A Novel Enhancer of the Wound Healing Process

Werner, Sabine

doi:10.1016/j.ajpath.2011.09.001

Cited by 29 publications

(14 citation statements)

References 25 publications

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“…Normal wound healing in healthy mice appears to be naturally optimised and it has been notoriously hard to experimentally improve this process 2 , 43 . Indeed, the increase in the number of nerve-derived cells in the wound of Pten cKO mice did neither lead to a significant acceleration of the wound closure D7 (86.3 ± 5.0% covered by epidermis in control vs. 87.2 ± 5.1% in Pten cKO) nor did it alter the area of HPE (0.250 ± 0.02 vs. 0.278 ± 0.03 mm 2 ), wound width (2.12 ± 0.09 vs. 1.90 ± 0.10 mm) or length of wound epithelium (1.81 ± 0.06 vs. 1.68 ± 0.08 mm), measured at the same time point (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Indeed, loss of injury-activated glia also affected the area of newly formed, HPE. However, expansion of peripheral glia in the wound bed did not influence this process, presumably because it is naturally optimised in murine skin wound healing 43 . Nonetheless, our data speak for multiple effects of injury-activated glia and point to a therapeutic potential of these cells and/or of their secretome in human wound healing.…”

Section: Discussionmentioning

confidence: 95%

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Injury-activated glial cells promote wound healing of the adult skin in mice

et al. 2018

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Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-β signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 95%

Injury-activated glial cells promote wound healing of the adult skin in mice

et al. 2018

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“…Although the effects of ivermectin on neuronal and glial growth in vivo were quite striking, it is important to acknowledge that the drug’s effect on wound closure was not as profound. It is accepted that wound healing in healthy mice is particularly difficult to improve experimentally, 36 and more specifically, the BALB/c wildtype mice used in this study are known to heal relatively quickly. 37 It will be important to assess whether this drug can also play a role in improving nerve regeneration in other models, in which the nerve defect is more profound and/or impaired.…”

Section: Discussionmentioning

confidence: 99%

Ivermectin Promotes Peripheral Nerve Regeneration during Wound Healing

Cairns¹,

Giordano²,

Conte³

et al. 2018

ACS Omega

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Peripheral nerves have the capacity to regenerate due to the presence of neuroprotective glia of the peripheral nervous system, Schwann cells. Upon peripheral nerve injury, Schwann cells create a permissive microenvironment for neuronal regrowth by taking up cytotoxic glutamate and secreting neurotrophic signaling molecules. Impaired peripheral nerve repair is often caused by a defective Schwann cell response after injury, and there is a critical need to develop new strategies to enhance nerve regeneration, especially in organisms with restricted regenerative potential, such as humans. One approach is to explore mechanisms in lower organisms, in which nerve repair is much more efficient. A recent study demonstrated that the antiparasitic drug, ivermectin, caused hyperinnervation of primordial eye tissue in Xenopus laevis tadpoles. Our study aimed to examine the role of ivermectin in mammalian nerve repair. We performed in vitro assays utilizing human induced neural stem cells (hiNSCs) in co-culture with human dermal fibroblasts (hDFs) and found that ivermectin-treated hDFs promote hiNSC proliferation and migration. We also characterized the effects of ivermectin on hDFs and found that ivermectin causes hDFs to uptake extracellular glutamate, secrete glial cell-derived neurotrophic factor, develop an elongated bipolar morphology, and express glial fibrillary acidic protein. Finally, in a corresponding in vivo model, we found that localized ivermectin treatment in a dermal wound site induced the upregulation of both glial and neuronal markers upon healing. Taken together, we demonstrate that ivermectin promotes peripheral nerve regeneration by inducing fibroblasts to adopt a glia-like phenotype.

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“…Unlike burn wounds, skin wound biopsies exhibit few residual necrotic tissues, which may aggravate local inflammation. However, these wounds are acute; thus, their healing processes are similar (18). For keratinised epithelial cells, the increase in CAR expression in mouse skin wound biopsies was consistent with the upregulation in burn wounds.…”

Section: Discussionmentioning

confidence: 99%

Effects of heat stress on the expression of the coxsackievirus and adenovirus receptor in mouse skin keratinocytes

Deng

Jia

Chen

et al. 2013

Experimental and Therapeutic Medicine

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The aim of this study was to investigate the effects of heat stress on the expression of the coxsackievirus and adenovirus receptor (CAR) in mouse skin keratinocytes. Twenty BALB/c mice were randomly divided into two groups: the sham heat (control) and scald groups. Skin specimens were obtained 6 h after the treatments. Changes in the expression of CAR in skin keratinocyte samples were detected by immunohistochemistry, quantitative polymerase chain reaction and western blotting. In an in vitro assay, mouse skin keratinocytes were cultured and randomly divided into two groups: the normal control and heat stress groups. Six hours subsequently, the changes in CAR expression in the two groups were estimated by flow cytometry to determine the differences between the two groups. Heat stress significantly increased the expression of CAR in the mouse skin keratinocytes (P<0.05). The upregulation of CAR in mouse keratinocytes in burn wounds may be beneficial for restoring healing in organisms.

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A Novel Enhancer of the Wound Healing Process

Cited by 29 publications

References 25 publications

Injury-activated glial cells promote wound healing of the adult skin in mice

Injury-activated glial cells promote wound healing of the adult skin in mice

Ivermectin Promotes Peripheral Nerve Regeneration during Wound Healing

Effects of heat stress on the expression of the coxsackievirus and adenovirus receptor in mouse skin keratinocytes

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