Role of HDAC1 in senescence, aging, and cancer

Willis-Martinez, Danielle; Richards, Hunter W.; Timchenko, Nikolai A.; Medrano, Estela E.

doi:10.1016/j.exger.2009.10.001

Cited by 72 publications

(65 citation statements)

References 59 publications

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“…Histone deacetylases related to Hdac3, Hdac1, and Sirt1, are known to play important roles in aging liver (Jin et al, 2011; Willis-Martinez et al, 2010). Liver-specific deletion of Hdac3 leads to fatty liver, a phenotype associated with aging, due to de-repression of nuclear hormone receptor-dependent gene expression (Sun et al, 2012) (Knutson et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Aging is associated with increased prevalence of metabolic disease and cancer, reduced capacity for tissue regeneration, and physical decline (Rodriguez et al, 2007; Willis-Martinez et al, 2010). In particular, triglyceride accumulation is the common metabolic phenotype of aging liver and of metabolic syndrome, an age-related disorder that increases the risk of developing diabetes and cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

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Changes in Nucleosome Occupancy Associated with Metabolic Alterations in Aged Mammalian Liver

et al. 2014

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Summary Aging is accompanied by physiological impairments, which, in insulin-responsive tissues, including the liver, predispose individuals to metabolic disease. However, the molecular mechanisms underlying these changes remain largely unknown. Here, we analyze genome-wide profiles of RNA and chromatin organization in the liver of young (3 months) and old (21 months) mice. Transcriptional changes suggest that de-repression of the nuclear receptors PPARα, PPARγ, and LXRα in aged mouse liver leads to activation of targets regulating lipid synthesis and storage, whereas age-dependent changes in nucleosome occupancy are associated with binding sites for both known regulators (forkhead factors and nuclear receptors) and for novel candidates associated with nuclear lamina (Hdac3 and Srf) implicated to govern metabolic function of aging liver. Winged-helix transcription factor Foxa2 and nuclear receptor co-repressor Hdac3 exhibit reciprocal binding pattern at PPARα targets contributing to gene expression changes that lead to steatosis in aged liver.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Changes in Nucleosome Occupancy Associated with Metabolic Alterations in Aged Mammalian Liver

et al. 2014

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“…Some findings imply functional roles for HDAC2 in the maturation of neural cells 10, 11, 27-29, especially in migration and differentiation 13. In addition, HDAC2 can affect basic excitatory neurotransmission 26, 29, 30. Thus, the specific characteristics of HDAC2 expression may be one of the key elements of normal development of the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Spatiotemporal Expression of HDAC2 during the Postnatal Development of the Rat Hippocampus

Hou¹,

Gong²,

Bi³

et al. 2014

Int. J. Med. Sci.

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Background: Histone acetylation, which is a chromatin modification of histone tails, can dynamically regulate the expression of various genes in normal development. HDAC2 is a negative regulatory factor of acetylation and closely related to learning and memory. NSE is a nerve marker and vital for maintaining physiological functions in nervous system. Currently, few studies associated with the expression pattern of HDAC2 in postnatal rat hippocampus have been reported. This study aimed to explore the temporal and spatial expression pattern of HDAC2, helping to reveal the expression characteristics of HDAC2 during postnatal neuronal maturation. Materials and Methods: With NSE as a biomarker of neuronal maturation at postnatal days 1, 3, 7 and weeks 2, 4, and 8 (P1D, P3D, P7D, P2W, P4W, P8W), the expression patterns of HDAC2 in rat hippocampus were examined using real-time PCR and western blotting. Additionally, the subcellular distribution of HDAC2 was analysed by immunofluorescence. Results: We found that HDAC2 was highly expressed in the neonatal period and decreased gradually. HDAC2 expression was widely distributed in neurons of hippocampal CA1, CA3 and DG regions and gradually shifted from the nucleus to the cytoplasm during postnatal development. Altogether, the expression of HDAC2 decreased gradually with different subcellular localizations throughout development. Conclusions: The observed results indicate that the expression levels of HDAC2 become lower and with different subcellular localizations in neurons during hippocampal neuronal maturation, suggesting the specific expression characteristics of HDAC2 might play an important role during postnatal learning-memory function and development.

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“…This allele will enable dissection of the spatiotemporally specific expression patterning of Hdac1 in development and disease. HDAC1 expression variance is important in a number of human diseases, including several cancers (Kawai et al, 2003; Halkidou et al, 2004; Willis-Martinez et al, 2010). With this allele, the spatiotemporal expression dynamics of Hdac1 can be explored in mouse models of these diseases.…”

Section: Discussionmentioning

confidence: 99%

Histone deacetylase 1 and 2 are essential for murine neural crest proliferation, pharyngeal arch development, and craniofacial morphogenesis

Milstone

Lawson

Trivedi

2017

Developmental Dynamics

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Background Craniofacial anomalies involve defective pharyngeal arch development and neural crest function. Copy number variation at 1p35, containing histone deacetylase 1 (Hdac1), or 6q21-22, containing Hdac2, are implicated in patients with craniofacial defects, suggesting an important role in guiding neural crest development. However, the roles of Hdac1 and Hdac2 within neural crest cells remain unknown. Results The neural crest and its derivatives express both Hdac1 and Hdac2 during early murine development. Ablation of Hdac1 and Hdac2 within murine neural crest progenitor cells cause severe hemorrhage, atrophic pharyngeal arches, defective head morphogenesis, and complete embryonic lethality. Embryos lacking Hdac1 and Hdac2 in the neural crest exhibit decreased proliferation and increased apoptosis in both the neural tube and the first pharyngeal arch. Mechanistically, loss of Hdac1 and Hdac2 upregulates cyclin-dependent kinase inhibitors Cdkn1a, Cdkn1b, Cdkn1c, Cdkn2b, Cdkn2c, and Tp53 within the first pharyngeal arch. Conclusions Our results show that Hdac1 and Hdac2 function redundantly within the neural crest to regulate proliferation and the development of the pharyngeal arches via repression of cyclin-dependent kinase inhibitors.

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Role of HDAC1 in senescence, aging, and cancer

Cited by 72 publications

References 59 publications

Changes in Nucleosome Occupancy Associated with Metabolic Alterations in Aged Mammalian Liver

Changes in Nucleosome Occupancy Associated with Metabolic Alterations in Aged Mammalian Liver

Spatiotemporal Expression of HDAC2 during the Postnatal Development of the Rat Hippocampus

Histone deacetylase 1 and 2 are essential for murine neural crest proliferation, pharyngeal arch development, and craniofacial morphogenesis

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