Function of aquaporins in sepsis: a systematic review

Rump, Katharina; Adamzik, Michael

doi:10.1186/s13578-018-0211-9

Cited by 70 publications

(56 citation statements)

References 73 publications

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“…AQPs, a family of water channel proteins expressed in various cell types, are implicated in brain edema formation (34). Despite a low protein identity (ϳ11%) with conventional AQPs such as AQP-1 and 4, AQP11 is indeed a functional water channel that permeates both water and glycerol (35)(36)(37).…”

Section: Mir-27a-3p Maintains Bbb Integrity Following Ichmentioning

confidence: 99%

miR-27a-3p protects against blood–brain barrier disruption and brain injury after intracerebral hemorrhage by targeting endothelial aquaporin-11

Jin

Zhu

et al. 2018

Journal of Biological Chemistry

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Previous studies have reported that miR-27a-3p is down-regulated in the serum of patients with intracerebral hemorrhage (ICH), but the implication of miR-27a-3p down-regulation in post-ICH complications remains elusive. Here we verified miR-27a-3p levels in the serum of ICH patients by real-time PCR and observed that miR-27a-3p is also significantly reduced in the serum of these patients. We then further investigated the effect of miR-27a-3p on post-ICH complications by intraventricular administration of a miR-27a-3p mimic in rats with collagenaseinduced ICH. We found that the hemorrhage markedly reduced miR-27a-3p levels in the hematoma, perihematomal tissue, and serum and that intracerebroventricular administration of the miR-27a-3p mimic alleviated behavioral deficits 24 h after ICH. Moreover, ICH-induced brain edema, vascular leakage, and leukocyte infiltration were also attenuated by this mimic. Of note, miR-27a-3p mimic treatment also inhibited neuronal apoptosis and microglia activation in the perihematomal zone. We further observed that the miR-27a-3p mimic suppressed the up-regulation of aquaporin-11 (AQP11) in the perihematomal area and in rat brain microvascular endothelial cells (BMECs). Moreover, miR-27a-3p down-regulation increased BMEC monolayer permeability and impaired BMEC proliferation and migration. In conclusion, miR-27a-3p down-regulation contributes to brain edema, blood-brain barrier disruption, neuron loss, and neurological deficits following ICH. We conclude that application of exogenous miR-27a-3p may protect against post-ICH complications by targeting AQP11 in the capillary endothelial cells of the brain. This study was supported by a grant from the National Natural Science Foundation of China (81271291). The authors declare that they have no conflicts of interest with the contents of this article. This article contains Fig. S1.

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Section: Mir-27a-3p Maintains Bbb Integrity Following Ichmentioning

confidence: 99%

miR-27a-3p protects against blood–brain barrier disruption and brain injury after intracerebral hemorrhage by targeting endothelial aquaporin-11

Jin

Zhu

et al. 2018

Journal of Biological Chemistry

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“…Regarding genetic variations, several candidate genes such as those for cytochrome P450 and interleukins have been implicated [ 15 , 16 ]. Aquaporins (AQPs) are related to immune cell and kidney function [ 17 ] and thus, might be of special interest. In the last years, the effects of AQPs on both graft rejection and CMV infection have garnered attention in immunological responses studies [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

The Aquaporin 3 Promoter Polymorphism −1431 A/G is Associated with Acute Graft Rejection and Cytomegalovirus Infection in Kidney Recipients Due to Altered Immune Cell Migration

Rump

Rahmel

Rustige

et al. 2020

Cells

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Major complications after kidney transplantation are graft rejection and cytomegalovirus (CMV) infection, which are related to T-cell function, which depends on aquaporin 3 (AQP3) expression. The impact of the AQP3 A(−1431)G promoter polymorphism in kidney transplant recipients was unelucidated and we explored the effect of AQP3 polymorphism on immune cell function and its association with graft rejection and CMV infection in 237 adult patients within 12 months after transplantation. AQP3 promoter polymorphism was molecular and functional characterized. Kaplan–Meier plots evaluated the relationship between genotypes and the incidence of CMV infection and graft rejection. AQP3 A(−1431)G A-allele was associated with enhanced immune cell migration and AQP3 expression in T-cells. The incidences of rejection were 45.4% for the A-allele and 27.1% for G-allele carriers (p = 0.005) and the A-allele was a strong risk factor (hazard ratio (HR): 1.95; 95% CI: 1.216 to 3.127; p = 0.006). The incidences for CMV infection were 21% for A-allele and 35% for G-allele carriers (p = 0.013) and G-allele was an independent risk factor (p = 0.023), with a doubled risk for CMV infection (HR: 1.9; 95% CI: 1.154 to 3.128; p = 0.012). Hence, A-allele confers more resistance against CMV infection, but susceptibility to graft rejection mediated by T-cells. Thus, AQP3-genotype adapted management of immunosuppression and antiviral prophylaxis after kidney transplantation seems prudent.

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“…AQP3 is an aquaporin that transports water, glycerol and small solutes through the plasma membrane; its function is not limited to liquid transport but also involves cell proliferation, migration, 25) skin hydration, 26) wound healing, 27) and tumorigenesis. 28) There is a high level of AQP3 expression in the intestinal tract, 9) regu-lating the absorption and secretion of liquid and maintaining the steady state. Previous studies have shown that targeted regulation of AQP3 can induce intestinal injury and intestinal bacterial translocation.…”

Section: Discussionmentioning

confidence: 99%

“…Studies showed that AQPs expressed abundantly in intestinal epithelial cells, and AQPs was involved in the secretion of intestinal mucus. Aquaporin-3 (AQP3) is hydrophobic, weighs 30 kDa and belongs to the aquaporin family, which is expressed in various parts of the intestine, 9) regulating the proliferation and migration of intestinal epithelial cells and transporting glycerol and hydrogen peroxide. In recent years, an increasing number of studies have found that the abnormal expression of AQPs during sepsis induces injuries to multiple important organs, including the heart, brain, kidney, and lung, indicating that AQPs may be an important biomarker of sepsis.…”

Section: Introductionmentioning

confidence: 99%

Role of Aquaporin-3 in Intestinal Injury Induced by Sepsis

Zhu

Yefeng

Teng

et al. 2019

Biological & Pharmaceutical Bulletin

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Aquaporin-3 (AQP3) is expressed in various parts of the intestine, where it regulates the proliferation and migration of intestinal epithelial cells and the transport of glycerol and hydrogen peroxide. Our study aimed to investigate the effect on the expression of AQP3 of intestinal injury in septic mice and whether oral administration of glycerol can reduce intestinal epithelial injury and barrier disorder by acting as a partial substitute for the function of AQP3. We established a sepsis model by cecal ligation and perforation (CLP) in mice. Sepsis induced intestinal injury, as demonstrated by the disordered destruction of the morphology of the intestinal mucosa, time-dependent increases in Chiu's score (p < 0.05), significantly increased (p < 0.05) plasma concentrations of determination of the levels of diamine oxidase (DAO) and intestinal fatty acidbinding protein 2 (FABP2), and time-dependent downregulation of the expression of AQP3 and occluding (p < 0.05). While the administration of oral glycerol partially ameliorated the sepsis-induced injury of the intestinal mucosa, as shown by the partial recovery of the morphological structure, with decreased Chiu's score, decreased plasma concentrations of DAO and intestinal-type FABP2, upregulated expression of occludin and decreased mortality rate (Sepsis vs. Sepsis Glycerol, p < 0.05). The results showed that the expression levels of AQP3 and occludin were downregulated after septic intestinal injury, while treatment with glycerol, which acts as a substitute for AQP3, partly ameliorated intestinal injury and improved the survival rate. This preliminary experiment suggests that AQP3 may protect the intestinal tract against the effects of sepsis.

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Function of aquaporins in sepsis: a systematic review

Cited by 70 publications

References 73 publications

miR-27a-3p protects against blood–brain barrier disruption and brain injury after intracerebral hemorrhage by targeting endothelial aquaporin-11

miR-27a-3p protects against blood–brain barrier disruption and brain injury after intracerebral hemorrhage by targeting endothelial aquaporin-11

The Aquaporin 3 Promoter Polymorphism −1431 A/G is Associated with Acute Graft Rejection and Cytomegalovirus Infection in Kidney Recipients Due to Altered Immune Cell Migration

Role of Aquaporin-3 in Intestinal Injury Induced by Sepsis

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