ArticleAmerican journal of physiology. Renal physiology2012
Collecting duct cells that lack normal cilia have mislocalized vasopressin-2 receptors.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Loss of primary cilia increases polycystin-2 and TRPV4 and the appearance of a nonselective cation channel in the mouse cortical collecting duct.American journal of physiology. Renal physiology · 2019Article
- Inhibition of non-receptor tyrosine kinase Src induces phosphoserine 256-independent aquaporin-2 membrane accumulation.The Journal of physiology · 2019Article
- Salt-deficient diet exacerbates cystogenesis in ARPKD via epithelial sodium channel (ENaC).EBioMedicine · 2019Article
- A new coupling of an acid-base transporter to PKD and cyst formation.The Journal of physiology · 2019Article
- Ciliogenesis is reciprocally regulated by PPARA and NR1H4/FXR through controlling autophagy in vitro and in vivo.Autophagy · 2018Article
- Heterotrimeric G protein signaling in polycystic kidney disease.Physiological genomics · 2016Review
- Molecular pathways and therapies in autosomal-dominant polycystic kidney disease.Physiology (Bethesda, Md.) · 2015Review
- Activation of the intrarenal renin-angiotensin-system in murine polycystic kidney disease.Physiological reports · 2015Article
- Epidermal growth factor-induced proliferation of collecting duct cells from Oak Ridge polycystic kidney mice involves activation of Na+/H+ exchanger.American journal of physiology. Cell physiology · 2014Article
- Nedd9 restrains renal cystogenesis in Pkd1-/- mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- ADAM17 promotes proliferation of collecting duct kidney epithelial cells through ERK activation and increased glycolysis in polycystic kidney disease.American journal of physiology. Renal physiology · 2014Article
- Peroxiredoxin VI oxidation in cerebrospinal fluid correlates with traumatic brain injury outcome.Free radical biology & medicine · 2014Article
- Article
- Vasopressin-2 receptor signaling and autosomal dominant polycystic kidney disease: from bench to bedside and back again.Journal of the American Society of Nephrology : JASN · 2014Review
- Primary cilia and kidney injury: current research status and future perspectives.American journal of physiology. Renal physiology · 2013Review
- Transport, cilia, and PKD: must we in (cyst) on interrelationships? Focus on "Increased Na+/H+ exchanger activity on the apical surface of a cilium-deficient cortical collecting duct principal cell model of polycystic kidney disease".American journal of physiology. Cell physiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Polycystic kidney disease (PKD) is a ciliopathy characterized by renal cysts and hypertension. These changes are presumably due to altered fluid and electrolyte transport in the collecting duct (CD). This is the site where vasopressin (AVP) stimulates vasopressin-2 receptor (V2R)-mediated aquaporin-2 (AQP2) insertion into the apical membrane. Since cysts frequently occur in the CD, we studied V2R and AQP2 trafficking and function in CD cell lines with stunted and normal cilia [cilia (-), cilia (+)] derived from the orpk mouse (hypomorph of the Tg737/Ift88 gene). Interestingly, only cilia (-) cells grown on culture dishes formed domes after apical AVP treatment. This observation led to our hypothesis that V2R mislocalizes to the apical membrane in the absence of a full-length cilium. Immunofluorescence indicated that AQP2 localizes to cilia and in a subapical compartment in cilia (+) cells, but AQP2 levels were elevated in both apical and basolateral membranes in cilia (-) cells after apical AVP treatment. Western blot analysis revealed V2R and glycosylated AQP2 in biotinylated apical membranes of cilia (-) but not in cilia (+) cells. In addition, apical V2R was functional upon apical desmopressin (DDAVP) treatment by demonstrating increased cAMP, water transport, and benzamil-sensitive equivalent short-circuit current (I(sc)) in cilia (-) cells but not in cilia (+) cells. Moreover, pretreatment with a PKA inhibitor abolished DDAVP stimulation of I(sc) in cilia (-) cells. Thus we propose that structural or functional loss of cilia leads to abnormal trafficking of AQP2/V2R leading to enhanced salt and water absorption. Whether such apical localization contributes to enhanced fluid retention and hypertension in PKD remains to be determined.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.