The Epigenetic Regulation of Wound Healing

Lewis, Christopher J.; Mardaryev, Andrei N.; Sharov, Andrey A.; Fessing, Michael Y.; Botchkarev, Vladimir A.

doi:10.1089/wound.2014.0522

Cited by 49 publications

(49 citation statements)

References 80 publications

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“…Previous studies found Hdac1/2 expression in human migrating wound epithelial tongue [127,128] and also in normal and keloid scars. [129] Moreover, another group investigated the differential effects of different classes of HDAC chemical inhibitors during wound healing.…”

Section: Histone Methylation and Acetylation During Re-epithelizationmentioning

confidence: 96%

“…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%

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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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Section: Histone Methylation and Acetylation During Re-epithelizationmentioning

confidence: 96%

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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“…Epigenetic mechanisms are important in regulating the wound healing processes, including keratinocyte proliferation, differentiation, and migration, together with dermal regeneration and neoangiogenesis (Lewis et al, 2014). The histone deacetylase (HDAC) inhibitor trichostatin A (TSA) has potent antifibrogenic effects in a mouse model of bleomycininduced skin fibrosis (Huber et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Caveolin-1 Controls Hyperresponsiveness to Mechanical Stimuli and Fibrogenesis-Associated RUNX2 Activation in Keloid Fibroblasts

Hsu

Lin

Harn

et al. 2018

Journal of Investigative Dermatology

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Keloids are pathological scars characterized by excessive extracellular matrix production that are prone to form in body sites with increased skin tension. CAV1, the principal coat protein of caveolae, has been associated with the regulation of cell mechanics, including cell softening and loss of stiffness sensing ability in NIH3T3 fibroblasts. Although CAV1 is present in low amounts in keloid fibroblasts (KFs), the causal association between CAV1 down-regulation and its aberrant responses to mechanical stimuli remain unclear. In this study, atomic force microscopy showed that KFs were softer than normal fibroblasts with a loss of stiffness sensing. The decrease of CAV1 contributed to the hyperactivation of fibrogenesis-associated RUNX2, a transcription factor germane to osteogenesis/chondrogenesis, and increased migratory ability in KFs. Treatment of KFs with trichostatin A, which increased the acetylation level of histone H3, increased CAV1 and decreased RUNX2 and fibronectin. Trichostatin A treatment also resulted in cell stiffening and decreased migratory ability in KFs. Collectively, these results suggest a role for CAV1 down-regulation in linking the aberrant responsiveness to mechanical stimulation and extracellular matrix accumulation with the progression of keloids, findings that may lead to new developments in the prevention and treatment of keloid scarring.

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“…Cellular responses after injury rely on transient changes in the expression of a great number of genes. Recent findings suggest that epigenetic changes play an important part in the modification of gene expression, but the mechanisms of dynamic epigenetic remodeling during wound healing are virtually unexplored (Lewis et al, 2014). Within this context, the study by Na et al (2016) focuses on the role of the Jumonji domaincontaining protein D3 (JMJD3) histone demethylase in modulating the function of keratinocytes after injury.…”

mentioning

confidence: 99%

Epigenetic Control of Skin Re-Epithelialization: the NF-kB/JMJD3 Connection

Odorisio

2016

Journal of Investigative Dermatology

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Major changes in gene expression must occur at wound site to establish the cellular responses required for rapid healing. Although epigenetic remodeling plays a role in gene modulation, the mechanisms responsible for epigenetic regulation during healing are largely unknown. The study from Na et al. sheds light on the role of histone demethylase Jumonji domain-containing protein D3 in promoting keratinocyte function after injury, and it links Jumonji domain-containing protein D3-dependent gene expression to NK-kB activity.

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The Epigenetic Regulation of Wound Healing

Cited by 49 publications

References 80 publications

Epigenetic control in skin development, homeostasis and injury repair

Epigenetic control in skin development, homeostasis and injury repair

Caveolin-1 Controls Hyperresponsiveness to Mechanical Stimuli and Fibrogenesis-Associated RUNX2 Activation in Keloid Fibroblasts

Epigenetic Control of Skin Re-Epithelialization: the NF-kB/JMJD3 Connection

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