Comparisons of keloid scars with normal skin samples that do not have the single-nucleotide polymorphism allele and were derived from different anatomical sites showed stronger expressions of NEDD4 TV3 and activated forms of NF-κB and STAT3 in keloid scars.
Immunohistochemistry confirms that STAT3 (Tyr705 phospho-STAT3) is activated and β-catenin is up-regulated in the dermis of keloid clinical specimens and keloid skin equivalent implants from the humanized mouse model.
The data we provided herein enrich the knowledge regarding the molecular mechanism of NEDD4 involved in the pathogenesis of keloid, defining a new regulatory role for STAT3 in keloid.
We revealed that NTP suppressed KF cell migration via down-regulation of EGFR and STAT3 and reduced collagen production via supressing transforming growth factor-β.