AQP5 ELISA kit
- Known as:
- AQP5 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-AQP5-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- AQP5 ELISA kit
Related genes to: AQP5 ELISA kit
- Gene:
- AQP5 NIH gene
- Name:
- aquaporin 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-25
- Date modifiied:
- 2016-10-05
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- Obesity is a major risk factor for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and its progressive form, Metabolic Dysfunction-Associated Steatohepatitis (MASH). Bacterial cyclodipeptides (CDPs) have previously been shown to modulate PI3K/Akt/mTOR signaling and transcriptional programs involved in lipid and cholesterol metabolism, highlighting their potential to regulate metabolic homeostasis. Given the central role of the PI3K/Akt/FoxO1 pathway in regulating aquaporins, inflammatory cytokines, and metabolic homeostasis during obesity and MASLD, the therapeutic potential of CDPs was evaluated in a rat model of MASLD. Treatment of obese animals with CDPs decreased body weight and abdominal and thoracic circumferences. The obesogenic diet induced liver damage after the 34th week, which was alleviated by ten weeks of CDP treatment administered three times a week. This reduced the number and size of lipid droplets and inflammatory infiltrates. Additionally, CDPs improved parameters associated with atherogenic dyslipidemia and metabolic dysfunction, including triglycerides and cholesterol, as well as hepatic injury markers. These changes were accompanied by restoration of mitochondrial membrane potential and a significant reduction in mitochondrial ROS generation. CDP treatment in obese animals restored protein expression levels of aquaporins AQP1, AQP5, AQP8, and AQP9 and downregulated the expression of the inflammatory markers NF-κB and IL-1β. Interestingly, the downstream cellular mediator GAB1 from the PI3K/Akt/FoxO1 pathway was also downregulated. These findings demonstrate that CDP treatment restored the expression of glycerol/water transporting aquaporins altered during obesity and MASLD. Overall, CDPs ameliorated MASLD in obese animals through coordinated modulation of lipid metabolism, mitochondrial function, aquaporin expression, and PI3K/Akt/FoxO1 signaling associated with inflammation, supporting their potential as therapeutic candidates for metabolic liver disease. - Source: PubMed
Publication date: 2026/08/12
Figueroa-Guzmán CitlaliGaona-García Roxana YCampos-Morales Marlene EMartínez-Alcantar LorenaCampos-García Jesús - Breast cancer remains a leading cause of global mortality in women, with therapy resistance posing a major challenge to successful treatment. Chemotherapy-induced oxidative stress can trigger adaptive survival mechanisms through the antioxidative transcription factor NRF2 and membrane pores known as peroxiporins. Peroxiporins regulate cellular redox homeostasis by controlling the flux of H2O2, potentially driving the development of chemoresistance in aggressive subtypes. This study investigated the expression of peroxiporins, AQP3 and AQP5, and the antioxidative transcription factor NRF2, before and after chemotherapy to determine their role in chemotherapy resistance in HER2-positive and triple negative breast cancer. - Source: PubMed
Publication date: 2026/08/10
Guteša IlijaBubanovic SandaVodopic TonciMlinaric MonikaGrgat KrešimirCipak Gašparovic Ana - Idiopathic pulmonary fibrosis (IPF) is one of the most severe forms of idiopathic interstitial pneumonia. Increasing evidence indicates that the gradual accumulation of senescent fibroblasts and alveolar epithelial cells contributes significantly to IPF pathogenesis, suggesting senescence as a potentially targetable process. Recurrent injury to the alveolar epithelium promotes senescence in epithelial cells, impairing their regenerative capacity and thereby predisposing the tissue to fibrotic degeneration. Although epithelial senescence is strongly implicated in the initiation and progression of lung fibrosis, the mechanisms through which it drives IPF remain challenging, partially due to the lack of physiologically relevant in vitro models capable of recapitulating lung architecture under both normal and pathological conditions. The objective of the present study was to develop a reproducible alveolosphere model in healthy and senescent conditions as a preliminary approach to investigate epithelial features that may be relevant to aspects of the IPF microenvironment. An alveolosphere system was generated by culturing alveolar epithelial cells with or without basement membrane components in combination with alveolar/epithelial optimized medium. Cultures were maintained for 3, 6, and 8 days, and cell viability together with morphological assessment confirmed the absence of cytotoxicity. The expression of keratin 8/18 and AQP5 was consistent with the maintenance of epithelial and alveolar-associated features. Cellular senescence was induced by exposing alveolospheres to doxorubicin for 24 h. Subsequent analyses of viability, along with the expression of senescent and pro-fibrotic markers, inflammatory mediators, and tissue remodeling factors, such as MMPs, were carried out in senescent 3D structures. The results demonstrated robust cell viability at all time points, supported by morphological observations. Marker expression suggested preservation of key epithelial characteristics, while senescence-inducing conditions were associated with an increase in senescence-associated, pro-fibrotic, inflammatory, and matrix-modulating markers. Collectively, these findings describe the preliminary establishment of a cost-effective and reproducible alveolosphere platform that may represent a useful starting point for studying epithelial senescence and its potential association with pro-fibrotic signaling relevant to aspects of IPF pathogenesis. Furthermore, this model may provide a basis for the preliminary evaluation of senotherapeutic compounds aimed at delaying or preventing the onset of cellular senescence. - Source: PubMed
Publication date: 2026/07/10
Longhin AuroraGatta ValentinaTeti GabriellaFalconi Mirella - Dry eye disease (DED) is a multifactorial ocular surface disorder characterized by inflammation, oxidative stress, tear film instability, and secretory dysfunction. This study investigated the protective effects of Lute-gen, a lutein and zeaxanthin-based formulation, in both in vitro and in vivo DED models. Human corneal epithelial (HCE-T) cells were stimulated with TNF-α, while dry eye was induced in female Sprague-Dawley rats using subcutaneous scopolamine (SCP) administration. In HCE-T cells, Lute-gen showed no cytotoxicity, restored cell viability, reduced intracellular ROS, and was associated with increased expression of antioxidant-related markers (Nrf2, HO-1, SOD, CAT, and GPx), reduced expression of inflammatory mediators (TLR4/MyD88/NF-κB/NLRP3), and increased expression of AQP3 and AQP5. In SCP-induced rats, Lute-gen significantly improved tear secretion and reduced corneal fluorescein staining. Histopathological analyses revealed restoration of conjunctival goblet cells, mucin staining, corneal epithelial integrity, acinar area and cell density, and lacrimal gland architecture, with reduced inflammatory infiltration. Immunofluorescence further demonstrated reduced TLR4 and MMP9 immunoreactivity and decreased CD68 inflammatory cell infiltration. Molecular analyses showed reduced expression of inflammatory cytokines and NF-κB/MAPK/MMP signaling-related inflammatory mediators, together with restoration of AQP1, AQP3, and AQP5 expression in corneal tissues. Collectively, these findings suggest that Lute-gen treatment was associated with improvements in dry eye-related pathological changes, including restoration of antioxidant-related markers, attenuation of inflammatory responses, restoration of aquaporin expression, and preservation of ocular surface and lacrimal gland integrity. These preclinical findings support further mechanistic investigations and the future clinical evaluation of Lute-gen as a potential nutritional intervention for dry eye disease. - Source: PubMed
Publication date: 2026/07/13
Sood RachitSanjay Lee Hae-Jeung - - Source: PubMed
Publication date: 2026/07/22
Ning XinXu WeiMa JiaxinChen SiningMa Rong