Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death
Louafi, F. ; Stewart, C. E. H. ; Perks, C. M. ; Thomas, M. G. ; Holly, J. M. P.
Oxford, UK : Munksgaard International Publishers
Published 2003
Oxford, UK : Munksgaard International Publishers
Published 2003
| ISSN: |
1600-0625
|
|---|---|
| Source: |
Blackwell Publishing Journal Backfiles 1879-2005
|
| Topics: |
Medicine
|
| Notes: |
Abstract: 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 [leu27 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.
|
| Type of Medium: |
Electronic Resource
|
| URL: |
| _version_ | 1798290491298545664 |
|---|---|
| autor | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. |
| autorsonst | Thomas, M. G. Holly, J. M. P. |
| book_url | http://dx.doi.org/10.1034/j.1600-0625.2003.00080.x |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLZ242384587 |
| insertion_date | 2012-04-27 |
| issn | 1600-0625 |
| journal_name | Experimental dermatology |
| materialart | 1 |
| notes | Abstract: 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 [leu27 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. |
| package_name | Blackwell Publishing |
| publikationsjahr_anzeige | 2003 |
| publikationsjahr_facette | 2003 |
| publikationsjahr_intervall | 7999:2000-2004 |
| publikationsjahr_sort | 2003 |
| publikationsort | Oxford, UK |
| publisher | Munksgaard International Publishers |
| reference | 12 (2003), S. 0 |
| search_space | articles |
| shingle_author_1 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. |
| shingle_author_2 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. |
| shingle_author_3 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. |
| shingle_author_4 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. |
| shingle_catch_all_1 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death Munksgaard International Publishers Abstract: 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 [leu27 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. 1600-0625 16000625 |
| shingle_catch_all_2 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death Munksgaard International Publishers Abstract: 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 [leu27 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. 1600-0625 16000625 |
| shingle_catch_all_3 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death Munksgaard International Publishers Abstract: 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 [leu27 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. 1600-0625 16000625 |
| shingle_catch_all_4 | Louafi, F. Stewart, C. E. H. Perks, C. M. Thomas, M. G. Holly, J. M. P. Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death Munksgaard International Publishers Abstract: 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 [leu27 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. 1600-0625 16000625 |
| shingle_title_1 | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| shingle_title_2 | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| shingle_title_3 | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| shingle_title_4 | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| sigel_instance_filter | dkfz geomar wilbert ipn albert |
| source_archive | Blackwell Publishing Journal Backfiles 1879-2005 |
| timestamp | 2024-05-06T08:17:34.884Z |
| titel | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| titel_suche | Role of the IGF-II receptor in mediating acute, non-genomic effects of retinoids and IGF-II on keratinocyte cell death |
| topic | WW-YZ |
| uid | nat_lic_papers_NLZ242384587 |