What is it about?
Recessive dystrophic epidermolysis bullosa (RDEB) is a mechanobullous disease caused by mutations in the COL7A1 gene that encodes type VII collagen (C7) at the dermal–epidermal junction. We demonstrated previously that intradermal injections of allogeneic fibroblasts in RDEB can increase C7 expression at the DEJ. Here, we proved that the elevated COL7A1expression is paralleled by increased expression of HB-EGF and, in vitro, incubation of keratinocytes and fibroblasts with HB-EGF leads to increased COL7A1 expression, potentially via increased AP-1 transcription factor.
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Why is it important?
Allogeneic fibroblasts induce subclinical inflammation, leading to upregulation of HB-EGF probably by the recipients’ own keratinocytes, which may be sustained for several months in an autocrine manner.
Perspectives
Our observation is of interest in trying to dissect a potential ‘‘magic bullet’’ from cell therapy for RDEB, notwithstanding the caveat that HB-EGF contributes to tumorigenicity.
Nikoletta Nagy
Read the Original
This page is a summary of: HB-EGF Induces COL7A1 Expression in Keratinocytes and Fibroblasts: Possible Mechanism Underlying Allogeneic Fibroblast Therapy in Recessive Dystrophic Epidermolysis Bullosa, Journal of Investigative Dermatology, August 2011, Elsevier,
DOI: 10.1038/jid.2011.85.
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