Last update 01 Nov 2024

AQP3

Last update 01 Nov 2024

Basic Info

Synonyms

AQP-3, AQP3, Aquaglyceroporin-3

+ [6]

Introduction

Water channel required to promote glycerol permeability and water transport across cell membranes (PubMed:12239222, PubMed:30420639). Acts as a glycerol transporter in skin and plays an important role in regulating SC (stratum corneum) and epidermal glycerol content. Involved in skin hydration, wound healing, and tumorigenesis. Provides kidney medullary collecting duct with high permeability to water, thereby permitting water to move in the direction of an osmotic gradient. Slightly permeable to urea and may function as a water and urea exit mechanism in antidiuresis in collecting duct cells. It may play an important role in gastrointestinal tract water transport and in glycerol metabolism (By similarity).

Drugs associated with AQP3

DFP00173

Target

AQP3

Mechanism

AQP3 inhibitors

Active Org.

University of Lund

Originator Org.

University of Lund

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2024014523

Patent Mining

Target

AQP3

Mechanism-

Active Org.

Keio University

Originator Org.

Keio University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with AQP3

100 Translational Medicine associated with AQP3

0 Patents (Medical) associated with AQP3

1,591

Literatures (Medical) associated with AQP3

01 Jan 2025·Journal of Ethnopharmacology

Improvement effect and mechanism of XuanFuDaiZhe tang on rats with diarrheal irritable bowel syndrome induced by colorectal dilation

Article

Author: Zhang, Kuo ; Wu, Chunfu ; Li, Shile ; Gu, Guanliang ; Cong, Huan ; Wang, Shasha ; Pang, Jie ; Jing, Weiliang ; Yang, Jingyu

ETHNOPHARMACOLOGICAL RELEVANCEXuanFuDaiZhe Tang (XFDZT) is used in traditional Chinese medicine (TCM) to treat diarrhoea-predominant irritable bowel syndrome (IBS-D). Our laboratory has demonstrated that XFDZT remarkably improves various gastrointestinal motility disorders in animal models. However, previous studies have only focused on one or several protein targets without systematically investigating dynamic changes and protein interrelations.AIM OF THE STUDYTo explore the mechanisms underlying the therapeutic action of XFDZT in IBS-D using a network pharmacology approach and in vivo experiments.MATERIALS AND METHODSThe active compounds of XFDZT were selected from TCM Systems Pharmacology and TCM Integrated databases, and potential targets were identified using the Swiss Target Prediction databases. Targets related to IBS-D were mined from the DisGeNet, Drug Bank, and Therapeutic Target databases. The intersecting protein-protein interactions (PPIs) of the drug-disease crossover genes were analysed, and a central PPI network was constructed using the STRING database and Cytoscape 3.7.2. Following Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, a gene pathway network was constructed to identify key target genes and pathways. Using haematoxylin and eosin staining and western blotting, we validated how XFDZT controls water expression in the body to treat IBS-D infection.RESULTSFirst, the results showed that XFDZT contained 1037 active ingredients and 1458 corresponding targets. After intersecting the 252 IBS targets, 108 targets were identified. The main targets of XFDZT were albumin, aquaporins such as AQP1 and AQP3, calmodulin, and the cellular enzyme CYP2C9. GO and KEGG enrichment predicted that the action pathways were the neuroactive ligand-receptor interaction, calcium signalling pathway, serotonergic synapse signalling pathway, cGMP-PKG signalling pathway, cAMP signalling pathway, and MLCK-MLC signalling pathway. Second, an IBS-D rat model was constructed using colorectal dilation (CRD). CRD can significantly induce IBS-D symptoms such as diarrhoea, abdominal pain, and anxiety and depression-like behaviour in rats. XFDZT (10, 20, and 40 g/kg) administered for 14, 21, and 28 days significantly reversed these changes in IBS-D rats in a time- and dose-dependent manner, suggesting that XFDZT significantly improved IBS-D. Finally, the mechanism by which XFDZT improves IBS-D was explored from the perspective of AQPs, tight junction proteins, and motility-related proteins in colon tissue. Compared with the control group, the protein expression of AQP1, AQP3, and AQP8 in the colon tissue of IBS-D rats was significantly downregulated, whereas the protein expression of AQP7 was significantly upregulated. The expression of tight junction-related proteins claudin-1, occludin, and ZO-1 in colon tissue was significantly downregulated, whereas the expression of motility-related proteins p-MLC, MLC, MLCK, and CaM in colon tissue was significantly upregulated, suggesting that IBS-D rats had AQP disorders, epithelial intercellular connections, and motility in colon tissue. The above changes were significantly reversed by XFDZT administration (5, 10, and 20 g/kg) for 14 days.CONCLUSIONXFDZT significantly improved diarrhoea, abdominal pain, anxiety, and depression in IBS-D rats, and its mechanism of action may be related to the regulation of AQPs, tight junction proteins, and the MLCK-MLC pathway. This study provided a pharmacological experimental basis for the development of XFDZT as a novel drug for the treatment of IBS-D.

31 Dec 2024·Renal Failure

FTO attenuates TNF-α-induced damage of proximal tubular epithelial cells in acute pancreatitis-induced acute kidney injury via targeting AQP3 in an N6-methyladenosine-dependent manner

Article

Author: Pu, Yu ; Li, Yong ; Liang, Qi ; Li, Xinghui ; Liu, Lu ; Chen, Shujun

BACKGROUNDAcute kidney injury (AKI) is a frequent complication of severe acute pancreatitis (SAP). Previous investigations have revealed the involvement of FTO alpha-ketoglutarate-dependent dioxygenase (FTO) and aquaporin 3 (AQP3) in AKI. Therefore, the aim of this study is to explore the association of FTO and AQP3 on proximal tubular epithelial cell damage in SAP-induced AKI.METHODSAn in-vitro AKI model was established in human proximal tubular epithelial cells (PTECs) HK-2 via tumor necrosis factor-α (TNF-α) induction (20 ng/mL), after which FTO and AQP3 expression was manipulated and quantified by quantitative real-time PCR and Western blotting. The viability and apoptosis of PTECs under various conditions, and reactive oxygen species (ROS), superoxide dismutase (SOD), and malonaldehyde (MDA) levels within these cells were measured using commercial assay kits and flow cytometry. Methylated RNA immunoprecipitation and mRNA stability assays were performed to elucidate the mechanism of FTO-mediated N6-methyladenosine (m⁶A) modification. Western blotting was performed to quantify β-catenin protein levels in the PTECs.RESULTSFTO overexpression attenuated the TNF-α-induced decrease in viability and SOD levels, elevated apoptosis, increased levels of ROS and MDA, and diminished TNF-α-induced AQP3 expression and reduced β-catenin expression, but its silencing led to contradictory results. FTO negatively modulates AQP3 levels in RTECs in an m⁶A-depednent manner and compromises AQP3 stability. In addition, all FTO overexpression-induced effects in TNF-α-induced PTECs were neutralized following AQP3 upregulation.CONCLUSIONFTO alleviates TNF-α-induced damage to PTECs in vitro by targeting AQP3 in an m⁶A-dependent manner.

01 Dec 2024·Biochemical and Biophysical Research Communications

Maternal alcohol consumption up to mouse organogenesis disrupts fetal-placental interface at mid-gestation associated with dysregulation of AQP3 immunoexpression

Article

Author: Damiano, Alicia E. ; Cebral, Elisa ; Damiano, Alicia E ; Gualdoni, Gisela Soledad ; Barril, Camila

Adequate trophoblast development during placentation involves the AQP3 regulation. The link between potential placental fetal-maternal interface abnormalities and AQP3 expression after perigestational alcohol intake was not explored yet. Female mice were treated (TF) with 10 % ethanol in drinking water before and up to day 10 of gestation, and control females (CF) with ethanol-free water. At gestational day 13, TFs showed increased fetal/placental weight ratio and reduced histological placental thickness compared to CFs. TF-placentas had disorganized fetal face layers, increased junctional zone (JZ), and decreased labyrinth (Lab). Concomitantly, immunoexpression of cleaved caspase-3 significantly increased in TF-JZ and Lab vs controls. Consistent with placental changes, AQP3 expression was higher in junctional trophoblast giant cells (TGCs), glycogen cells (GCs), spongiotrophoblasts (spg), and lab-syncytiotrophoblasts compared to CF-placentas. This study reveals, for the first time, that perigestational alcohol consumption up to organogenesis causes abnormal placental development associated with dysregulation of AQP3 expression.

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AQP3

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