Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In searching for a basolateral membrane water transporter in rat kidney with homology to channel forming integral protein (CHIP28), water channel-collecting duct (WCH-CD), and mercurial-insensitive water channel (MIWC), we cloned a new member of the major intrinsic protein family (GLIP, GLycerol Intrinsic Protein). GLIP cDNA had an 855-base pair open reading frame encoding a 30.5-kDa protein with 19-23% amino acid identity to the water channels and 36% identity to the bacterial glycerol facilitator GlpF. Northern blot analysis showed a 5.5-kilobase mRNA encoding GLIP in kidney, brain, and lung; RT-PCR/Southern blot analysis indicated expression of GLIP in kidney, brain, lung, eye, colon, stomach, and skeletal muscle, but not in heart, liver, and spleen. In situ hybridization in rat kidney showed GLIP mRNA expression in medullary collecting duct. Immunofluorescence with a peptide-derived polyclonal antibody showed GLIP protein expression in basolateral membrane of kidney collecting duct principal cells and brain meningeal cells. Functional measurements in Xenopus oocytes expressing GLIP cRNA showed a > 20-fold increase in [3H]glycerol uptake compared with water-injected oocytes; glycerol uptake was inhibited 88% by diisothiocyanodisulfonic stilbene (0.2 mM) and 36% by phloretin (0.25 mM). GLIP did not function as a transporter for water, urea, inositol, glucose, lactate, and monovalent ions. Glycerol uptake in oocytes expressing CHIP28 and MIWC was not different from that in water-injected controls. GLIP represents the first mammalian water channel homolog that selectively transports a solute other than water. The physiological substrate(s) and role(s) of GLIP remain to be elucidated.
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PMID:Cloning of a water channel homolog expressed in brain meningeal cells and kidney collecting duct that functions as a stilbene-sensitive glycerol transporter. 806 28

The nephroprotective effects of pentoxifylline, a methylxantine, were studied in glycerol-induced acute renal failure. Glycerol treated rats exhibited collecting duct and medullary ascending limb dilation and casts, with focal tubular damage, confined mainly to the superficial cortex. In the interstitium focal mononuclear infiltration was observed. In some glomeruli there was swelling of mesangial spaces and mesangial cells. Pentoxifylline injected to glycerol pretreated rats exerted a protective effect. Only few groups of proximal tubules in the subcapsulary region of renal cortex showed necrosis and tubulorhexis. There were not leukocyte infiltrations or vascular congestion. Morphometric analysis showed increased surface area fraction of tubular lumen in rats treated with glycerol (p < 0.01) compared to those in controls. Intratubular cast formations in rats treated with glycerol alone were significantly higher than in rats given pentoxifylline in addition to glycerol. Kidney cortex ectopeptidases (APA, APN and DPP IV) were not significantly changed after glycerol administration. Serum creatinine and blood urea were markedly increased in glycerol treated rats, however, pentoxifylline reduced significantly their levels. This study in glycerol-induced acute renal failure showed a marked renal morphologic and functional protection by pentoxifylline.
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PMID:Nephroprotective effects of pentoxifylline in experimental myoglobinuric acute renal failure. 1250 69