MiR-23b Promotes the Migration of Keratinocytes Through Downregulating TIMP3.
BACKGROUND
Wound healing is a complex process aiming at repairing the damaged skin. MiR-23b has been reported to be upregulated during wound healing. In this study, we intended to explore the working mechanism of miR-23b during wound healing.


METHODS
Quantitative real-time polymerase chain reaction was performed to detect the enrichment of miR-23b and tissue inhibitor of metalloproteinase-3 (TIMP3) in HaCaT cells. Scratch wound assay was carried out to measure the migration of HaCaT cells. The target of miR-23b was predicted by microT-CDS software, and the combination was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. The abundance of TIMP3 protein was detected by Western blot assay.


RESULTS
The abundance of miR-23b was positively related to the concentration and time of transforming growth factor β1 treatment in HaCaT cells. MiR-23b promoted the migration of keratinocytes. TIMP3 was a direct target of miR-23b and was negatively regulated by miR-23b. TIMP3 inhibited the migration of keratinocytes. MiR-23b accelerated the migration of keratinocytes by downregulating the abundance of TIMP3.


CONCLUSIONS
MiR-23b promoted the migration of keratinocytes partly through reducing the enrichment of TIMP3. MiR-23b might be a promising target for the treatment of wound healing-associated diseases.
['Hu|Hua|H|', 'Tang|Jun|J|', 'Liu|Chuanqi|C|', 'Cen|Ying|Y|']
D002460:Cell Line D002465:Cell Movement D015536:Down-Regulation D015603:Keratinocytes D035683:MicroRNAs D019717:Tissue Inhibitor of Metalloproteinase-3 D014162:Transfection D053773:Transforming Growth Factor beta1 D014945:Wound Healing
MiR-23b Migration TIMP3 Wound healing