PHOSPHOLIPASE A(2) ISOFORMS ARE ALTERED IN CHRONIC-PANCREATITIS

Citation
M. Kashiwagi et al., PHOSPHOLIPASE A(2) ISOFORMS ARE ALTERED IN CHRONIC-PANCREATITIS, Annals of surgery, 227(2), 1998, pp. 220-228
Citations number
41
Categorie Soggetti
Surgery
Journal title
ISSN journal
00034932
Volume
227
Issue
2
Year of publication
1998
Pages
220 - 228
Database
ISI
SICI code
0003-4932(1998)227:2<220:PAIAAI>2.0.ZU;2-7
Abstract
Objective To determine ii phospholipase A(2) (PLA(2)) type II and type IV mRNA expression and protein are altered in chronic pancreatitis. S ummary Background Data PLA(2)s have an important regulatory function i n several signaling pathways, especially in inflammation. In this stud y, we examined the expression of three PLA(2) isoforms (type I, type I I, and type IV) in chronic pancreatitis. Methods The distribution of P LA(2) was studied in 15 pancreas samples obtained from patients with c hronic pancreatitis using immunohistochemical, Northern blot, and in s itu hybridization techniques. Normal pancreas obtained from healthy or gan donors served as control. Results Northern blot analysis revealed enhanced mRNA levels of PLA(2) type II (5.7-fold) and type IV (5.1-fol d) in chronic pancreatitis (p < 0.01) versus normal pancreas. In norma l pancreas, intense PLA(2) type I immunostaining was present in acinar cells, whereas PLA(2) type II immunostaining was visible only in some acinar cells. In chronic pancreatitis, PLA(2) type II immunostaining was present more frequently and with higher intensity in acinar cells. Furthermore, PLA(2) type II immunoreactivity was more abundant in met aplastic ductal cells in the chronic pancreatitis samples. By in situ hybridization, areas with ductal metaplasia in chronic pancreatitis ex hibited intense PLA(2) type IV mRNA signals. All chronic pancreatitis tissues with concomitantly increased mRNA expression for PLA(2) type I I and type IV exhibited a higher degree of degeneration, ductal metapl asia, and fibrosis. Conclusions Upregulation of PLA(2) types II and IV in areas with more histologic damage suggests that these PLA(2) isofo rms might contribute to the morphologic changes that occur in chronic pancreatitis.