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1.
Biol Res ; 48: 23, 2015 May 06.
Artículo en Inglés | MEDLINE | ID: mdl-25943891

RESUMEN

BACKGROUND: Hepcidin, encoding by HAMP gene, is the pivotal regulator of iron metabolism, controlling the systemic absorption and transportation of irons from intracellular stores. Abnormal levels of HAMP expression alter plasma iron parameters and lead to iron metabolism disorders. Therefore, it is an important goal to understand the mechanisms controlling HAMP gene expression. RESULTS: Overexpression of Sox2 decrease basal expression of HAMP or induced by IL-6 or BMP-2, whereas, knockdown of Sox2 can increase HAMP expression, furthermore, two potential Sox2-binding sites were identified within the human HAMP promoter. Indeed, luciferase experiments demonstrated that deletion of any Sox2-binding site impaired the negative regulation of Sox2 on HAMP promoter transcriptional activity in basal conditions. ChIP experiments showed that Sox2 could directly bind to these sites. Finally, we verified the role of Sox2 to negatively regulate HAMP expression in human primary hepatocytes. CONCLUSION: We found that Sox2 as a novel factor to bind with HAMP promoter to negatively regulate HAMP expression, which may be further implicated as a therapeutic option for the amelioration of HAMP-overexpression-related diseases, including iron deficiency anemia.


Asunto(s)
Regulación Neoplásica de la Expresión Génica/genética , Hepatocitos/metabolismo , Hepcidinas/genética , Factores de Transcripción SOXB1/genética , Anemia/genética , Anemia/metabolismo , Sitios de Unión , Proteína Morfogenética Ósea 2/metabolismo , Técnicas de Silenciamiento del Gen , Vectores Genéticos , Células Hep G2 , Hepcidinas/metabolismo , Humanos , Interleucina-6/metabolismo , Hierro/metabolismo , Luciferasas , Plásmidos/genética , Regiones Promotoras Genéticas/genética , Factores de Transcripción SOXB1/metabolismo
2.
Biol. Res ; 48: 1-8, 2015. graf
Artículo en Inglés | LILACS | ID: biblio-950787

RESUMEN

BACKGROUND: Hepcidin, encoding by HAMP gene, is the pivotal regulator of iron metabolism, controlling the systemic absorption and transportation of irons from intracellular stores. Abnormal levels of HAMP expression alter plasma iron parameters and lead to iron metabolism disorders. Therefore,itis animportant goal to understand the mechanisms controlling HAMP gene expression. RESULTS: Overexpression of Sox2 decrease basal expression of HAMP or induced by IL-6 or BMP-2, whereas, knockdown of Sox2 can increase HAMP expression, furthermore, two potential Sox2-binding sites were identified within the human HAMP promoter. Indeed, luciferase experiments demonstrated that deletion of any Sox2-binding site impaired the negative regulation of Sox2 on HAMP promoter transcriptional activity in basal conditions. ChIP experiments showed that Sox2 could directly bind to these sites. Finally, we verified the role of Sox2 to negatively regulate HAMP expression in human primary hepatocytes. CONCLUSION: We found that Sox2 as a novel factor to bind with HAMP promoter to negatively regulate HAMP expression, which may be further implicated as a therapeutic option for the amelioration of HAMP-overexpression-related diseases, including iron deficiency anemia.


Asunto(s)
Humanos , Regulación Neoplásica de la Expresión Génica/genética , Hepatocitos/metabolismo , Factores de Transcripción SOXB1/genética , Hepcidinas/genética , Plásmidos/genética , Sitios de Unión , Interleucina-6/metabolismo , Regiones Promotoras Genéticas/genética , Proteína Morfogenética Ósea 2/metabolismo , Factores de Transcripción SOXB1/metabolismo , Técnicas de Silenciamiento del Gen , Células Hep G2 , Hepcidinas/metabolismo , Vectores Genéticos , Anemia/genética , Anemia/metabolismo , Hierro/metabolismo , Luciferasas
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