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Potential role of protease-activated receptor-2-stimulated activation of cytosolic phospholipase A(2) in intestinal myofibroblast proliferation: Implications for stricture formation in Crohns disease
Kalmar University .
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
Kalmar University .
2009 (engelsk)Inngår i: JOURNAL OF CROHNS and COLITIS, ISSN 1873-9946, Vol. 3, nr 1, s. 15-24Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background and aims: Myofibroblast hyperplasia contributes to muscularis mucosae thickening and stricture formation in Crohns disease (CD). Protease-activated receptor-2 (PAR-2) and cytosolic phospholipase A(2) (cPLA(2)) are known regulators of cell growth, but their significance in intestinal myofibroblast proliferation remain to be elucidated. The principle aims of the present study were to investigate if PAR-2 is expressed in the expanded muscularis mucosa in ileal CD specimens, if inflammatory cytokines may stimulate PAR-2 expression in intestinal myofibroblasts, and if PAR-2 and cPLA(2). may regulate intestinal myofibroblast growth.

Methods: Immunohistochemistry was used for detection of PAR-2 in ileal CD specimens. Studies on PAR-2 expression, PLA(2) activation and cell growth were performed in a human intestinal myofibroblast cell tine, CCD-18Co. PAR-2 expression was investigated by RT-PCR and immunocytochemistry. PLA(2) activity was analyzed by quantification of released C-14-arachidonic acid (C-14-AA). Cell growth was examined by H-3-thymidine incorporation and cell counting.

Results: The thickened muscularis mucosae of the CD specimens showed strong PAR-2 expression. In cultured myofibroblasts, tumor necrosis factor-alpha (TNF-alpha) up-regulated PAR-2 mRNA and protein, and potentiated PAR-2-stimutated C-14-AA release by two known PAR-2 activators, trypsin and SLIGRL-NH2. The release of C-14-AA was dependent on cPLA(2). Trypsin stimulated the proliferation of serum-starved cells, and inhibition of cPLA(2) reduced normal cell growth and abolished the growth-promoting effect of trypsin.

Conclusions: The results suggest that PAR-2-mediated cPLA(2) activation might be of importance in intestinal myofibroblast proliferation. The results also point to the possibility that PAR-2 upregulation by inflammatory cytokines, like TNF-alpha, may modulate this effect.

sted, utgiver, år, opplag, sider
2009. Vol. 3, nr 1, s. 15-24
Emneord [en]
Crohns disease, Intestinal myofibroblasts, Phospholipase A(2), Protease-activated receptor-2, Tumor necrosis factor-alpha
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-17284DOI: 10.1016/j.crohns.2008.10.002OAI: oai:DiVA.org:liu-17284DiVA, id: diva2:208145
Tilgjengelig fra: 2009-03-16 Laget: 2009-03-16 Sist oppdatert: 2009-08-17

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