GPR35 agonists (YE120, zaprinast, and pamoic acid) promoted wound repair in a very focus-dependent fashion independently of cell proliferation, whereas a particular GPR35 antagonist CID2745687, forskolin, and pertussis toxin reversed the YE120-induced outcome. YE120 improved the mRNA expression of fibronectin and its receptor integrin α5, and ERK1
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