CAJ | 학술논문

目的：探讨P57kip2、CDK5在神经管发育缺陷（NTD）发生过程中与正常组织的差异表达，为研究正常神经胚形成的分子机制提供线索。方法用含有1100余个已知基因的中密度芯片比较胚胎（embryonic，E）9．5、10．5d正常与同期维甲酸（RA）诱导致NTD小鼠神经管组织的P57kip2、CDK5基因表达差异，并对芯片结果进行Northern杂交验证。结果通过比较P57kip2、CDK5基因在正常E9．5d与E10．5d、E9．5d-NTD、E10．5d-NTD的表达差异，发现在正常神经胚形成前后P57kip2、CDK5表达显著上调，在RA诱导致NTD（包括E9．5d与E10．5d两个时相）P57kip2、CDK5在RA作用后呈现下调趋势。结论P57kip2、CDK5参与了神经管发育缺陷的发生过程，为研究正常神经胚形成的分子机制提供了有益线索。
목적：탐토P57kip2、CDK5재신경관발육결함（NTD）발생과정중여정상조직적차이표체，위연구정상신경배형성적분자궤제제공선색。방법용함유1100여개이지기인적중밀도심편비교배태（embryonic，E）9．5、10．5d정상여동기유갑산（RA）유도치NTD소서신경관조직적P57kip2、CDK5기인표체차이，병대심편결과진행Northern잡교험증。결과통과비교P57kip2、CDK5기인재정상E9．5d여E10．5d、E9．5d-NTD、E10．5d-NTD적표체차이，발현재정상신경배형성전후P57kip2、CDK5표체현저상조，재RA유도치NTD（포괄E9．5d여E10．5d량개시상）P57kip2、CDK5재RA작용후정현하조추세。결론P57kip2、CDK5삼여료신경관발육결함적발생과정，위연구정상신경배형성적분자궤제제공료유익선색。
Objective To investigate the differential expression of P57kip2 and CDK5 in neural tube defects t(NTD) from the normal ,and provide the clue for the research of the molecular mechanism of the normal neurula formation .Methods A cDNA mi-croarray containing 1 100 known genes was used to compare differences in P57kip2 and CDK5 gene expression between the normal control group and the retinoic acid(RA)-induced NTD group on embryonic(E) day 9 .5 and 10 .5 .Two differentially expressed genes were randomly selected from the two groups for Northern blotting to verify the results of the cDNA microarray .Results Compared the differences of between P57kip2 and CDK5 in normal and E9 .5 d ,E10 .5 d ,E9 .5 d-NTD ,E10 .5 d-NTD ,P57kip2 and CDK5 expression was significantly up-regulated in the before and after the formation of the normal neurulation ,but them showed a downward trend in retinoic acid (RA)-induced NTD(including two phase E9 .5 d and E10 .5 d) .Conclusion P57kip2 and CDK5 in-volved in the physiological process of NTD ,and provide the useful clue for the research of the molecular mechanism of the normal neurula formation .