Histone Deacetylase 2 Is Upregulated in Normal and Keloid Scars

O’Connor, Edmund J. Fitzgerald; Badshah, Irbaz I; Addae, Lucy Y; Kundasamy, Preeya; Thanabalasingam, Sukanthini; Abioye, Daniel; Soldin, Mark; Shaw, Tanya J.

doi:10.1038/jid.2011.432

Cited by 39 publications

(23 citation statements)

References 15 publications

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“…The altered expression levels when compared to normal skin fibroblasts were also maintained by keloid fibroblasts over the culture lifetime. This again suggests sustained modulation of gene expression and implicates epigenetic change as being important in the maintenance of the keloid fibroblast phenotype …”

Section: Epigenetic Mechanisms In Keloid Scarringmentioning

confidence: 84%

From genetics to epigenetics: new insights into keloid scarring

Deng

Alghamdi

et al. 2017

Cell Proliferation

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Keloid scarring is a dermal fibroproliferative response characterized by excessive and progressive deposition of collagen; aetiology and molecular pathology underlying keloid formation and progression remain unclear. Genetic predisposition is important in the pathogenic processes of keloid formation, however, environmental factors and epigenetic mechanisms may also play pivotal roles. Epigenetic modification is a recent area of investigation in understanding the molecular pathogenesis of keloid scarring and there is increasing evidence that epigenetic changes may play a role in induction and persistent activation of fibroblasts in keloid scars. Here we have reviewed three epigenetic mechanisms: DNA methylation, histone modification and the role of non-coding RNAs. We also review the evidence that these mechanisms may play a role in keloid formation - in future, it may be possible that epigenetic markers may be used instead of prognostic or diagnostic markers here. However, there is a significant amount of work required to increase our current understanding of the role of epigenetic modification in keloid disease.

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Section: Epigenetic Mechanisms In Keloid Scarringmentioning

confidence: 84%

From genetics to epigenetics: new insights into keloid scarring

Deng

Alghamdi

et al. 2017

Cell Proliferation

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“…More evidence enforces the postulation that HDAC inhibitors directly regulate transdifferentiation of fibroblasts to myofibroblasts. 72 During scar formation, the HDAC2 protein amount is dramatically increased 73 and renal fibrosis is also successfully controlled by HDAC inhibitors. 74 75 …”

Section: The Role Of Hdacs In Cardiovascular Diseasesmentioning

confidence: 99%

HDAC and HDAC Inhibitor: From Cancer to Cardiovascular Diseases

2016

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Histone deacetylases (HDACs) are epigenetic regulators that regulate the histone tail, chromatin conformation, protein-DNA interaction, and even transcription. HDACs are also post-transcriptional modifiers that regulate the protein acetylation implicated in several pathophysiologic states. HDAC inhibitors have been highlighted as a novel category of anti-cancer drugs. To date, four HDAC inhibitors, Vorinostat, Romidepsin, Panobinostat, and Belinostat, have been approved by the United States Food and Drug Administration. Principally, these HDAC inhibitors are used for hematologic cancers in clinic with less severe side effects. Clinical trials are continuously expanding to address other types of cancer and also nonmalignant diseases. HDAC inhibition also results in beneficial outcomes in various types of neurodegenerative diseases, inflammation disorders, and cardiovascular diseases. In this review, we will briefly discuss 1) the roles of HDACs in the acquisition of a cancer's phenotype and the general outcome of the HDAC inhibitors in cancer, 2) the functional relevance of HDACs in cardiovascular diseases and the possible therapeutic implications of HDAC inhibitors in cardiovascular disease.

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“…Although histone acetylation is now well established to regulate gene expression during skin development and homeostasis, there is less information regarding its role during wound healing in the skin. Previous studies found Hdac1/2 expression in human migrating wound epithelial tongue and also in normal and keloid scars . Moreover, another group investigated the differential effects of different classes of HDAC chemical inhibitors during wound healing …”

Section: Epigenetic Reprogramming During Injury‐induced Epidermis Regmentioning

confidence: 99%

Epigenetic control in skin development, homeostasis and injury repair

Kang

Chovatiya

Tumbar

2019

Experimental Dermatology

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Cell‐type‐ and cell‐state‐specific patterns of covalent modifications on DNA and histone tails form global epigenetic profiles that enable spatiotemporal regulation of gene expression. These epigenetic profiles arise from coordinated activities of transcription factors and epigenetic modifiers, which result in cell‐type‐specific outputs in response to dynamic environmental conditions and signalling pathways. Recent mouse genetic and functional studies have highlighted the physiological significance of global DNA and histone epigenetic modifications in skin. Importantly, specific epigenetic profiles are emerging for adult skin stem cells that are associated with their cell fate plasticity and proper activity in tissue regeneration. We can now begin to draw a more comprehensive picture of how epigenetic modifiers orchestrate their cell‐intrinsic role with microenvironmental cues for proper skin development, homeostasis and wound repair. The field is ripe to begin to implement these findings from the laboratory into skin therapies.

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Histone Deacetylase 2 Is Upregulated in Normal and Keloid Scars

Cited by 39 publications

References 15 publications

From genetics to epigenetics: new insights into keloid scarring

From genetics to epigenetics: new insights into keloid scarring

HDAC and HDAC Inhibitor: From Cancer to Cardiovascular Diseases

Epigenetic control in skin development, homeostasis and injury repair

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