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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 05641naa a2201153 4500 | |
| 001 | oai:gup.ub.gu.se/321216 | |
| 003 | SwePub | |
| 008 | 240528s2022 | |||||||||||000 ||eng| | |
| 009 | oai:prod.swepub.kib.ki.se:150779665 | |
| 024 | 7 | a https://gup.ub.gu.se/publication/3212162 URI |
| 024 | 7 | a https://doi.org/10.1007/s00109-022-02244-w2 DOI |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1507796652 URI |
| 040 | a (SwePub)gud (SwePub)ki | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Fritz, N.4 aut |
| 245 | 1 0 | a The serotonin receptor 3E variant is a risk factor for female IBS-D |
| 264 | c 2022-09-19 | |
| 264 | 1 | b Springer Science and Business Media LLC,c 2022 |
| 520 | a Irritable bowel syndrome (IBS) is a gut-brain disorder of multifactorial origin. Evidence of disturbed serotonergic function in IBS accumulated for the 5-HT3 receptor family. 5-HT(3)Rs are encoded by HTR3 genes and control GI function, and peristalsis and secretion, in particular. Moreover, 5-HT3R antagonists are beneficial in the treatment of diarrhea predominant IBS (IBS-D). We previously reported on functionally relevant SNPs in HTR3A c.-42C > T (rs1062613), HTR3C p.N163K (rs6766410), and HTR3E c.*76G > A (rs56109847 = rs62625044) being associated with IBS-D, and the HTR3B variant p.Y129S (rs1176744) was also described within the context of IBS. We performed a multi-center study to validate previous results and provide further evidence for the relevance of HTR3 genes in IBS pathogenesis. Therefore, genotype data of 2682 IBS patients and 9650 controls from 14 cohorts (Chile, Germany (2), Greece, Ireland, Spain, Sweden (2), the UK (3), and the USA (3)) were taken into account. Subsequent meta-analysis confirmed HTR3E c.*76G > A (rs56109847 = rs62625044) to be associated with female IBS-D (OR = 1.58; 95% CI (1.18, 2.12)). Complementary expression studies of four GI regions (jejunum, ileum, colon, sigmoid colon) of 66 IBS patients and 42 controls revealed only HTR3E to be robustly expressed. On top, HTR3E transcript levels were significantly reduced in the sigma of IBS patients (p = 0.0187); more specifically, in those diagnosed with IBS-D (p = 0.0145). In conclusion, meta-analysis confirmed rs56109847 = rs62625044 as a risk factor for female IBS-D. Expression analysis revealed reduced HTR3E levels in the sigmoid colon of IBS-D patients, which underlines the relevance of HTR3E in the pathogenesis of IBS-D. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Gastroenterologi0 (SwePub)302132 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Gastroenterology and Hepatology0 (SwePub)302132 hsv//eng |
| 653 | a Irritable bowel syndrome | |
| 653 | a Serotonin type 3 receptor | |
| 653 | a IBS-D | |
| 653 | a Females | |
| 653 | a irritable-bowel-syndrome | |
| 653 | a microrna-510 target site | |
| 653 | a functional variant | |
| 653 | a htr3a gene | |
| 653 | a association | |
| 653 | a polymorphism | |
| 653 | a c178t | |
| 653 | a 3a | |
| 653 | a responsiveness | |
| 653 | a impact | |
| 653 | a Genetics & Heredity | |
| 653 | a Research & Experimental Medicine | |
| 700 | 1 | a Berens, S.4 aut |
| 700 | 1 | a Dong, Y. J.4 aut |
| 700 | 1 | a Martinez, C.4 aut |
| 700 | 1 | a Schmitteckert, S.4 aut |
| 700 | 1 | a Houghton, L. A.4 aut |
| 700 | 1 | a Goebel-Stengel, M.4 aut |
| 700 | 1 | a Wahl, V.4 aut |
| 700 | 1 | a Kabisch, M.4 aut |
| 700 | 1 | a Gotze, D.4 aut |
| 700 | 1 | a D'Amato, M.4 aut |
| 700 | 1 | a Zheng, T. H.4 aut |
| 700 | 1 | a Roth, R.4 aut |
| 700 | 1 | a Monnikes, H.4 aut |
| 700 | 1 | a Tesarz, J.4 aut |
| 700 | 1 | a Engel, F.4 aut |
| 700 | 1 | a Gauss, A.4 aut |
| 700 | 1 | a Raithel, M.4 aut |
| 700 | 1 | a Andresen, V.4 aut |
| 700 | 1 | a Keller, J.4 aut |
| 700 | 1 | a Frieling, T.4 aut |
| 700 | 1 | a Pehl, C.4 aut |
| 700 | 1 | a Stein-Thoringer, C.4 aut |
| 700 | 1 | a Clarke, G.4 aut |
| 700 | 1 | a Kennedy, P. J.4 aut |
| 700 | 1 | a Cryan, J. F.4 aut |
| 700 | 1 | a Dinan, T. G.4 aut |
| 700 | 1 | a Quigley, E. M. M.4 aut |
| 700 | 1 | a Spiller, R.4 aut |
| 700 | 1 | a Beltran, C.4 aut |
| 700 | 1 | a Madrid, A. M.4 aut |
| 700 | 1 | a Torres, V.4 aut |
| 700 | 1 | a Mayer, E. A.4 aut |
| 700 | 1 | a Sayuk, G.4 aut |
| 700 | 1 | a Gazouli, M.4 aut |
| 700 | 1 | a Karamanolis, G.4 aut |
| 700 | 1 | a Bustamante, M.4 aut |
| 700 | 1 | a Estivil, X.4 aut |
| 700 | 1 | a Rabionet, R.4 aut |
| 700 | 1 | a Hoffmann, P.4 aut |
| 700 | 1 | a Nothen, M. M.4 aut |
| 700 | 1 | a Heilmann-Heimbach, S.4 aut |
| 700 | 1 | a Schmidt, B.4 aut |
| 700 | 1 | a Franke, A.4 aut |
| 700 | 1 | a Lieb, W.4 aut |
| 700 | 1 | a Herzog, W.4 aut |
| 700 | 1 | a Boeckxstaens, G.4 aut |
| 700 | 1 | a Wouters, M. M.4 aut |
| 700 | 1 | a Simrén, Magnus,d 1966u Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine4 aut0 (Swepub:gu)xsimrm |
| 700 | 1 | a Rappold, G. A.4 aut |
| 700 | 1 | a Vicario, M.4 aut |
| 700 | 1 | a Santos, J.4 aut |
| 700 | 1 | a Schaefert, R.4 aut |
| 700 | 1 | a Lorenzo-Bermejo, J.4 aut |
| 700 | 1 | a Niesler, B.4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för medicin4 org |
| 773 | 0 | t Journal of Molecular Medicine-Jmmd : Springer Science and Business Media LLCg 100:11, s. 1617-1627q 100:11<1617-1627x 0946-2716x 1432-1440 |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/321216 |
| 856 | 4 8 | u https://doi.org/10.1007/s00109-022-02244-w |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:150779665 |
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