卡哈尔间质细胞
CD44细胞
伊马替尼
病理
免疫染色
免疫印迹
免疫组织化学
生物
免疫荧光
细胞
川东北117
医学
癌症研究
川地34
免疫学
抗体
干细胞
细胞生物学
基因
生物化学
髓系白血病
遗传学
作者
Juan Han,Lei Zhang,Xia Li,Yaping Chen,Rong Yuan,Bai-gang Yan
出处
期刊:Cells Tissues Organs
[S. Karger AG]
日期:2020-01-01
卷期号:209 (4-6): 200-208
摘要
Loss of Kit protein expression is proven to influence the plasticity of interstitial cells of Cajal (ICCs) and may contribute to gastrointestinal (GI) dysfunctions. The role and fate of Kit negative ICCs are unclear, and cell-specific markers for the Kit ICCs are unknown. In this study, we treated adult mice with imatinib (a Kit signaling blocker) for 8 or 16 days and investigated whether CD44 is a specific marker for the Kit negative ICCs in the adult mouse colon. We aimed at examining the protein and mRNA level of CD44 and Kit by using Western blot and real-time RT-PCR, respectively. Our results indicated that Kit expression was downregulated for both protein and mRNA levels after imatinib treatment for 8 or 16 days as compared to the vehicle-treated mice. Interestingly, CD44 expression remained unchanged throughout the treatment. Immunostaining on whole-mount preparations for Kit and CD44 showed that CD44 was exclusively co-localized with Kit in the ICCs of the vehicle-treated mouse colon. After imatinib treatment, a number of CD44+/Kit- cells with elaborated processes were observed with an evident decrease of Kit+ cell number within the muscular layers (ICC-IM) and around the myenteric nerve plexus (ICC-MY) as compared to vehicle-treated mice. After discontinuing imatinib for 16 days, Kit+ ICC-MY and ICC-IM were completely co-localized with normalization of CD44 and Kit+ cell numbers. Overall, our results identify CD44 as a cell-specific surface marker for Kit-ICCs and may be useful to understand the role and fate of Kit- ICCs in GI disorders.
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