ArticleHuman mutation2011
Human dermal fibroblasts derived from oculodentodigital dysplasia patients suggest that patients may have wound-healing defects.
Article in Human mutation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Macrophage-Fibroblast Crosstalk Shapes Wound Repair Signaling In Vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Towards a Better Understanding of Genotype-Phenotype Correlations and Therapeutic Targets for Cardiocutaneous Genes: The Importance of Functional Studies above Prediction.International journal of molecular sciences · 2022Review
- Restraint of Human Skin Fibroblast Motility, Migration, and Cell Surface Actin Dynamics, by Pannexin 1 and P2X7 Receptor Signaling.International journal of molecular sciences · 2021Article
- Connexins and Disease.Cold Spring Harbor perspectives in biology · 2018Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Disease-linked connexin26 S17F promotes volar skin abnormalities and mild wound healing defects in mice.Cell death & disease · 2017Article
- Specificity of the connexin W3/4 locus for functional gap junction formation.Channels (Austin, Tex.) · 2016Article
- Specific functional pathologies of Cx43 mutations associated with oculodentodigital dysplasia.Molecular biology of the cell · 2016Article
- The Role of Connexins in Wound Healing and Repair: Novel Therapeutic Approaches.Frontiers in physiology · 2016Review
- Connexins and pannexins in the integumentary system: the skin and appendages.Cellular and molecular life sciences : CMLS · 2015Review
- Prognostic impact of reduced connexin43 expression and gap junction coupling of neoplastic stromal cells in giant cell tumor of bone.PloS one · 2015Article
- Intracellular Cleavage of the Cx43 C-Terminal Domain by Matrix-Metalloproteases: A Novel Contributor to Inflammation?Mediators of inflammation · 2015Review
- Expression and function of connexin 43 in human gingival wound healing and fibroblasts.PloS one · 2015Article
- Panx1 regulates cellular properties of keratinocytes and dermal fibroblasts in skin development and wound healing.The Journal of investigative dermatology · 2014Article
- Functional assessment of gap junctions in monolayer and three-dimensional cultures of human tendon cells using fluorescence recovery after photobleaching.Journal of biomedical optics · 2014Article
- Neurological manifestations of oculodentodigital dysplasia: a Cx43 channelopathy of the central nervous system?Frontiers in pharmacology · 2013Review
- Structure and functional studies of N-terminal Cx43 mutants linked to oculodentodigital dysplasia.Molecular biology of the cell · 2012Article
- Gap junctions in inherited human disorders of the central nervous system.Biochimica et biophysica acta · 2012Review
- Characterization of gap junction proteins in the bladder of Cx43 mutant mouse models of oculodentodigital dysplasia.The Journal of membrane biology · 2012Article
- Connexins and pannexins: Coordinating cellular communication in the testis and epididymis.Spermatogenesis · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Oculodentodigital dysplasia (ODDD) is primarily an autosomal dominant human disease caused by any one of over 60 mutations in the GJA1 gene encoding the gap junction protein Cx43. In the present study, wound healing was investigated in a G60S ODDD mutant mouse model and by using dermal fibroblasts isolated from two ODDD patients harboring the p.D3N and p.V216L mutants along with dermal fibroblasts isolated from their respective unaffected relatives. Punch biopsies revealed a delay in wound closure in the G60S mutant mice in comparison to wild-type littermates, and this delay appeared to be due to defects in the dermal fibroblasts. Although both the p.D3N and p.V216L mutants reduced gap junctional intercellular communication in human dermal fibroblasts, immunolocalization studies revealed that Cx43 gap junctions were prevalent at the cell surface of p.D3N expressing fibroblasts but greatly reduced in p.V216L expressing fibroblasts. Mutant expressing fibroblasts were further found to have reduced proliferation and migration capabilities. Finally, in response to TGFβ1, mutant expressing fibroblasts expressed significantly less alpha smooth muscle actin suggesting they were inefficient in their ability to differentiate into myofibroblasts. Collectively, our results suggest that ODDD patients may have subclinical defects in wound healing due to impaired function of dermal fibroblasts.
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