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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 379 - 384 (6page)
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Dexamethasone converts pluripotent pancreatic AR42J cels into exocrine cells expressing diges-tive enzymes. In order to adress molecular me-chanism of this diferentiation, we have investi-gated the role of mitogen-activated protein (MAP) kinase pathway and gene expresions of p21waf1/cip1 and nuclear oncogenes (c-fos and c-myc) during AR42J cell diferentiation. Dexamethasone marked-ly increased the intracellular and secreted amylase contents as wel as its mRNA level. However, cell growth and DNA content were significantly de-creased. With these phenotypic changes, AR42J cells induced transient mRNA expression of p21waf1/cip1gene, which reached maximal level by 6 h and then declined gradualy toward basal state. In contrast to p21waf1/cip1, c-fos gene expres-sion was transiently inhibited by 6 h and then recovered to basal level by 24 h. Increased c-myc expression detected after 3 h, peaked by 12 h, and remained elevated during the rest of observation. Dexamethasone inhibited epidermal growth factor- induced phosphorylation of extracelular signal regulated kinase. Inhibition of MAP kinase pathway by PD98059 resulted in further elevation of the de-xamethasone-induced amylase mRNA and p21waf1/cip1 gene expression. These results sugest that p21waf1/cip1 and nuclear oncogenes are involved in dexamethasone-induced diferentiation and inhi-bition of MAP kinase pathway accelerates the con-version of undiferentiated AR42J cels into am-ylase-secreting exocrine cels.
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