Dermal Wound Healing Is Subject to Redox Control

Roy, Sashwati; Khanna, Savita; Nallu, Kishore; Hunt, Thomas K.; Sen, Chandan K.

doi:10.1016/j.ymthe.2005.07.684

Cited by 383 publications

(371 citation statements)

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“…Moderate hypoxia, a potent angiogenic stimulus, induces Ets-1 promoter activity and Ets-1 expression via activation of HIF (43). Hydrogen peroxide, a well known pro-angiogenic stimulus (44,45), activates nuclear factor (erythroid-derived 2)-like 2, leading to binding to antioxidant response elements and subsequent enhancement of Ets-1 promoter activity (46). Retinoic acid induces angiogenesis (47), with concomitant induction of Ets-1 transactivation (48).…”

Section: Discussionmentioning

confidence: 99%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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Background:The role of miR-199a-5p in angiogenesis remains unclear. Results: miR-199a-5p exerts angiostatic effects by targeting Ets-1-MMP1 pathway and is down-regulated in skin wound healing. Conclusion: Down-regulation of miR-199a-5p switches on wound angiogenesis through derepressing of Ets-1-MMP1 pathway. Significance: This investigation provides novel mechanistic insight explaining miR-dependent regulation of wound angiogenesis and the foundation of developing therapeutic intervention in treating chronic nonhealing wounds.

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Section: Discussionmentioning

confidence: 99%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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“…The MoorLDI-Mark 2 laser Doppler bloodperfusion imager (Moor Instruments Ltd.) was used to map tissue blood flow, as described previously (4,36).…”

Section: Methodsmentioning

confidence: 99%

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

Biswas¹,

Roy²,

Banerjee³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Ischemia complicates wound closure. Here, we are unique in presenting a murine ischemic wound model that is based on bipedicle flap approach. Using this model of ischemic wounds we have sought to elucidate how microRNAs may be implicated in limiting wound reepithelialization under hypoxia, a major component of ischemia. Ischemia, evaluated by laser Doppler as well as hyperspectral imaging, limited blood flow and lowered tissue oxygen saturation. EPR oximetry demonstrated that the ischemic wound tissue had pO 2 <10 mm Hg. Ischemic wounds suffered from compromised macrophage recruitment and delayed wound epithelialization. Specifically, epithelial proliferation, as determined by Ki67 staining, was compromised. In vivo imaging showed massive hypoxia inducible factor-1α (HIF-1α) stabilization in ischemic wounds, where HIF-1α induced miR-210 expression that, in turn, silenced its target E2F3, which was markedly down-regulated in the wound-edge tissue of ischemic wounds. E2F3 was recognized as a key facilitator of cell proliferation. In keratinocytes, knock-down of E2F3 limited cell proliferation. Forced stabilization of HIF-1α using Ad-VP16-HIF-1α under normoxic conditions upregulated miR-210 expression, down-regulated E2F3, and limited cell proliferation. Studies using cellular delivery of miR-210 antagomir and mimic demonstrated a key role of miR-210 in limiting keratinocyte proliferation. In summary, these results are unique in presenting evidence demonstrating that the hypoxia component of ischemia may limit wound re-epithelialization by stabilizing HIF-1α, which induces miR-210 expression, resulting in the down-regulation of the cell-cycle regulatory protein E2F3.skin | tissue repair | wound healing

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“…By producing agents such as nitric oxide and triggering the hypoxia-inducible factor-1 α pathway, they assist in the removal of bacteria, the transition into the proliferative phase, and the induction of angiogenesis [ 32,33 ] . Other factors that trigger ROS production include local hypoxia and ischemia/reperfusion.…”

Section: Inflammation and Oxidative Stress In Chronic Woundsmentioning

confidence: 99%

Pathogenesis of wound healing disorders in the elderly

Makrantonaki

Wlaschek

Scharffetter‐Kochanek

2017

J Deutsche Derma Gesell

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Summary The elderly constitute the age group most susceptible to wound healing disorders and chronic wounds, the most prevalent being venous leg ulcers, pressure ulcers, and diabetic foot ulcers. However, other age‐associated diseases should also be taken into consideration in the diagnostic workup of chronic wounds, and not be underestimated. A better understanding of the pathomechanisms involved in the wound healing process is of key importance in combatting the difficulties associated with the treatment of chronic wounds. In recent decades, considerable progress has been made in the development of pioneering therapeutic strategies for chronic wounds. In this context, the use of growth factors and cytokines, tissue engineering, and cell therapy – including stem cells – have proven very promising. Nevertheless, prior to their introduction into routine clinical practice, large controlled clinical trials are required to assess the safety of these techniques.

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Dermal Wound Healing Is Subject to Redox Control

Cited by 383 publications

References 50 publications

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Hypoxia inducible microRNA 210 attenuates keratinocyte proliferation and impairs closure in a murine model of ischemic wounds

Pathogenesis of wound healing disorders in the elderly

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