UV induced responses of the human epidermal IGF system: Impaired anti-apoptotic effects of IGF-I in HaCaT keratinocytes
Autor: | Christopher J. Wraight, George A. Werther, Susan P. Thumiger, Timothy E. Adams, Stephanie R. Edmondson |
---|---|
Rok vydání: | 2005 |
Předmět: |
Keratinocytes
medicine.medical_specialty Time Factors Cell Survival Ultraviolet Rays Blotting Western Clinical Biochemistry Apoptosis Ligands Cell Line Endocrinology Growth factor receptor Cell Line Tumor Internal medicine medicine Homeostasis Humans RNA Messenger Insulin-Like Growth Factor I Phosphorylation Receptor Cell Proliferation integumentary system Reverse Transcriptase Polymerase Chain Reaction Chemistry Cell growth Receptors Somatomedin Cell Biology Molecular biology HaCaT Insulin-Like Growth Factor Binding Protein 3 medicine.anatomical_structure Cell culture Tyrosine Epidermis Keratinocyte |
Zdroj: | Growth Factors. 23:151-159 |
ISSN: | 1029-2292 0897-7194 |
DOI: | 10.1080/08977190500153680 |
Popis: | The insulin-like growth factor receptor (IGF-IR) is critical in epidermal development and IGF binding protein-3 (IGFBP-3), a modulator of cellular activity with or without IGF-dependence, co-localises with epidermal IGF-IRs. We have investigated whether the greater UV susceptibility of a human keratinocyte cell line (HaCaT) in comparison to normal human keratinocytes (NHKs) may involve differences in the IGF system. At 24 h after UV (960 mJ/cm(2) UVB), in comparison to NHKs, HaCaT keratinocytes exhibited significantly higher levels of apoptosis, refractoriness to IGF-I treatment and reduced IGF-IR phosphorylation. Secreted, intact IGFBP-3 (38-42 kDa) and IGFBP-3 mRNA abundance were reduced in HaCaT keratinocytes, but not consistently altered in NHKs. Immunoreactive IGFBP-3 fragments (16-11 kDa) were detected in both UV-exposed cultures. These data suggest that an altered IGF system contributes to HaCaT keratinocyte UV susceptibility and that following UV insult the IGF system may enhance keratinocyte viability and contribute to a return to epidermal homeostasis. |
Databáze: | OpenAIRE |
Externí odkaz: |