Abstract
Evaluation of: Xia W, Kong W, Wang Z et al. Increased CCN2 transcription in keloid fibroblasts requires cooperativity between AP-1 and SMAD binding sites. Ann Surg. 246(5), 886–895 (2007).
Keloid is a dermal fibroproliferative disorder characterized by the overgrowth of dense fibrous tissue coupled with excessive deposition of extracellular matrix components. The dysregulation of the immediate-early gene encoding connective tissue growth factor (CTGF), a key regulatory element in the wound-healing process, has been suggested to play a critical role in keloid pathogenesis. We review a recent paper by Xia et al., which examined the transcriptional regulatory mechanism(s) that contribute to the elevated transcription of the CTGF gene and its contribution to keloid phenotype. Results from this paper, together with the evidences from several recent studies, suggested that cooperative activities among several transcriptional regulatory elements (AP-1, SMAD, SP-1, SP-3 and TEF/TEAD) provide a fine-tuned regulatory mechanism for CTGF gene expression
Acknowledgements
We thank Katherine Long for her editorial assistance.
Financial & competing interests disclosure
This work was supported in part by NIH PHS grants K22 DE014847, RO3 DE016569 and RO3 CA114688 to X Zhou.The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.