PMID- 28901443
OWN - NLM
STAT- MEDLINE
DCOM- 20180604
LR  - 20181113
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 16
IP  - 5
DP  - 2017 Nov
TI  - Basic fibroblast growth factor increases IFT88 expression in chondrocytes.
PG  - 6590-6599
LID - 10.3892/mmr.2017.7449 [doi]
AB  - Intraflagellar transport protein 88 (IFT88) is protein crucial for the assembly 
      and maintenance of primary cilia in chondrocytes. Primary cilia regulate 
      mechanical and chemical signals in chondrocytes; however, the effects of 
      cytokines on IFT88 expression and cilia formation and maintenance remain to be 
      elucidated. Therefore, the role of basic fibroblast growth factor (bFGF) on IFT88 
      expression were examined in theATDC5 murine chondrocytic line, in order to 
      investigate the signaling pathways involved in this process. bFGF treatment 
      upregulated IFT88 expression in a dose‑ and time‑dependent manner in ATDC5 cells. 
      The effects of bFGF on IFT88 protein expression were suppressed in the presence 
      of the extracellular signal‑regulated protein kinase (ERK) inhibitor PD0325901 
      and the FGF receptor inhibitor BGJ398. In addition, treatment with 
      IFT88‑trageting small interfering (si)RNA downregulated the protein expression of 
      IFT88 and ERK, thus suggesting that the ERK signaling pathway may be involved in 
      the regulation of IFT88 expression in ATDC5 cells. bFGF treatment increased the 
      number of ciliated ATDC5 cells and primary cultured chondrocytes. Downregulation 
      of IFT88 expression by PD0325901, BGJ398, or IFT88‑targeting siRNA was revealed 
      to reduce the number of ciliated cells. bFGF also upregulated the mRNA and 
      protein expression of IFT88 in primary cultured chondrocytes. In conclusion, the 
      findings of the present study suggested that bFGF may enhance the expression of 
      IFT88, and promote primary cilia development, through the mitogen‑activated 
      protein kinase/ERK‑mediated pathway in chondrocytes.
FAU - Zhan, Daolu
AU  - Zhan D
AD  - Graduate School, Southern Medical University, Guangzhou, Guangdong 510515, P.R. 
      China.
FAU - Xiang, Wei
AU  - Xiang W
AD  - Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
FAU - Guo, Fengjing
AU  - Guo F
AD  - Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
FAU - Ma, Yuanzheng
AU  - Ma Y
AD  - Graduate School, Southern Medical University, Guangzhou, Guangdong 510515, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20170908
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Fibroblast Growth Factor)
RN  - 0 (Tg737Rpw protein, mouse)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 62031-54-3 (Fibroblast Growth Factors)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chondrocytes/*metabolism
MH  - Cilia/genetics/metabolism
MH  - Down-Regulation/genetics
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Fibroblast Growth Factors/*metabolism
MH  - MAP Kinase Signaling System/genetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - RNA, Messenger/genetics
MH  - Receptors, Fibroblast Growth Factor/*metabolism
MH  - Signal Transduction/genetics
MH  - Transcriptional Activation/genetics
MH  - Tumor Suppressor Proteins/genetics/*metabolism
MH  - Up-Regulation/genetics
PMC - PMC5865803
EDAT- 2017/09/14 06:00
MHDA- 2018/06/05 06:00
PMCR- 2017/09/08
CRDT- 2017/09/14 06:00
PHST- 2016/11/21 00:00 [received]
PHST- 2017/07/11 00:00 [accepted]
PHST- 2017/09/14 06:00 [pubmed]
PHST- 2018/06/05 06:00 [medline]
PHST- 2017/09/14 06:00 [entrez]
PHST- 2017/09/08 00:00 [pmc-release]
AID - mmr-16-05-6590 [pii]
AID - 10.3892/mmr.2017.7449 [doi]
PST - ppublish
SO  - Mol Med Rep. 2017 Nov;16(5):6590-6599. doi: 10.3892/mmr.2017.7449. Epub 2017 Sep 
      8.