PMID- 19798549
OWN - NLM
STAT- MEDLINE
DCOM- 20100513
LR  - 20211020
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 335
IP  - 1-2
DP  - 2010 Feb
TI  - Activation of RhoA and FAK induces ERK-mediated osteopontin expression in 
      mechanical force-subjected periodontal ligament fibroblasts.
PG  - 263-72
LID - 10.1007/s11010-009-0276-1 [doi]
AB  - The precise mechanism by which Rho kinase translates the mechanical signals into 
      OPN up-regulation in force-exposed fibroblasts has not been elucidated. Human 
      periodontal ligament fibroblasts (hPLFs) were exposed to mechanical force by 
      centrifuging the culture plates at a magnitude of 50 g/cm(2) for 60 min. At 
      various times of the force application, they were processed for analyzing cell 
      viability, trypan blue exclusion, and OPN expression at protein and RNA levels. 
      Cellular mechanism(s) of the force-induced OPN up-regulation was also examined 
      using various kinase inhibitors or antisense oligonucleotides specific to 
      mechanosensitive factors. Centrifugal force up-regulated OPN expression and 
      induced a rapid and transient increase in the phosphorylation of focal adhesion 
      kinase (FAK), extracellular signal-regulated kinase (ERK), and Elk1. 
      Pharmacological blockade of RhoA/Rho-associated coiled coil-containing kinase 
      (ROCK) signaling markedly reduced force-induced FAK and ERK1/2 phosphorylation. 
      Transfecting hPLFs with FAK antisense oligonucleotide diminished ERK1/2 
      activation and force-induced OPN expression. Further, ERK inhibitor inhibited 
      significantly OPN expression, Elk1 phosphorylation, and activator protein-1 
      (AP-1)-DNA binding activation, but not FAK phosphorylation, in the force-applied 
      cells. These results demonstrate that FAK signaling plays critical roles in 
      force-induced OPN expression in hPLFs through interaction with Rho/ROCK as 
      upstream effectors and ERK-Elk1/ERK-c-Fos as downstream effectors.
FAU - Hong, So-Yeon
AU  - Hong SY
AD  - Department of Orthodontics, Dental Clinic, School of Medicine, Ajou University, 
      Suwon 443-721, South Korea.
FAU - Jeon, Young-Mi
AU  - Jeon YM
FAU - Lee, Hyun-Jung
AU  - Lee HJ
FAU - Kim, Jong-Ghee
AU  - Kim JG
FAU - Baek, Jin-A
AU  - Baek JA
FAU - Lee, Jeong-Chae
AU  - Lee JC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091002
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 106441-73-0 (Osteopontin)
RN  - 124671-05-2 (RHOA protein, human)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (rho-Associated Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.6.5.2 (rhoA GTP-Binding Protein)
SB  - IM
MH  - Adult
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Fibroblasts/cytology/*metabolism
MH  - Focal Adhesion Protein-Tyrosine Kinases/*metabolism
MH  - Humans
MH  - Male
MH  - Osteopontin/*genetics/metabolism
MH  - Periodontal Ligament/cytology/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Stress, Mechanical
MH  - Transcription Factor AP-1/metabolism
MH  - Transfection
MH  - rho-Associated Kinases/metabolism
MH  - rhoA GTP-Binding Protein/*metabolism
EDAT- 2009/10/03 06:00
MHDA- 2010/05/14 06:00
CRDT- 2009/10/03 06:00
PHST- 2009/06/04 00:00 [received]
PHST- 2009/09/16 00:00 [accepted]
PHST- 2009/10/03 06:00 [entrez]
PHST- 2009/10/03 06:00 [pubmed]
PHST- 2010/05/14 06:00 [medline]
AID - 10.1007/s11010-009-0276-1 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2010 Feb;335(1-2):263-72. doi: 10.1007/s11010-009-0276-1. Epub 
      2009 Oct 2.