Role For Apoptosis-associated Proteins Fas, FasL And Bcl-2 In Abnormal Proliferation, Differentiation And Apoptosis Of Epithelial Cells In Nasal Polyps

BACKGROUND/OBJACTIVES ; Proliferation, apoptosis and differentiation, three kinds of cellular essential physiological characteristics, are nearly relative to maintenance physiological functions, and to pathogenesis, in organism. It has been approved disorders of proliferation, apoptosis and differentiation of epithelial cells in nasal polyps being associated with the pathogenesis of nasal polyps. Investigations on proliferation, apoptosis and differentiation of epithelial cells in nasal polyps, consequently, help to deep understand the pathogenesis of nasal polyps. Interaction among Fas-FasL system mediated apoptosis mechanism, Bcl-2 mediated apoptosis inhibition mechanism and FasL mediated cell immune escape mechanism, plays an important role in regulating control on the balance between proliferation and apoptosis as well as cellular differentiation. METHORDS: 29 nasal polyp cases in treatment group, 11 normal inferior turbinate cases in control group. All specimens were proved by formallin-fixed paraffin-embedded hematoxylin-eosin staining. By immunohistochemical staining [Elivision? two-step kit (Maxim Biotech Cat.No.9801, 9804)],we researched the protein expressions of Fas, FasL, Bcl-2 , PCNA, CK14, CK18 and CK13. Through TUNEL technique [In Situ Cell Death Detection Kit, POD (Roche Molecular Biochemicals Cat.No. 1684817)], we surveyed apoptosis cells in site. RESULTS; (1) Both PIPcNA(53.60 11.10)andAK29.48 8.20)of epithelial cells in nasal polyps are prominently larger than that of epithelial cells in normal inferior turbinate (30.02 5.89, 5.33 2.79, respectively) .(2)Of epithelial cells in nasal polyps , PIpcNA (53.60 11.10) > AI (29.48 8.20) .(3) PIpcNA/AK 1.95 0.66) of epithelial cells in nasal polyps is less than that of epithelial cells in normal inferior turbinate ( 6.93 3.32 ) . This demonstrates that increasing range of proliferation actability of epithelialcells in nasal polyps is inconsistent with that of apoptosis actability, which is of larger increasing range. (4)PIcK14 (39.74 10.65), PIcKi8 (62.12 15.15)and LERcK13(13/28) of epithelial cells in nasal polyps are all prominently larger than that of epithelial cells in normal inferior turbinate (12.34 6.86, 41.73 8.62, 2/11, respectively) .Beyond epithelia in nasal polyps, micro-glands with higher CK18 protein expression are associated with CK18-positive epithelial cells in nasal polyps, continuously and gradually changing in microtopography. In epithelial cells of nasal polyps, "gland-like cells" hyperplasia, squamatization and inverted papilloma-like transformation phenomenon's are more common. (5)PIFas (27.70 10.06)> PlfasL (33.97 18.56) and PIBcl-2 (49.7U12.38) of epithelial cells in nasal polyps are all prominently larger than that of epithelial cells in normal inferior turbinate (11.03 4.05, 9.28 3.35, 8.58 4.84, respectively) . Of epithelial cells in nasal polyps, PIpasL (33.97 18.56) and PIBd-2 (49.71 12.38) are all prominently larger than PIFas (27.70 10.06). PIpasL/PIFas (1.57 1.28) of epithelial cells in nasal polyps is of no significant difference compared with that of epithelial cells in normal inferior turbinate (1.00 0.58) , however, PlBci-2/PIpas (2.53 2.35) of epithelial cells in nasal polyps is prominently larger than that of epithelial cells in normal inferior turbinate (0.88 0.59) CONCLUSIONS; (1)Increasing range of proliferation actability of epithelial cells in nasal polyps is inconsistent with that of apoptosis actability, the latter is of larger increasing range. However, proliferation actability, taking one with another, is higher than apoptosis actability of epithelial cells in nasal polyps, resulting in apoptosis insufficient to balance proliferation accompanied by increasing cell accumulation. This may be the reason why over-proliferation and abnormal cellular differentiation of epithelial cells in nasal...