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Fibroblast growth factor (Fgf) 23 gene transcription depends on actin cytoskeleton reorganization
Author(s) -
Fajol Abul,
Honisch Sabina,
Zhang Bingbing,
Schmidt Sebastian,
Alkahtani Saad,
Alarifi Saud,
Lang Florian,
Stournaras Christos,
Föller Michael
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12096
Subject(s) - cytochalasin d , microbiology and biotechnology , fibroblast growth factor , actin , mdia1 , actin remodeling , actin cytoskeleton , biology , chemistry , cytoskeleton , biochemistry , cell , receptor
FGF 23 regulates renal phosphate and vitamin D metabolism. Loss of FGF 23 results in massive calcification and rapid aging. FGF 23 production is stimulated by 1,25( OH ) 2 D 3 and NF κB signaling. Here, we report that treatment of UMR 106 osteoblast‐like cells with 1,25( OH ) 2 D 3 , inducing Fgf23 transcription, resulted in actin polymerization which was blocked by NF κB inhibitor wogonin. Interestingly, 1,25( OH ) 2 D 3 ‐induced Fgf23 gene transcription was abolished by the actin microfilament‐disrupting agent cytochalasin B, as well as by the inhibition of actin‐regulating Rac1/ PAK 1 signaling. Our results provide strong evidence that actin redistribution regulated by the Rac1/ PAK 1 pathway participates in 1,25( OH ) 2 D 3 ‐induced Fgf23 gene transcription.