Academic Journal

Role of the IGF‐II receptor in mediating acute, non‐genomic effects of retinoids and IGF‐II on keratinocyte cell death

التفاصيل البيبلوغرافية
العنوان: Role of the IGF‐II receptor in mediating acute, non‐genomic effects of retinoids and IGF‐II on keratinocyte cell death
المؤلفون: Louafi, F., Stewart, C. E. H., Perks, C. M., Thomas, M. G., Holly, J. M. P.
المصدر: Experimental Dermatology ; volume 12, issue 4, page 426-434 ; ISSN 0906-6705 1600-0625
بيانات النشر: Wiley
سنة النشر: 2003
المجموعة: Wiley Online Library (Open Access Articles via Crossref)
الوصف: In this study, we have examined the effects of retinoic acid (RA) on the human immortalized keratinocyte cell line (HaCaT). A significant twofold ( P < 0.01) increase in apoptotic cell death compared with the control was found within 24 h of treatment with 10 −5 M of RA. Apoptosis was confirmed by flow cytometry. Cycloheximide did not inhibit this acute RA‐induced apoptosis. Interestingly, insulin‐like growth factor‐II (IGF‐II, 50 ng/ml) was able to significantly (67.3%; P < 0.05) reduce RA effects, whereas IGF‐I (50 ng/ml) and insulin (75 ng/ml) were without effect. Furthermore, analogues of IGF‐II [leu 27 IGF‐II and Des(1‐6) IGF‐II], with altered affinities for the IGF‐I receptor and IGF‐binding proteins (IGFBPs), but retained affinities for the IGF‐II receptor, also completely inhibited (100%; P < 0.01) RA‐induced apoptosis, while an IGF‐I receptor antagonist did not reduce the survival effects of IGF‐II. Insulin pretreatment negates the survival effect of IGF‐II. In contrast, mannose 6 phosphate (M6P) did not alter RA or IGF‐II actions. These results indicate that rapid induction of cell death by RA is independent of production or secretion of new proteins. The inhibition of RA action by IGF‐II was independent of its ability to signal through the IGF‐I receptor or to interact with IGFBPs.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1034/j.1600-0625.2003.00080.x
الاتاحة: http://dx.doi.org/10.1034/j.1600-0625.2003.00080.x
https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1034%2Fj.1600-0625.2003.00080.x
https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1600-0625.2003.00080.x
Rights: http://onlinelibrary.wiley.com/termsAndConditions#vor
رقم الانضمام: edsbas.92C53D3B
قاعدة البيانات: BASE
الوصف
DOI:10.1034/j.1600-0625.2003.00080.x