High throughput screening of biologically functional small molecules for modulating the expression of FGFR1OP2/wit3.0 in fibroblasts.
Oral wounds heal rapidly without scarring through yet unknown molecular mechanisms. A small cytoskeleton molecule identified in oral wound fibroblasts, FGFR1OP2/wit3.0, has been shown to accelerate wound closure in vitro and in vivo. The objective of this study was to elucidate the transcriptional mechanism of FGFR1OP2/ wit3.0 in fibroblasts using a high throughput drug-screening platform. This pilot study identified chemical compounds that could effectively modulate the FGFR1OP2/wit3.0 expression for future studies on effective wound management.
Weintraub Center for Reconstructive Biotechnology, University of California, Los Angeles School of Dentistry, USA. willcheng@ucla.edu
William
W
Cheng
Ichiro
I
Nishimura
D000199:Actins / Q000378:metabolism; D000818:Animals; D018929:Cell Culture Techniques; D002460:Cell Line; D048430:Cell Shape; D002478:Cells, Cultured; D003593:Cytoplasm / Q000648:ultrastructure; D003598:Cytoskeletal Proteins / Q000235:genetics*; D053595:Embryonic Stem Cells / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism*; D055785:Gene Knockdown Techniques; D020868:Gene Silencing; D057166:High-Throughput Screening Assays; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018613:Microscopy, Confocal; D009154:Mutation / Q000235:genetics; D010865:Pilot Projects; D034741:RNA, Small Interfering / Q000502:physiology; D012867:Skin / Q000166:cytology; D014158:Transcription, Genetic / Q000235:genetics*; D014162:Transfection
D000199:Actins; D003598:Cytoskeletal Proteins; C547759:FGFR1OP2 protein, mouse; D034741:RNA, Small Interfering