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

Myo-inositol is a major compatible osmolyte in the renal medulla and is accumulated in cells under hypertonic conditions by uptake via a Na+/myo-inositol cotransporter (SMIT). SMIT is regulated by extracellular osmolarity at the transcription level. We investigated localization of SMIT in rat kidney by immunohistochemical staining using an anti-SMIT-antibody raised against a synthetic peptide corresponding to part of SMIT and by in situ hybridization. SMIT protein localized predominantly to the basolateral membranes of cells of the thick ascending limb of Henle (TAL) and inner medullary collecting duct (IMCD). Macula densa (MD) cells, identified as the Tamm-Horsfall-protein (THP)-unreactive cells surrounded by THP-reactive TAL cells, also stained for anti-SMIT. In situ hybridization yielded the intense SMIT signals in the TAL and IMCD and also in the juxtaglomerular (JG) region. Prior loading of the animal with a high concentration of NaCl rapidly induced SMIT mRNA; furosemide down-regulated it. The high level of SMIT expression suggests that MD cells are exposed to hypertonicity at the basolateral surface. Because SMIT expression seemed to be proportional to the magnitude of NaCl reabsorption, it may be a good marker for examination of the tubuloglomerular feedback mechanism in vivo.
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PMID:Expression of the Na+/myo-inositol cotransporter in the juxtaglomerular region. 973 84

Intracellular ionic strength may play an important role in regulating the expression of genes encoding osmolyte-accumulating molecules. To establish whether a strict relation exists between these variables, intracellular ionic strength (sum of Na+, Cl- and K+ concentrations) and the relative abundance of mRNA derived from various tonicity-sensitive genes was examined using electron microprobe analysis and Northern blots on primary cultures of rat papillary collecting duct (PCD) cells following acute or long-term alterations in medium tonicity. Hypertonic medium (450 mosmol kg(-1)) evoked an initial rise in intracellular ionic strength (269 +/- 5 vs. 194 +/- 7 mmol (kg wet weight (wt))(-1) in isotonic controls; means +/- S.E.M.), which subsequently declined gradually, and a significantly higher abundance of bgt1 (Na+- and Cl- -dependent betaine transporter), smit (Na+/myo-inositol cotransporter), ar (aldose reductase) and osp94 (osmotic stress protein 94) mRNAs. Conversely, exposure to hypotonic medium (200 mosmol kg(-1)) for 12 h was associated with significantly reduced intracellular ionic strength (153 +/- 4 mmol (kg wet wt)(-1)) and significantly reduced the abundance of smit and ar mRNAs. PCD cells preconditioned in hypotonic medium and re-exposed to isotonic medium showed significantly higher abundance of these mRNAs than isotonic controls, although the intracellular ionic strength did not differ. Two further tonicity-sensitive genes responded differently to medium tonicity: while the abundance of hsp70 (heat shock protein 70) mRNA increased significantly following both hypo- and hypertonic stress, inos (inducible nitric oxide synthase) mRNA abundance correlated inversely with medium tonicity. These findings support the view that the effect of intracellular ionic strength on the expression of bgt1, smit, ar and osp94 is modulated by additional factors such as cell volume, and that its effect on the pathways regulating hsp70 and inos is even more complex.
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PMID:Relationship between intracellular ionic strength and expression of tonicity-responsive genes in rat papillary collecting duct cells. 1218 Dec 87