Gene expression of taurine transporter and taurine biosynthetic enzymes in brain of rats with acute or chronic hyperosmotic plasma. A comparative study with gene expression of myo-inositol transporter, betaine transporter and sorbitol biosynthetic enzyme.
Cells exposed to hyperosmotic conditions maintain their volume by accumulating organic osmolytes. Taurine is considered as an osmolyte in brain cells. Accumulation of other osmolytes (sorbitol, myo-inositol and betaine), was shown in renal cells to result from an upregulation of the expression of the genes regulating osmolyte cell content. We have investigated the gene expression of the taurine transporter (TauT) and of the taurine biosynthetic enzymes, cysteine dioxygenase (CDO) and cysteine sulfinate decarboxylase (CSD) by measuring their mRNA levels in brain of salt-loaded rats. mRNA levels of genes previously identified as osmosensitive, namely aldose reductase (AR), myo-inositol transporter (SMIT) and betaine transporter (BGT1) were also determined. In whole brain, TauT-, SMIT- and BGT1-mRNA levels were significantly increased following acute salt-loading but SMIT-mRNA levels only remained elevated following chronic salt-loading while CDO-, CSD- and AR-mRNA levels remained unchanged in both conditions. Following acute salt-loading, mRNA levels of TauT, CDO, CSD, SMIT, BGT1 and AR were increased in cerebral cortex while SMIT- and BGT1-mRNA levels only were increased in striatum and habenula.TauT, CDO and CSD genes may be upregulated in brain of salt-loaded rats but the upregulation of the TauT gene appears more widespread. TauT, CDO and CSD are thus putative osmosensitive genes. However the actual pattern (amplitude, time course and regional occurrence) of the upregulation of each of the putative (TauT, CDO and CSD) and established (AR, SMIT and BGT1) osmosensitive genes differs markedly. This indicates that there exist other factors in brain cells which can selectively prevent the upregulation of these genes by hyperosmolarity.
Bitoun
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Institut National de la Santé et de la Recherche Médicale, Unité INSERM 433, Faculté de médecine RTH Laennec, Rue Guillaume Paradin, F 69372, Lyon, France.
Tappaz
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D000208:Acute Disease; D000449:Aldehyde Reductase / Q000235:genetics; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002262:Carboxy-Lyases / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics*; D002908:Chronic Disease; D050558:Cysteine Dioxygenase; D049308:Dioxygenases; D050485:GABA Plasma Membrane Transport Proteins; D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins / Q000235:genetics*; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics*; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D009928:Organ Specificity; D010105:Oxygenases / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D012462:Saline Solution, Hypertonic; D013012:Sorbitol / Q000378:metabolism; D027981:Symporters; D013654:Taurine / Q000096:biosynthesis; D013997:Time Factors; D014883:Water-Electrolyte Imbalance / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology*; D000099247:Taurine Transporters
D000449:Aldehyde Reductase; D002262:Carboxy-Lyases; D002352:Carrier Proteins; D050558:Cysteine Dioxygenase; D049308:Dioxygenases; D050485:GABA Plasma Membrane Transport Proteins; D006360:Heat-Shock Proteins; D008562:Membrane Glycoproteins; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D010105:Oxygenases; D012462:Saline Solution, Hypertonic; D013012:Sorbitol; D027981:Symporters; D013654:Taurine; D000099247:Taurine Transporters; C072207:betaine plasma membrane transport proteins; C073884:SLC5A3 protein, human; C019972:sulfoalanine decarboxylase