- Tytuł:
- The expression of apoptosis-related proteins in patients with ulcerative colitis
- Autorzy:
-
Niewiarowska, K.
Lebelt, A.
Gryko, M.
Pryczynicz, A.
Famulski, W.
Czyżewska, J.
Kemona, A.
Piekarska-Dymicka, V.
Jagodzińska, D.
Guzińska-Ustymowicz, K. - Powiązania:
- https://bibliotekanauki.pl/articles/1916338.pdf
- Data publikacji:
- 2014
- Wydawca:
- Uniwersytet Medyczny w Białymstoku
- Tematy:
-
Ulcerative colitis
Bcl-xl
Bax
Bid
Bcl-2 - Opis:
- Purpose: Recent literature data indicate a key role of apoptosis in the pathogenesis of inflammatory bowel disease. The aim of the study was to evaluate the expression of Bax, Bid, Bcl-2 and Bcl-xl in non-dysplastic and dysplastic epithelium in inflamated mucosa of patients with ulcerative colitis. Methods: The study consists of 18 patients with diagnosed ulcerative colitis. The expression of proteins was determined immunohistochemically. Results: Lack of Bax expression in normal epithelium of the inflamed intestinal mucosa (94.4%) and a weak expression of this protein were found in dysplastic glandular cells (67%). The Bax expression of dysplastic epithelium correlates with reduced severity of chronic inflammation (p<0.005). Bid expression in non-dysplastic glands was found in 67% of cases vs. 16% in dysplastic epithelium that was associated with the occurrence of epithelial erosions or ulcers (p<0.05). Moderate cytoplasmic expression of Bcl-xl was noted in 27.7% of patients in normal epithelium and in 66.1% within dysplastic lesions. Bcl-xl expression in dysplastic glandular cells correlated with the presence of neutrophils in the lamina propria (p <0.05). Conclusions: The immunohistochemical expressions of Bax, Bcl-2 and Bcl-xl increase and Bid protein expression decreases in dysplastic glandular tubes as compared to non-dysplastic intestinal epithelium in inflamed mucosa, which may suggest an imbalance of controlled cell death in ulcerative colitis.
- Źródło:
-
Progress in Health Sciences; 2014, 4, 1; 75-82
2083-1617 - Pojawia się w:
- Progress in Health Sciences
- Dostawca treści:
- Biblioteka Nauki
Artykuł