TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro

Linda Harkness, Hanna Taipaleenmaki, Anna-Marja Saamanen, Moustapha Kassem, Basem Abdallah

Publikation: Konferencebidrag uden forlag/tidsskriftPosterForskning

Resumé

DLK1/FA1 (delta like-1 homolog/Fetal Antigen-1) is a novel surface marker for embryonic chondroprogenitor cells undergoing lineage progression from proliferation to prehypertrophic stages. However, mechanisms mediating control of its expression during chondrogenesis are not known. Thus, we examined the effect of a number of signalling molecules on DLK1 expression during in vitro chondrogenic differentiation in mouse embryonic limb bud mesenchymal micromass cultures and mouse embryonic fibroblast (MEF) pellet cultures. Dlk1 was initially expressed during mesenchymal condensation and chondrocyte proliferation, in parallel with expression of Sox9 and Col2a1, and was down-regulated upon expression of Col10a1 by hypertrophic chondrocytes. Among a number of molecules that affected chondrogenesis, TGF-b signalling regulated Dlk1expression. TGF-b1-induced chondrogenesis was associated with decreased Dlk1 expression and these effects were abolished by the TGF-b signalling inhibitor SB4311542 suggesting an involvement of DLK1/FA1 in mediating the function of TGF-b1 signalling in chondrogenesis. In support of this hypothesis, we found that TGF-b1 enhanced chondrocyte differentiation in dlk1-/- MEF compared to wild type MEF. In conclusion, our data identified TGF-b-1 as an upstream negative regulator of Dlk1 expression and function during the early events of embryonic chondrogenesis. The cross-talk between TGF-b1 and DLK1 showed promotion of early chondrogenesis during embryonic endochondral bone formation process.
OriginalsprogEngelsk
Publikationsdato15. jun. 2011
StatusUdgivet - 15. jun. 2011

Fingeraftryk

Chondrogenesis
Chondrocytes
Fibroblasts
Limb Buds
Cell Lineage
Osteogenesis
In Vitro Techniques

Citer dette

Harkness, L., Taipaleenmaki, H., Saamanen, A-M., Kassem, M., & Abdallah, B. (2011). TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro.
Harkness, Linda ; Taipaleenmaki, Hanna ; Saamanen, Anna-Marja ; Kassem, Moustapha ; Abdallah, Basem. / TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro.
@conference{d67b68fdc15e4598a2e6d892c42f310b,
title = "TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro",
abstract = "DLK1/FA1 (delta like-1 homolog/Fetal Antigen-1) is a novel surface marker for embryonic chondroprogenitor cells undergoing lineage progression from proliferation to prehypertrophic stages. However, mechanisms mediating control of its expression during chondrogenesis are not known. Thus, we examined the effect of a number of signalling molecules on DLK1 expression during in vitro chondrogenic differentiation in mouse embryonic limb bud mesenchymal micromass cultures and mouse embryonic fibroblast (MEF) pellet cultures. Dlk1 was initially expressed during mesenchymal condensation and chondrocyte proliferation, in parallel with expression of Sox9 and Col2a1, and was down-regulated upon expression of Col10a1 by hypertrophic chondrocytes. Among a number of molecules that affected chondrogenesis, TGF-b signalling regulated Dlk1expression. TGF-b1-induced chondrogenesis was associated with decreased Dlk1 expression and these effects were abolished by the TGF-b signalling inhibitor SB4311542 suggesting an involvement of DLK1/FA1 in mediating the function of TGF-b1 signalling in chondrogenesis. In support of this hypothesis, we found that TGF-b1 enhanced chondrocyte differentiation in dlk1-/- MEF compared to wild type MEF. In conclusion, our data identified TGF-b-1 as an upstream negative regulator of Dlk1 expression and function during the early events of embryonic chondrogenesis. The cross-talk between TGF-b1 and DLK1 showed promotion of early chondrogenesis during embryonic endochondral bone formation process.",
author = "Linda Harkness and Hanna Taipaleenmaki and Anna-Marja Saamanen and Moustapha Kassem and Basem Abdallah",
year = "2011",
month = "6",
day = "15",
language = "English",

}

Harkness, L, Taipaleenmaki, H, Saamanen, A-M, Kassem, M & Abdallah, B 2011, 'TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro'.

TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro. / Harkness, Linda; Taipaleenmaki, Hanna; Saamanen, Anna-Marja; Kassem, Moustapha; Abdallah, Basem.

2011.

Publikation: Konferencebidrag uden forlag/tidsskriftPosterForskning

TY - CONF

T1 - TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro

AU - Harkness, Linda

AU - Taipaleenmaki, Hanna

AU - Saamanen, Anna-Marja

AU - Kassem, Moustapha

AU - Abdallah, Basem

PY - 2011/6/15

Y1 - 2011/6/15

N2 - DLK1/FA1 (delta like-1 homolog/Fetal Antigen-1) is a novel surface marker for embryonic chondroprogenitor cells undergoing lineage progression from proliferation to prehypertrophic stages. However, mechanisms mediating control of its expression during chondrogenesis are not known. Thus, we examined the effect of a number of signalling molecules on DLK1 expression during in vitro chondrogenic differentiation in mouse embryonic limb bud mesenchymal micromass cultures and mouse embryonic fibroblast (MEF) pellet cultures. Dlk1 was initially expressed during mesenchymal condensation and chondrocyte proliferation, in parallel with expression of Sox9 and Col2a1, and was down-regulated upon expression of Col10a1 by hypertrophic chondrocytes. Among a number of molecules that affected chondrogenesis, TGF-b signalling regulated Dlk1expression. TGF-b1-induced chondrogenesis was associated with decreased Dlk1 expression and these effects were abolished by the TGF-b signalling inhibitor SB4311542 suggesting an involvement of DLK1/FA1 in mediating the function of TGF-b1 signalling in chondrogenesis. In support of this hypothesis, we found that TGF-b1 enhanced chondrocyte differentiation in dlk1-/- MEF compared to wild type MEF. In conclusion, our data identified TGF-b-1 as an upstream negative regulator of Dlk1 expression and function during the early events of embryonic chondrogenesis. The cross-talk between TGF-b1 and DLK1 showed promotion of early chondrogenesis during embryonic endochondral bone formation process.

AB - DLK1/FA1 (delta like-1 homolog/Fetal Antigen-1) is a novel surface marker for embryonic chondroprogenitor cells undergoing lineage progression from proliferation to prehypertrophic stages. However, mechanisms mediating control of its expression during chondrogenesis are not known. Thus, we examined the effect of a number of signalling molecules on DLK1 expression during in vitro chondrogenic differentiation in mouse embryonic limb bud mesenchymal micromass cultures and mouse embryonic fibroblast (MEF) pellet cultures. Dlk1 was initially expressed during mesenchymal condensation and chondrocyte proliferation, in parallel with expression of Sox9 and Col2a1, and was down-regulated upon expression of Col10a1 by hypertrophic chondrocytes. Among a number of molecules that affected chondrogenesis, TGF-b signalling regulated Dlk1expression. TGF-b1-induced chondrogenesis was associated with decreased Dlk1 expression and these effects were abolished by the TGF-b signalling inhibitor SB4311542 suggesting an involvement of DLK1/FA1 in mediating the function of TGF-b1 signalling in chondrogenesis. In support of this hypothesis, we found that TGF-b1 enhanced chondrocyte differentiation in dlk1-/- MEF compared to wild type MEF. In conclusion, our data identified TGF-b-1 as an upstream negative regulator of Dlk1 expression and function during the early events of embryonic chondrogenesis. The cross-talk between TGF-b1 and DLK1 showed promotion of early chondrogenesis during embryonic endochondral bone formation process.

M3 - Poster

ER -

Harkness L, Taipaleenmaki H, Saamanen A-M, Kassem M, Abdallah B. TGFb signalling inhibits DLK1 expression during chondrogenesis in vitro. 2011.