p38 but not p53 is responsible for UVA-induced MCPIP1 expression.
Mech Ageing Dev
; 172: 96-106, 2018 06.
Article
em En
| MEDLINE
| ID: mdl-29103983
ABSTRACT
MCPIP1 (Monocyte Chemotactic Protein-1 Induced Protein) is an important regulator of inflammation and cell apoptosis, but its role in UVA-induced stress response in the epidermis has never been studied. We have found that moderate apoptosis-inducing dose of UVA (27J/cm2) increases the level of MCPIP1 expression in HaCaT cells and normal human keratinocytes (NHEK) within 6-9h after the treatment. MCPIP1 upregulation was dependent on the induction of p38, but not p53, as demonstrated by using p38 inhibitor SB203580 and p53 inducer RG7388, respectively. This increase was also blocked by antioxidants (α-tocopherol and ascorbic acid), suggesting the involvement of MCPIP1 in UVA-induced oxidative stress response. Si-RNA-mediated down-regulation of MCPIP1 expression in HaCaT cells resulted in increased sensitivity to UVA-induced DNA damage and apoptosis. This was accompanied by decreased phosphorylation of p53 and p38 in MCPIP1-silenced cells following UVA irradiation. The activation of p38 in response to low doses of ultraviolet radiation was postulated to be protective for p53-inactive cells. Therefore, MCPIP1 may favor the survival of p53-defective HaCaT cells by sustaining the activation of p38. This creates a loop of mutual positive regulation between p38 and MCPIP1 protein in HaCaT cells, providing the protection against the consequences of UVA irradiation.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Ribonucleases
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Fatores de Transcrição
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Raios Ultravioleta
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Regulação da Expressão Gênica
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Proteína Supressora de Tumor p53
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Apoptose
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Proteínas Quinases p38 Ativadas por Mitógeno
Limite:
Humans
Idioma:
En
Revista:
Mech Ageing Dev
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
Polônia