Anaemia Stimulates Aquaporin 1 Expression in the Fetal Sheep Heart

Jonker, Sonnet S.; Davis, Lowell E.; Bilt, Jarmila D. W. van der; Hadder, Bryanna; Hohimer, A. Roger; Giraud, G; Thornburg, Kent L.

doi:10.1113/eph8802626

Cited by 23 publications

(12 citation statements)

References 36 publications

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“…It has been hypothesized that the transmembrane ion current of myocardial cells, mediated by AQP1, requires rapid equilibrium of internal and external osmotic pressure (21,22). In a previous report, it was demonstrated that AQP1 expression was increased in anemic fetuses compared to agematched controls, suggesting that AQP1 plays an important role in physiological accommodation to fetal anemia (23). In this study, left ventricular mRNA and protein expression levels of AQP1 were measured following CPB surgery and the water content of myocardial muscle was determined.…”

Section: Discussionmentioning

confidence: 99%

Aquaporin 1 plays an important role in myocardial edema caused by cardiopulmonary bypass surgery in goat

Yan

Huang

Ding

et al. 2013

International Journal of Molecular Medicine

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Myocardial stunning, which is closely related to myocardial edema, is a severe complication that may occur following cardiac surgery. In this study, we examined the expression of aquaporin 1 (AQP1) and Connexin 43 (Cx43) following cardiopulmonary bypass (CPB) surgery in goats. We assessed myocardial muscle tissue water content according to changes in dry-wet weight. Our results showed that AQP1 expression and myocardial muscle tissue water content increased significantly 6 h after CPB surgery, reaching peak levels 48 h after surgery; additionally, the protein expression of Cx43 was inversely correlated with AQP1 expression. Overexpression of AQP1 during CPB surgery enhanced the degree of myocardial edema, whereas the addition of water channel protein inhibitor Hg2+ in cold crystalloid cardioplegia and knockdown of AQP1 during surgery weakened the degree of myocardial edema. These findings revealed that the severity of myocardial edema after CPB surgery is correlated with AQP1 protein expression levels, suggesting the important role played by AQP1 protein in the regulation of Cx43 in the pathological progression of myocardial edema.

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Section: Discussionmentioning

confidence: 99%

Aquaporin 1 plays an important role in myocardial edema caused by cardiopulmonary bypass surgery in goat

Yan

Huang

Ding

et al. 2013

International Journal of Molecular Medicine

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“…Later in gestation one report suggested that total cardiac AQP1 levels reflected predominantly vascular sites, and that the total amount could be increased by fetal anemia [84]. …”

Section: Aquaporins In the Heart – Changes With Intrauterine Growth Rmentioning

confidence: 99%

Aquaporins in development – a review

Liu

Wintour

2005

Reprod Biol Endocrinol

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Water homeostasis during fetal development is of crucial physiologic importance. It depends upon maternal fetal fluid exchange at the placenta and fetal membranes, and some exchange between fetus and amniotic fluid can occur across the skin before full keratinization. Lungs only grow and develop normally with fluid secretion, and there is evidence that cerebral spinal fluid formation is important in normal brain development. The aquaporins are a growing family of molecular water channels, the ontogeny of which is starting to be explored. One question that is of particular importance is how well does the rodent (mouse, rat) fetus serve as a model for long-gestation mammals such as sheep and human? This is particularly important for organs such as the lung and the kidney, whose development before birth is very much less in rodents than in the long-gestation species.

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“…At present, 13 types of AQP proteins (AQP-0-AQP-12) have been identified in mammals ( 7 ). AQP-1 is concentrated in microvascular endothelial cells and cardiomyocytes in myocardium ( 8 ). Furthermore, AQP-1 is highly expressed in cardiomyocytes and vascular endothelial cells in rabbits with chronic myocardial ischemia ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen‑rich solution against myocardial injury and aquaporin expression via the PI3K/Akt signaling pathway during cardiopulmonary bypass in rats

et al. 2018

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Myocardial ischemia, hypoxia and reperfusion injury are induced by aortic occlusion, cardiac arrest and resuscitation during cardiopulmonary bypass (CPB), which can severely affect cardiac function. The aim of the present study was to investigate the effects of hydrogen-rich solution (HRS) and aquaporin (AQP) on cardiopulmonary bypass (CPB)-induced myocardial injury, and determine the mechanism of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Sprague Dawley rats were divided into a sham operation group, a CPB surgery group and a HRS group. A CPB model was established, and the hemodynamic parameters were determined at the termination of CPB. The myocardial tissues were observed by hematoxylin and eosin, and Masson staining. The levels of myocardial injury markers [adult cardiac troponin I (cTnI), lactate dehydrogenase (LDH), creatine kinase MB (CK-MB) and brain natriuretic peptide (BNP)], inflammatory factors [interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α)] and oxidative stress indicators [superoxide dismutase (SOD), malondialdehyde (MDA) and myeloperoxidase (MPO)] were determined by ELISA. Furthermore, H9C2 cells were treated with HRS following hypoxia/reoxygenation. Cell viability and cell apoptosis were investigated. The expression of apoptosis regulator Bcl-2 (Bcl-2), apoptosis regulator Bax (Bax), caspase 3, AQP-1, AQP-4, phosphorylated (p)-Akt, heme oxygenase 1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) were investigated using western blotting and quantitative-polymerase chain reaction of tissues and cells. Following CPB, myocardial cell arrangement was disordered, myocardial injury markers (cTnI, LDH, CK-MB and BNP), inflammatory cytokines (IL-1β, IL-6 and TNF-α) and MDA levels were significantly increased compared with the sham group; whereas the SOD levels were significantly downregulated following CPB compared with the sham group. HRS attenuated myocardial injury, reduced the expression levels of cTnI, LDH, CK-MB, BNP, IL-1β, IL-6, TNF-α, MDA and MPO, and increased SOD release. Levels of Bcl-2, AQP-1, AQP-4, p-Akt, HO-1 and Nrf2 were significantly increased following HRS; whereas Bax and caspase-3 expression levels were significantly reduced following CPB. HRS treatment significantly increased the viability of myocardial cells, reduced the rate of myocardial cell apoptosis and the release of MDA and LDH compared with the CPB group. A PI3K inhibitor (LY294002) was revealed to reverse the protective effect of HRS treatment. HRS was demonstrated to attenuate CPB-induced myocardial injury, suppress AQP-1 and AQP-4 expression following CPB treatment and protect myocardial cells via the PI3K/Akt signaling pathway.

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Anaemia Stimulates Aquaporin 1 Expression in the Fetal Sheep Heart

Cited by 23 publications

References 36 publications

Aquaporin 1 plays an important role in myocardial edema caused by cardiopulmonary bypass surgery in goat

Aquaporin 1 plays an important role in myocardial edema caused by cardiopulmonary bypass surgery in goat

Aquaporins in development – a review

Hydrogen‑rich solution against myocardial injury and aquaporin expression via the PI3K/Akt signaling pathway during cardiopulmonary bypass in rats

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