Paracrine and autocrine signals promoting full chondrogenic differentiation of a mesoblastic cell line

被引：21

作者：

Locker, M

Kellermann, O

Boucquey, M

Khun, H

Huerre, M

Poliard, A

机构：

[1] ONRS, UPR 1983, Lab Differenciat Cellulaire & Prions, Villejuif, France

[2] Catholic Univ Louvain, Ludwig Inst Canc Res, Brussels Branch, Brussels, Belgium

[3] Catholic Univ Louvain, Ludwig Inst Canc Res, Cellular Genet Unit, Brussels, Belgium

[4] Inst Pasteur, Unite Anatomopathol, Paris, France

来源：

JOURNAL OF BONE AND MINERAL RESEARCH | 2004年 / 19卷 / 01期

关键词：

mesodermal progenitor; chonrogenesis; bone morphogenetic protein/Smad; type II collagen mRNA splicing; Sox9; paracrine signaling; dexamethasone;

D O I：

10.1359/JBMR.0301206

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The pluripotent mesoblastic C1 cell line was used under serum-free culture conditions to investigate how paracrine and autocrine signals cooperate to drive chondrogenesis. Sequential addition of two systemic hormones, dexamethasone and triiodothyronine, permits full chondrogenic differentiation. The cell intrinsic activation of the BMP signaling pathway and Sox9 expression occurring on mesoblastic condensation is insufficient for recruitment of the progenitors. Dexamethasone-dependent Sox9 upregulation is essential for chondrogenesis.

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页码：100 / 110

页数：11

相关论文

共 48 条

[1] The transcrintion factor Sox9 has essential roles in successive steps of the chondrocyte differentiation pathway and is required for expression of Sox5 and Sox6 [J].

Akiyama, H ;

Chaboissier, MC ;

Martin, JF ;

Schedl, A ;

de Crombrugghe, B .

GENES & DEVELOPMENT, 2002, 16 (21) :2813-2828

[2]

Alini M, 1996, J BONE MINER RES, V11, P105

[3] Bone morphogenetic protein (BMP) localization in developing human and rat growth plate, metaphysis, epiphysis, and articular cartilage [J].

Anderson, HC ;

Hodges, PT ;

Aguilera, XM ;

Missana, L ;

Moylan, PE .

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 2000, 48 (11) :1493-1502

[4] Smads as transcriptional co-modulators [J].

Attisano, L ;

Wrana, JL .

CURRENT OPINION IN CELL BIOLOGY, 2000, 12 (02) :235-243

[5] THYROXINE IS THE SERUM FACTOR THAT REGULATES MORPHOGENESIS OF COLUMNAR CARTILAGE FROM ISOLATED CHONDROCYTES IN CHEMICALLY-DEFINED MEDIUM [J].

BALLOCK, RT ;

REDDI, AH .

JOURNAL OF CELL BIOLOGY, 1994, 126 (05) :1311-1318

[6] Haploinsufficiency of Sox9 results in defective cartilage primordia and premature skeletal mineralization [J].

Bi, WM ;

Huang, WD ;

Whitworth, DJ ;

Deng, JM ;

Zhang, ZP ;

Behringer, RR ;

de Crombrugghe, B .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (12) :6698-6703

[7] Sox9 is required for cartilage formation [J].

Bi, WM ;

Deng, JM ;

Zhang, ZP ;

Behringer, RR ;

de Crombrugghe, B .

NATURE GENETICS, 1999, 22 (01) :85-89

[8] INDUCTION OF PROLIFERATION OR HYPERTROPHY OF CHONDROCYTES IN SERUM-FREE CULTURE - THE ROLE OF INSULIN-LIKE GROWTH FACTOR-I, INSULIN, OR THYROXINE [J].

BOHME, K ;

CONSCIENCEEGLI, M ;

TSCHAN, T ;

WINTERHALTER, KH ;

BRUCKNER, P .

JOURNAL OF CELL BIOLOGY, 1992, 116 (04) :1035-1042

[9] Chondrocyte-specific enhancer elements in the Col11a2 gene resemble the Col2a1 tissue-specific enhancer [J].

Bridgewater, LC ;

Lefebvre, V ;

de Crombrugghe, B .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (24) :14998-15006

[10] Mechanisms of glucocorticoid action in bone [J].

Canalis, E ;

Delany, AM .

NEUROENDOCRINE IMMUNE BASIS OF THE RHEUMATIC DISEASES II, PROCEEDINGS, 2002, 966 :73-81

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