Distribution of aquaporin water channels AQP1 and AQP5 in the ductal system of the human pancreas

Burghardt, Beáta; Elkjær, Marie-Louise; Kwon, Tae‐Hwan; Rácz, Gábor; Varga, Gábor; Steward, Martin C.; Nielsen, Søren

doi:10.1136/gut.52.7.1008

Cited by 157 publications

(157 citation statements)

References 48 publications

Supporting

Mentioning

138

Contrasting

Unclassified

Order By: Relevance

“…Other reports have alluded to the role of other AQPs in the development of human cancer [6,8,9]. For example, expression of AQP3 was increased in renal cell cancer, as was AQP5 in pancreatic cancer [9,10]. AQP1 appears to be involved in cell cycle control [8,11], and expression of hAQP1, hAQP3, and hAQP5 have been shown to be simultaneously induced during lymphocyte activation [12].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of AQP5, a putative oncogene, promotes cell growth and transformation

et al. 2008

View full text Add to dashboard Cite

Overexpression of several aquaporins has been reported in different types of human cancer but the role of AQPs in human carcinogenesis has not yet been clearly defined. Here, we demonstrate that ectopic expression of human AQP5 (hAQP5), a water channel expressed in lung, salivary glands, and kidney, induces many phenotypic changes characteristic of transformation both in vitro and in vivo. Furthermore, the cell proliferative ability of AQP5 appears to be dependent upon the phosphorylation of a cAMP-protein kinase (PKA) consensus site located in a cytoplasmic loop of AQP5. In addition, phosphorylation of the PKA consensus site was found to be phosphorylated preferentially in tumors. These findings altogether indicate that hAQP5 plays an important role in human carcinogenesis and, furthermore, provide an attractive therapeutic target.

show abstract

Section: Introductionmentioning

confidence: 99%

Overexpression of AQP5, a putative oncogene, promotes cell growth and transformation

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Glycerol transport through AQP3 also contributes to the generation of ATP for cell proliferation and tumorigenesis (7). AQP5 is widely overexpressed in pancreatic cancer and appears to be involved in cell proliferation (8).…”

Section: Introductionmentioning

confidence: 99%

AQP5: A novel biomarker that predicts poor clinical outcome in colorectal cancer

Shan

Cui

et al. 2014

Oncology Reports

View full text Add to dashboard Cite

Abstract. The aquaporins (AQPs) are water channel proteins that exhibit several properties related to tumor development. However, the expression and clinical significance of AQP5 in colorectal cancer, particularly the correlation with circulating tumor cells (CTCs), has not been elucidated. The aim of the present study was to determine whether or not the expression of AQP5 is a strong prognostic biomarker for colorectal cancer. The results showed that of 45 tumor specimens, 14 (31.1%) had high levels of expression of AQP5, 29 (64.4%) exhibited a moderate (intermediate) level of staining, and 2 (4.4%) had an absence of AQP5 staining. AQP5 was only occasionally detected in para-neoplastic [3/45 (6.67%)] and normal tissues [3/45 (6.67%)]. AQP5 protein overexpression frequently accompanied gene amplification detection with fluorescence in situ hybridization (FISH). Moreover, AQP5 expression in colorectal cancer cells was upregulated compared to normal colon cells. AQP5 overexpression was also associated with TNM stage (P=0.002), lymph node metastasis (P=0.016), and distant metastasis (P=0.000). The relationships between age, gender, histologic grade and tumor size with expression of AQP5 were not significant (P>0.05). A positive correlation between the number of CTCs and AQP5 expression (P<0.05) was demonstrated. In addition, patients who did not express AQP5 had a superior cumulative survival rate compared to patients with AQP5 positivity. AQP5 may be used as a novel biomarker for colorectal cancer aggressiveness and metastasis, but it does not reflect drug resistance.

show abstract

“…Aquaporin (AQP)-5 is on the apical membrane at several sites in mammals, including secretory cells in salivary, lacrimal, sweat, and airway submucosal glands, corneal epithelium, nasopharyngeal and bronchial epithelium, and type I pneumocytes of the lung (2)(3)(4)(5). Studies of isolated salivary gland epithelial cells (6) and type I pneumocytes (7) demonstrate that AQP5 confers high level membrane water permeability to the cell and that cellular responses to an initial osmotic challenge as well as subsequent regulatory volume changes require AQP5 (6).…”

mentioning

confidence: 99%

Transient receptor potential vanilloid 4 regulates aquaporin-5 abundance under hypotonic conditions

Sidhaye

Güler

Schweitzer

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Aquaporin-5 (AQP5) is expressed in epithelia of lung, cornea, and various secretory glands, sites where extracellular osmolality is known to fluctuate. Hypertonic aquaporin (AQP) induction has been described, but little is known about the effects of a hypotonic environment on AQP abundance. We report that, when mouse lung epithelial cells were exposed to hypotonic medium, a doseresponsive decrease in AQP5 abundance was observed. Hypotonic reduction of AQP5 was blocked by ruthenium red, methanandamide, and miconazole, agents that inhibit the cation channel transient receptor potential vanilloid (TRPV) 4 present in lung epithelial cells. Several observations indicate that TRPV4 participates in hypotonic reduction of AQP5, including a requirement for extracellular calcium to achieve AQP5 reduction; an increase in intracellular calcium in mouse lung epithelial (MLE) cells after hypotonic stimulation; and reduction of AQP5 abundance after addition of the TRPV4 agonist 4␣-Phorbol-12,13-didecanoate (4␣-PDD). Similarly, addition of hypotonic PBS to mouse trachea in vivo decreased AQP5 within 1 h, an effect blocked by ruthenium red. To confirm a functional interaction, AQP5 was expressed in control or TRPV4-expressing human embryonic kidney (HEK) cells. Hypotonic reduction of AQP5 was observed only in the presence of TRPV4 and was blocked by ruthenium red. Combined with earlier studies, these observations indicate that AQP5 abundance is tightly regulated along a range of osmolalities and that AQP5 reduction by extracellular hypotonicity can be mediated by TRPV4. These findings have direct relevance to regulation of membrane water permeability and water homeostasis in epithelia of the lung and other organs.epithelium ͉ lung ͉ membrane permeability ͉ osmotic stress ͉ calcium channel A quaporin water channel proteins participate in a wide array of physiological processes and are the primary determinants of membrane osmotic water permeability (1). Aquaporin (AQP)-5 is on the apical membrane at several sites in mammals, including secretory cells in salivary, lacrimal, sweat, and airway submucosal glands, corneal epithelium, nasopharyngeal and bronchial epithelium, and type I pneumocytes of the lung (2-5). Studies of isolated salivary gland epithelial cells (6) and type I pneumocytes (7) demonstrate that AQP5 confers high level membrane water permeability to the cell and that cellular responses to an initial osmotic challenge as well as subsequent regulatory volume changes require AQP5 (6).AQP5 abundance is regulated by numerous stimuli, including TNF-␣ (8), adenoviral infection (9), cAMP (10, 11), and hypertonic stress (12, 13). The general paradigm of aquaporin induction by extracellular hypertonicity is well established because, in addition to AQP5, hypertonic induction of AQP1 (14-16), AQP3 (13,17,18), AQP4 (19,20), and AQP9 (20) has been reported. In contrast, the effects of reduced extracellular osmolality on aquaporin abundance have not been reported.Transient receptor potential-vanilloid (TRPV) 4 is a nonselective cati...

show abstract

Distribution of aquaporin water channels AQP1 and AQP5 in the ductal system of the human pancreas

Cited by 157 publications

References 48 publications

Overexpression of AQP5, a putative oncogene, promotes cell growth and transformation

Overexpression of AQP5, a putative oncogene, promotes cell growth and transformation

AQP5: A novel biomarker that predicts poor clinical outcome in colorectal cancer

Transient receptor potential vanilloid 4 regulates aquaporin-5 abundance under hypotonic conditions

Contact Info

Product

Resources

About