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Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice.

Demyanenko IA, Popova EN, Zakharova VV, Ilyinskaya OP, Vasilieva TV, Romashchenko VP, Fedorov AV, Manskikh VN, Skulachev MV, Zinovkin RA, Pletjushkina OY, Skulachev VP, Chernyak BV - Aging (Albany NY) (2015)

Bottom Line: This effect resembled SkQ1-induced differentiation of fibroblasts to myofibroblast, observed earlierin vitro.The Transforming Growth Factor beta (TGFb) produced by SkQ1-treated fibroblasts was found to stimulated motility of endothelial cells in vitro, an effect which may underlie pro-angiogenic action of SkQ1 in the wounds.Prevention of excessive reaction of endothelium to the pro-inflammatory cytokine(s) might account for anti-inflammatory effect of SkQ1.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia.

ABSTRACT
The process of skin wound healing is delayed or impaired in aging animals. To investigate the possible role of mitochondrial reactive oxygen species (mtROS) in cutaneous wound healing of aged mice, we have applied the mitochondria-targeted antioxidant SkQ1. The SkQ1 treatment resulted in accelerated resolution of the inflammatory phase, formation of granulation tissue, vascularization and epithelization of the wounds. The wounds of SkQ1-treated mice contained increased amount of myofibroblasts which produce extracellular matrix proteins and growth factors mediating granulation tissue formation. This effect resembled SkQ1-induced differentiation of fibroblasts to myofibroblast, observed earlierin vitro. The Transforming Growth Factor beta (TGFb) produced by SkQ1-treated fibroblasts was found to stimulated motility of endothelial cells in vitro, an effect which may underlie pro-angiogenic action of SkQ1 in the wounds. In vitro experiments showed that SkQ1 prevented decomposition of VE-cadherin containing contacts and following increase in permeability of endothelial cells monolayer, induced by pro-inflammatory cytokine TNF. Prevention of excessive reaction of endothelium to the pro-inflammatory cytokine(s) might account for anti-inflammatory effect of SkQ1. Our findings point to an important role of mtROS in pathogenesis of age-related chronic wounds.

No MeSH data available.


Related in: MedlinePlus

SkQ1 accelerates wound closure in old miceFull-thickness 7×7 mm excisions were made on the interscapular area of the back skin of young (6 month, n=12), old (24 month, n=12) and old mice received SkQ1 (100 nmol/kg of body weight per day) during the last 8 month of life (n=10). (a) Representative photos of wounds, (b) dynamics of wound closure. Data are presented as mean ± SD; *P < 0.05 for SkQ1-treated versus old mice.
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Figure 1: SkQ1 accelerates wound closure in old miceFull-thickness 7×7 mm excisions were made on the interscapular area of the back skin of young (6 month, n=12), old (24 month, n=12) and old mice received SkQ1 (100 nmol/kg of body weight per day) during the last 8 month of life (n=10). (a) Representative photos of wounds, (b) dynamics of wound closure. Data are presented as mean ± SD; *P < 0.05 for SkQ1-treated versus old mice.

Mentions: In line with the previously published data [33, 34], old mice suffered from severely impaired wound healing. This effect was completely abolished in 24 month old animals treated with SkQ1 for last 8 months (Fig. 1).


Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice.

Demyanenko IA, Popova EN, Zakharova VV, Ilyinskaya OP, Vasilieva TV, Romashchenko VP, Fedorov AV, Manskikh VN, Skulachev MV, Zinovkin RA, Pletjushkina OY, Skulachev VP, Chernyak BV - Aging (Albany NY) (2015)

SkQ1 accelerates wound closure in old miceFull-thickness 7×7 mm excisions were made on the interscapular area of the back skin of young (6 month, n=12), old (24 month, n=12) and old mice received SkQ1 (100 nmol/kg of body weight per day) during the last 8 month of life (n=10). (a) Representative photos of wounds, (b) dynamics of wound closure. Data are presented as mean ± SD; *P < 0.05 for SkQ1-treated versus old mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4543037&req=5

Figure 1: SkQ1 accelerates wound closure in old miceFull-thickness 7×7 mm excisions were made on the interscapular area of the back skin of young (6 month, n=12), old (24 month, n=12) and old mice received SkQ1 (100 nmol/kg of body weight per day) during the last 8 month of life (n=10). (a) Representative photos of wounds, (b) dynamics of wound closure. Data are presented as mean ± SD; *P < 0.05 for SkQ1-treated versus old mice.
Mentions: In line with the previously published data [33, 34], old mice suffered from severely impaired wound healing. This effect was completely abolished in 24 month old animals treated with SkQ1 for last 8 months (Fig. 1).

Bottom Line: This effect resembled SkQ1-induced differentiation of fibroblasts to myofibroblast, observed earlierin vitro.The Transforming Growth Factor beta (TGFb) produced by SkQ1-treated fibroblasts was found to stimulated motility of endothelial cells in vitro, an effect which may underlie pro-angiogenic action of SkQ1 in the wounds.Prevention of excessive reaction of endothelium to the pro-inflammatory cytokine(s) might account for anti-inflammatory effect of SkQ1.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia.

ABSTRACT
The process of skin wound healing is delayed or impaired in aging animals. To investigate the possible role of mitochondrial reactive oxygen species (mtROS) in cutaneous wound healing of aged mice, we have applied the mitochondria-targeted antioxidant SkQ1. The SkQ1 treatment resulted in accelerated resolution of the inflammatory phase, formation of granulation tissue, vascularization and epithelization of the wounds. The wounds of SkQ1-treated mice contained increased amount of myofibroblasts which produce extracellular matrix proteins and growth factors mediating granulation tissue formation. This effect resembled SkQ1-induced differentiation of fibroblasts to myofibroblast, observed earlierin vitro. The Transforming Growth Factor beta (TGFb) produced by SkQ1-treated fibroblasts was found to stimulated motility of endothelial cells in vitro, an effect which may underlie pro-angiogenic action of SkQ1 in the wounds. In vitro experiments showed that SkQ1 prevented decomposition of VE-cadherin containing contacts and following increase in permeability of endothelial cells monolayer, induced by pro-inflammatory cytokine TNF. Prevention of excessive reaction of endothelium to the pro-inflammatory cytokine(s) might account for anti-inflammatory effect of SkQ1. Our findings point to an important role of mtROS in pathogenesis of age-related chronic wounds.

No MeSH data available.


Related in: MedlinePlus