Spatial and temporal regulation of gene expression in the mammalian growth plate

被引:61
作者
Lui, Julian C. K. [4 ]
Andrade, Anenisia C. [1 ,2 ,3 ]
Forcinito, Patricia [4 ]
Hegde, Anita [4 ]
Chen, WeiPing [5 ]
Baron, Jeffrey [4 ]
Nilsson, Ola [1 ,2 ,3 ]
机构
[1] Karolinska Inst, Ctr Mol Med, SE-17176 Stockholm, Sweden
[2] Karolinska Inst, Pediat Endocrinol Unit, Dept Woman & Child Hlth, SE-17176 Stockholm, Sweden
[3] Karolinska Univ Hosp, SE-17176 Stockholm, Sweden
[4] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA
[5] NIDDK, Genom Core Lab, NIH, Bethesda, MD 20892 USA
基金
瑞典研究理事会;
关键词
Growth plate; Chondrocytes; Gene expression; Longitudinal bone growth; Differentiation; Senescence; MESSENGER-RNA LEVELS; CHONDROCYTE DIFFERENTIATION; CARTILAGE DEVELOPMENT; SKELETAL DEVELOPMENT; ZONE CHONDROCYTES; EPIPHYSEAL FUSION; BONE-DEVELOPMENT; NUCLEAR FACTOR; RESTING ZONE; FACTOR-BETA;
D O I
10.1016/j.bone.2010.01.373
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Growth plates are spatially polarized and structured into three histologically and functionally distinct layers the resting zone (RZ), proliferative zone (PZ), and hypertrophic zone (HZ). With age, growth plates undergo functional and structural senescent changes including declines of growth rate, proliferation rate, growth plate height and cell number. To explore the mechanisms responsible for spatially-associated differentiation and temporally-associated senescence of growth plate in an unbiased manner, we used microdissection to collect individual growth plate zones from proximal tibiae of 1-week rats and the PZ and early hypertrophic zones of growth plates from 3-, 6-, 9-, and 12-week rats and analyzed gene expression using microarray. We then used bioinformatic approaches to identify significant changes in biological functions, molecular pathways, transcription factors and also to identify specific gene products that can be used as molecular markers for individual zones or for temporal development. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:1380 / 1390
页数:11
相关论文
共 65 条
[1]   The role of the resting zone in growth plate chondrogenesis [J].
Abad, V ;
Meyers, JL ;
Weise, M ;
Gafni, RI ;
Barnes, KM ;
Nilsson, O ;
Bacher, JD ;
Baron, J .
ENDOCRINOLOGY, 2002, 143 (05) :1851-1857
[2]   C-type natriuretic peptide regulates endochondral bone growth through p38 MAP kinase-dependent and -independent pathways [J].
Agoston, Hanga ;
Khan, Sameena ;
James, Claudine G. ;
Gillespie, J. Ryan ;
Serra, Rosa ;
Stanton, Lee-Anne ;
Beier, Frank .
BMC DEVELOPMENTAL BIOLOGY, 2007, 7
[3]   Wnt gene expression in the post-natal growth plate: Regulation with chondrocyte differentiation [J].
Andrade, Anenisla C. ;
Nilsson, Ola ;
Barnes, Kevin M. ;
Baron, Jeffrey .
BONE, 2007, 40 (05) :1361-1369
[4]   Global analyses of gene expression in early experimental osteoarthritis [J].
Appleton, C. T. G. ;
Pitelka, V. ;
Henry, J. ;
Beier, F. .
ARTHRITIS AND RHEUMATISM, 2007, 56 (06) :1854-1868
[5]   MEF2C transcription factor controls chondrocyte hypertrophy and bone development [J].
Arnold, Michael A. ;
Kim, Yuri ;
Czubryt, Michael P. ;
Phan, Dillon ;
McAnally, John ;
Qi, Xiaoxia ;
Shelton, John M. ;
Richardson, James A. ;
Bassel-Duby, Rhonda ;
Olson, Eric N. .
DEVELOPMENTAL CELL, 2007, 12 (03) :377-389
[6]   A microarray approach for comparative expression profiling of the discrete maturation zones of mouse growth plate cartilage [J].
Belluoccio, Daniele ;
Bernardo, Bianca C. ;
Rowley, Lynn ;
Bateman, John F. .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS, 2008, 1779 (05) :330-340
[7]  
Bendall AJ, 2003, INT J DEV BIOL, V47, P335
[8]   A comparison of normalization methods for high density oligonucleotide array data based on variance and bias [J].
Bolstad, BM ;
Irizarry, RA ;
Åstrand, M ;
Speed, TP .
BIOINFORMATICS, 2003, 19 (02) :185-193
[9]   SERUM FRACTIONS AND RELATED AGONISTS WITH CALCIUM-MOBILIZING ACTIVITY IN THE BOVINE GROWTH-PLATE CHONDROCYTE [J].
BULMAN, WA ;
IANNOTTI, JP ;
GLOWACKI, K ;
BLEUIT, J .
JOURNAL OF ORTHOPAEDIC RESEARCH, 1995, 13 (02) :220-229
[10]   Inhibition of β-catenin signaling causes defects in postnatal cartilage development [J].
Chen, Mo ;
Zhu, Mei ;
Awad, Hani ;
Li, Tian-Fang ;
Sheu, Tzong-Jen ;
Boyce, Brendan F. ;
Chen, Di ;
O'Keefe, Regis J. .
JOURNAL OF CELL SCIENCE, 2008, 121 (09) :1455-1465