Genomic analysis of insulin-like growth factor-I gene transfer in thermally injured rats
Autor: | Mohan R. K. Dasu, David N. Herndon, Marcus Spies, J. Regino Perez-Polo |
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Rok vydání: | 2004 |
Předmět: |
Male
Programmed cell death Kininogen High-Molecular-Weight medicine.medical_treatment Thermal trauma Inflammation Dermatology Biology Immediate-Early Proteins RNA Complementary Rats Sprague-Dawley Insulin-like growth factor Western blot Gene expression medicine Animals RNA Messenger Insulin-Like Growth Factor I Gene Early Growth Response Protein 1 Oligonucleotide Array Sequence Analysis medicine.diagnostic_test Gene Transfer Techniques Molecular biology Rats DNA-Binding Proteins Insulin-Like Growth Factor Binding Protein 1 Liver Surgery DNA microarray medicine.symptom Burns Transcription Factors |
Zdroj: | Wound Repair and Regeneration. 12:217-224 |
ISSN: | 1524-475X 1067-1927 |
DOI: | 10.1111/j.1067-1927.2004.012114.x |
Popis: | Thermal trauma causes tissue damage by membrane destabilization and energy depletion at the cellular level, resulting in tissue necrosis and inflammation leading to delayed cell death. One therapeutic approach is to block the immediate triggering of the inflammatory cascade that results in prolonged hypermetabolic responses and immune dysfunction while promoting the expression of growth factors. In the present study, we determined hepatic gene expression responses to insulin-like growth factors-i (IGF-I) gene transfer to burned rats using high-density DNA microarray assays. The expression of 123 out of approximately 8,800 genes assayed (1.4% of total) were significantly altered. Of these, 42 genes were altered irrespective of treatment by burn trauma (p < 0.05). Changes in gene expression were confirmed by measuring mRNA levels using reverse transcription-polymerase chain reaction and protein levels by Western blot assays. DNA microarray analyses showed two major mechanisms that mediated beneficial outcomes after IGF-I gene transfer in the burned rat livers. These mechanisms were the stimulation of IGF binding protein potentiation of peripheral IGF-I and the inhibition of the burn-augmented pro-apoptotic and oxidative mitochondrial metabolites stimulated by thermal trauma. |
Databáze: | OpenAIRE |
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