Palatogenesis and cutaneous repair: A two‐headed coin

Biggs, Leah C.; Goudy, Steven L.; Dunnwald, Martine

doi:10.1002/dvdy.24224

Cited by 16 publications

(14 citation statements)

References 294 publications

(344 reference statements)

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“…Tgfb3 is an upstream regulator of Irf6 in oral keratinocytes and palatal epithelium during palatogenesis . Results from this study, although not formally tested, support a relationship between these two molecules in cutaneous wounds, similarly to what was observed for craniofacial development, and further validate our overall viewpoint that palatogenesis and cutaneous wounds are “two faces of the same coin” …”

Section: Discussionsupporting

confidence: 82%

“…7,40 Results from this study, although not formally tested, support a relationship between these two molecules in cutaneous wounds, similarly to what was observed for craniofacial development, and further validate our overall viewpoint that palatogenesis and cutaneous wounds are "two faces of the same coin". 41 The formation of the granulation tissue is dependent on the proper signaling between keratinocytes, innate immune cells, adipocytes, and fibroblasts with the requirement for the migration of collagen-producing fibroblasts to the injured site. 41 Although Irf6 is not detected in fibroblasts, it is expressed in both keratinocytes and innate immune cells, and has been previously reported as a repressor of inflammatory cytokines following endotoxic shock.…”

Section: Discussionmentioning

confidence: 99%

“…41 The formation of the granulation tissue is dependent on the proper signaling between keratinocytes, innate immune cells, adipocytes, and fibroblasts with the requirement for the migration of collagen-producing fibroblasts to the injured site. 41 Although Irf6 is not detected in fibroblasts, it is expressed in both keratinocytes and innate immune cells, and has been previously reported as a repressor of inflammatory cytokines following endotoxic shock. 8,39 The inflammatory phase of tissue repair is essential to the overall healing process, that must be accompanied by a return to normal levels for completion of the process.…”

Section: Discussionmentioning

confidence: 99%

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Interferon regulatory factor 6 is required for proper wound healing in vivo

Rhea

Canady

et al. 2019

Developmental Dynamics

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Background Van der Woude syndrome (VWS) is the most common form of syndromic orofacial cleft caused predominantly by mutations in Interferon Regulatory Factor 6 (IRF6). We previously reported that individuals with VWS have increased risk of wound healing complications following cleft repair compared with individuals with nonsyndromic orofacial clefts (nonsyndromic cleft lip and palate—NSCLP). In vitro, absence of IRF6 leads to impaired keratinocyte migration and embryonic wound healing. However, there is currently no data on tissue repair in adult animals and cells with reduced levels of IRF6 like in VWS. Results Excisional wounds of Irf6+/− and wild‐type animals were analyzed 4 and 7 days post‐wounding. Although all wounds were reepithelialized after 7 days, the epidermal and wound volume of repaired wounds was larger in Irf6+/−. These data were supported by increased keratinocyte proliferation in the neoformed epidermis and a less mature granulation tissue with increased cytokine levels. This effect was not cell autonomous, as Irf6+/− neonatal keratinocytes in vitro did not exhibit defects in scratch wound closure or proliferation. Keratinocytes from individuals with VWS also migrated similarly to keratinocytes from NSCLP individuals. Conclusions These data support a role for IRF6 in wound healing by regulating keratinocyte proliferation, granulation tissue maturation, and cytokine levels.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Interferon regulatory factor 6 is required for proper wound healing in vivo

Rhea

Canady

et al. 2019

Developmental Dynamics

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“…While these data show that Fz1 , Fz2 , and Fz7 synergize with other canonical and noncanonical pathway components, they do not definitively indicate which pathway(s) is/are affected by the different Frizzled mutations. Palate, ventricular septum, and neural tube closures are known to involve multiple signaling pathways (Biggs, Goudy, & Dunnwald, 2015), and it is therefore plausible that defects in more than one Frizzled-based pathway combine to produce a developmental defect.…”

Section: Frizzled1 Frizzled2 and Frizzled7mentioning

confidence: 99%

Frizzled Receptors in Development and Disease

Wang

Chang

Rattner

et al. 2016

Current Topics in Developmental Biology

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Frizzled proteins are the principal receptors for the Wnt family of ligands. They mediate canonical Wnt signaling together with Lrp5 and Lrp6 coreceptors. In conjunction with Celsr, Vangl, and a small number of additional membrane and membrane-associated proteins, they also play a central role in tissue polarity/planar cell polarity (PCP) signaling. Targeted mutations in 9 of the 10 mammalian Frizzled genes have revealed their roles in an extraordinarily diverse set of developmental and homeostatic processes, including morphogenetic movements responsible for palate, ventricular septum, ocular furrow, and neural tube closure; survival of thalamic neurons; bone formation; central nervous system (CNS) angiogenesis and blood–brain barrier formation and maintenance; and a wide variety of processes that orient subcellular, cellular, and multicellular structures relative to the body axes. The last group likely reflects the mammalian equivalent of tissue polarity/PCP signaling, as defined in Drosophila, and it includes CNS axon guidance, hair follicle and tongue papilla orientation, and inner ear sensory hair bundle orientation. Frizzled receptors are ubiquitous among multicellular animals and, with other signaling molecules, they very likely evolved to permit the development of the complex tissue architectures that provide multicellular animals with their enormous selective advantage.

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“…Also highlighted in this issue is the intimate connection between development, homeostasis, and disease. Most tissues have the capacity to repair damage, such as the skin (Biggs et al, ) and the liver (Cast et al, ), but others such as the heart and limbs lose this capacity during embryogenesis or during the early postnatal period. Many diseases such as muscular dystrophy (Chau and Kalsotra, ) and neurodegenerative disorders reflect an inability to repair damaged tissues as a result of faulty repair mechanisms or due to inherent barriers to repair.…”

mentioning

confidence: 99%