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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003684naa a2200457 4500
001oai:DiVA.org:umu-123411
003SwePub
008160701s2001 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1234112 URI
040 a (SwePub)umu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Wagner, C A4 aut
2451 0a Effects of the serine/threonine kinase SGK1 on the epithelial Na(+) channel (ENaC) and CFTR :b implications for cystic fibrosis.
264 1c 2001
338 a print2 rdacarrier
520 a Cystic fibrosis (CF) is characterized by impaired Cl(-) secretion and increased Na(+) reabsorption in several tissues including respiratory epithelium. Many CFTR mutations have been identified over the past years. However, only a poor correlation between the genotype and lung phenotype was found suggesting additional factors influencing the phenotype and course of the disease. The serine/threonine kinase SGK1 has recently been shown to stimulate the activity of the epithelial Na(+) channel ENaC. A variety of stimuli such as aldosterone, cell shrinkage, insulin or TGF-beta1 stimulate transcription and activate the SGK1 kinase. Here we further examined the effects of SGK1 on ENaC and CFTR which have mutual interactions and we analyzed sgk1 mRNA abundance in lung tissue from CF patients. Coexpression of CFTR and h-SGK1 in Xenopus oocytes increased ENaC currents as previously described. In addition CFTR mediated currents were also stimulated. h-SGK1 accelerated the expression of the amiloride sensitive Na(+)- current in Xenopus oocytes paralleled by increased ENaC-protein abundance in the oocyte membrane, an effect which was reversed by a h-SGK1(K127R) mutation lacking the ATP-binding site. The cation selectivity or Na(+) affinity were not affected. However, coexpression of h-SGK1 with ENaC altered the sensitivity of the Na(+)-channel to the inhibitors amiloride and triamterene. The inhibitory effect of CFTR expression on ENaC current was not affected by coexpression of h-SGK1 in Xenopus oocytes. Lung tissue from CF patients strongly expressed the serine/threonine kinase h-sgk1 which was not the case for non-CF lung tissue. Loss of CFTR function itself in a CF lung epithelial cell line did not increase SGK1 expression. In summary, enhanced expression of h-SGK1 in epithelial cells of CF-lung tissue may be a novel pathophysiological factor contributing to increased Na(+) channel activity and thus to increased Na(+) transport in CF.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Fysiologi0 (SwePub)301062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Physiology0 (SwePub)301062 hsv//eng
653 a fysiologi
653 a Physiology
7001 a Ott, Michael,d 1970-u Umeå universitet,Institutionen för folkhälsa och klinisk medicin4 aut0 (Swepub:umu)miot0002
7001 a Klingel, K4 aut
7001 a Beck, S4 aut
7001 a Melzig, J4 aut
7001 a Friedrich, B4 aut
7001 a Wild, K N4 aut
7001 a Bröer, S4 aut
7001 a Moschen, I4 aut
7001 a Albers, A4 aut
7001 a Waldegger, S4 aut
7001 a Tümmler, B4 aut
7001 a Egan, M E4 aut
7001 a Geibel, J P4 aut
7001 a Kandolf, R4 aut
7001 a Lang, F4 aut
7102 a Umeå universitetb Institutionen för folkhälsa och klinisk medicin4 org
7730 t Cellular Physiology and Biochemistryg 11:4q 11:4x 1015-8987x 1421-9778
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-123411

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