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Expression of protease-activated-receptor 2 (PAR-2) in human esophageal mucosa.

Artikel i vetenskaplig tidskrift
Författare Kamuran Inci
Anders Edebo
Lars Olbe
Anna Casselbrant
Publicerad i Scandinavian journal of gastroenterology
Volym 44
Nummer/häfte 6
Sidor 664-71
ISSN 1502-7708
Publiceringsår 2009
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för gastrokirurgisk forskning och utbildning
Sidor 664-71
Språk en
Länkar dx.doi.org/10.1080/0036552090278368...
Ämnesord Proteinase-activated receptors (PARs), PAR-2 receptor, esophageal mucosa, GERD, trypsin,
Ämneskategorier Kirurgi

Sammanfattning

OBJECTIVE: The role of duodenal reflux in gastroesophageal reflux disease (GERD) containing bile salts and pancreatic enzymes (with special attention to trypsin) is still under discussion. Proteinase-activated receptors (PARs) are a novel family and PAR-2 is a unique member of this family because it is activated by trypsin. The aim of the present study was to examine the presence and the position of the PAR-2 receptor in human esophageal mucosa in different subgroups of GERD. MATERIAL AND METHODS: Distal biopsies taken from healthy controls, patients with erosive reflux disease (ERD), patients with specialized intestinal metaplasia (SIM) and adenocarcinoma were analyzed for the PAR-2 receptor with reverse-transcription polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry. RESULTS: Gene transcripts for the PAR-2 receptor were found in all groups, with increased levels in SIM patients compared to controls. However, this visual pattern was not seen for the protein expression of the PAR-2 receptor showing no apparent quantitative differences between the groups. Immunohistochemistry revealed distinct staining for the PAR-2 receptor in the luminal part of the esophageal epithelium. CONCLUSIONS: The localization of the PAR-2 receptor indicates that the receptor can be cleaved and activated by trypsin in duodenogastric esophageal refluxate. The data thus suggest that the trypsin-PAR-2 pathway may be involved in the pathogenesis of GERD.

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