidin. Results Red blood cell edema increased significantly with gramicidin D at 20 (1.8%), 40 (6.7%), 60 (16.7%), and 80 (11.3%) ng/mL, reaching a peak at 60 ng/mL, compared to the control group (20 ng/mL, P = .019; 40, 60, and 80 ng/mL, P < .001). No significant RBC hemolysis was observed in any group. Edema induced by gramicidin D at 40 ng/mL was significantly reduced by US at 30 (3.4%; P = .003), 70 (4.4%; P = .001), and 100 (2.9%; P = .001) mW/cm2. Subsequent experiments showed that edema reduction by US ranged from 7% to 10%. Cotreatment with HgCl2 partially reversed the US effect and showed a significantly different level of edema compared to gramicidin D‐alone and US‐cotreated groups (P = .001). These results were confirmed by microscopic observation of RBC morphologic changes. Conclusions Low‐intensity US could reduce gramicidin D–induced RBC edema, and its effect appeared to at least partly involve regulation of AQP‐1 activity. These results suggest that low‐intensity US can be used as an alternative treatment to control edema and related disorders.

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“…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].…”

Section: Editorial Textmentioning

confidence: 99%

“…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].…”

Section: Editorial Textmentioning

confidence: 99%

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

Cited by 14 publications

References 14 publications

Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Cardioprotective effect of valsartan in mice with short-term high-salt diet by regulating cardiac aquaporin 1 and angiogenic factor expression

Effects of Low‐Intensity Ultrasound on Gramicidin D‐Induced Erythrocyte Edema

On the Role of Aquaporins in Myocardial Injury

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