Hdac-mediated control of endochondral and intramembranous ossification

Elizabeth W. Bradley, Meghan Elizabeth McGee Lawrence, Jennifer J. Westendorf

Research output: Contribution to journalReview article

34 Citations (Scopus)

Abstract

Histone deacetylases (Hdacs) remove acetyl groups (CH3CO-) from e-amino groups in lysine residues within histones and other proteins. This posttranslational (de) modification alters protein stability, protein-protein interactions, and chromatin structure. Hdac activity plays important roles in the development of all organs and tissues, including the mineralized skeleton. Bone is a dynamic tissue that forms and regenerates by two processes: endochondral and intramembranous ossification. Chondrocytes and osteoblasts are responsible for producing the extracellular matrices of skeletal tissues. Several Hdacs contribute to the molecular pathways and chromatin changes that regulate tissue-specific gene expression during chondrocyte and osteoblast specification, maturation, and terminal differentiation. In this review, we summarize the roles of class I and class II Hdacs in chondrocytes and osteoblasts. The effects of small molecule Hdac inhibitors on the skeleton are also discussed.

Original languageEnglish (US)
Pages (from-to)101-113
Number of pages13
JournalCritical Reviews in Eukaryotic Gene Expression
Volume21
Issue number2
StatePublished - Nov 14 2011
Externally publishedYes

Fingerprint

Osteogenesis
Histone Deacetylases
Chondrocytes
Osteoblasts
Skeleton
Chromatin
Proteins
Protein Stability
Post Translational Protein Processing
Histones
Lysine
Extracellular Matrix
Gene Expression
Bone and Bones

Keywords

  • Cartilage
  • Chondrocytes
  • Lysine deacetylase
  • Osteoblasts
  • Runx2

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

Cite this

Hdac-mediated control of endochondral and intramembranous ossification. / Bradley, Elizabeth W.; McGee Lawrence, Meghan Elizabeth; Westendorf, Jennifer J.

In: Critical Reviews in Eukaryotic Gene Expression, Vol. 21, No. 2, 14.11.2011, p. 101-113.

Research output: Contribution to journalReview article

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