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Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

Authors
 Su Jin Park  ;  Su Jin Kim  ;  Sung-Kil Lim  ;  Eun Jig Lee  ;  Myoung Hee Kim  ;  Seong Hwan Kim  ;  Ji Hyun Byun  ;  Yumie Rhee 
Citation
 Journal of Bone and Mineral Research, Vol.22(6) : 889-896, 2007 
Journal Title
 Journal of Bone and Mineral Research 
ISSN
 0884-0431 
Issue Date
2007
MeSH
3T3 Cells ; ATPases Associated with Diverse Cellular Activities ; Active Transport, Cell Nucleus/drug effects ; Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Adenosine Triphosphatases/physiology* ; Alkaline Phosphatase/genetics ; Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Apoptosis/physiology ; Cell Count ; Cell Differentiation/drug effects* ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell Proliferation/drug effects* ; Cells, Cultured ; Collagen Type I/genetics ; Fibroblast Growth Factor 2/pharmacology* ; Gene Expression/drug effects ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Mice ; Mice, Inbred ICR ; Microtubule-Associated Proteins ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Nuclear Proteins/physiology* ; Osteoblasts/cytology ; Osteoblasts/drug effects* ; Osteoblasts/metabolism ; Osteocalcin/genetics ; RNA, Small Interfering/genetics ; Skull/cytology ; Transfection ; Transforming Growth Factor beta1/pharmacology
Keywords
fidgetin-like 1 ; osteoblast ; basic fibroblast growth factor ; siRNA
Abstract
The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.
Full Text
http://onlinelibrary.wiley.com/doi/10.1359/jbmr.070311/abstract
DOI
10.1359/jbmr.070311
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Myoung Hee(김명희) ORCID logo https://orcid.org/0000-0001-5652-1452
Park, Su Jin(박수진)
Rhee, Yumie(이유미) ORCID logo https://orcid.org/0000-0003-4227-5638
Lee, Eun Jig(이은직) ORCID logo https://orcid.org/0000-0002-9876-8370
Lim, Sung Kil(임승길)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/96241
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