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IUGR prevents IGF-1 upregulation in juvenile male mice by perturbing postnatal IGF-1 chromatin remodeling.
Fung, Camille M; Yang, Yueqin; Fu, Qi; Brown, Ashley S; Yu, Baifeng; Callaway, Christopher W; Li, Jicheng; Lane, Robert H; McKnight, Robert A.
Afiliação
  • Fung CM; Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
  • Yang Y; 1] Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah [2] Institute of Cell Biology, Zhejiang University, Hangzhou, Zhejiang, China.
  • Fu Q; Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
  • Brown AS; Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
  • Yu B; Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
  • Callaway CW; Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
  • Li J; Institute of Cell Biology, Zhejiang University, Hangzhou, Zhejiang, China.
  • Lane RH; Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
  • McKnight RA; Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Pediatr Res ; 78(1): 14-23, 2015 Jul.
Article em En | MEDLINE | ID: mdl-25826117
BACKGROUND: Intrauterine growth restriction (IUGR) offspring with rapid catch-up growth are at increased risk for early obesity especially in males. Persistent insulin-like growth factor-1 (IGF-1) reduction is an important risk factor. Using a mouse model of maternal hypertension-induced IUGR, we examined IGF-1 levels, promoter DNA methylation, and histone H3 covalent modifications at birth (D1). We additionally investigated whether prenatal perturbations could reset at preadolescence (D21). METHODS: IUGR was induced via maternal thromboxane A2-analog infusion in mice. RESULTS: IUGR uniformly decreased D1 IGF-1 mRNA and protein levels with reduced promoter 1 (P1) transcription and increased P1 DNA methylation. IUGR males also had increased H3K4ac at exon 5 and 3' distal UTR. At D21, IUGR males continued to have decreased IGF-1 levels, originating from both P1 and P2 with reduced 1A variant. IUGR males also had decreased activation mark of H3K4me3 at P1 compared with sham males. In contrast, D21 IUGR females normalized their IGF-1 levels, in association with an increased activation mark of H3K4me3 at P1 compared with sham females. CONCLUSION: IUGR uniformly affected D1 hepatic IGF-1 epigenetic modifications in both sexes. However, at preadolescence, IUGR males are unable to correct for the prenatal reduction possibly due to a more perturbed IGF-1 chromatin structure.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fator de Crescimento Insulin-Like I / Regulação da Expressão Gênica no Desenvolvimento / Montagem e Desmontagem da Cromatina / Retardo do Crescimento Fetal Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: Pediatr Res Ano de publicação: 2015 Tipo de documento: Article País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fator de Crescimento Insulin-Like I / Regulação da Expressão Gênica no Desenvolvimento / Montagem e Desmontagem da Cromatina / Retardo do Crescimento Fetal Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: Pediatr Res Ano de publicação: 2015 Tipo de documento: Article País de publicação: Estados Unidos