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@article{2409957,
author = {Kratochvilova, Adela and Knopfová, Lucia and Gregorkova, Janka and Gruber, Reinhard and Janeckova, Eva and Chai, Yang and Matalova, Eva},
article_number = {September 2024},
doi = {http://dx.doi.org/10.1016/j.cdev.2024.203929},
keywords = {ECM; Fas ligand; Tgfb; Fosl2; Mef2c; Prrx1},
language = {eng},
issn = {2667-2901},
journal = {Cells & Development},
title = {FasL impacts Tgfb signaling in osteoblastic cells},
url = {https://www.sciencedirect.com/science/article/pii/S2667290124000305},
volume = {179},
year = {2024}
}
TY - JOUR
ID - 2409957
AU - Kratochvilova, Adela - Knopfová, Lucia - Gregorkova, Janka - Gruber, Reinhard - Janeckova, Eva - Chai, Yang - Matalova, Eva
PY - 2024
TI - FasL impacts Tgfb signaling in osteoblastic cells
JF - Cells & Development
VL - 179
IS - September 2024
SP - 1-6
EP - 1-6
PB - Elsevier B.V.
SN - 26672901
KW - ECM
KW - Fas ligand
KW - Tgfb
KW - Fosl2
KW - Mef2c
KW - Prrx1
UR - https://www.sciencedirect.com/science/article/pii/S2667290124000305
N2 - Fas ligand (FasL, CD178) belongs to classical apoptotic molecules, however, recent evidence expands the spectrum of FasL functions into non-apoptotic processes which also applies for the bone. Tgfb subfamily members (Tgfb1, Tgfb2, Tgfb3) represent major components in osteogenic pathways and extracellular matrix. Their possible association with FasL has not yet been investigated but can be postulated. To test such a hypothesis, FasL deficient (gld) calvaria-derived cells were examined with a focus on the expression of Tgfb receptor ligands. The qPCR analysis revealed significantly increased expression of Tgfb1, Tgfb2 and Tgfb3 in gld cells. To check the vice versa effect, the gld cells were stimulated by soluble FasL. As a consequence, a dramatic decrease in expression levels of all three ligands was observed. This phenomenon was also confirmed in IDG-SW3 (osteoblastic cells of endochondral origin). TFLink gateway identified Fosl2 as an exclusive candidate of FasL capable to impact expression of all three Tgfb ligands. However, Fosl2 siRNA did not cause any significant changes in expression of Tgfb ligands. Therefore, the upregulation of the three ligands is likely to occur separately. In this respect, we tested the only exclusive candidate transcription factor for Tgfb3, Prrx1. Additionally, an overlapping candidate for Tgfb1 and Tgfb2, Mef2c capable to modulate expression of sclerostin, was examined. Prrx1 as well as Mef2c were found upregulated in gld samples and their expression decreased after addition of FasL. The same effect of FasL treatment was observed in the IDG-SW3 model. Taken together, FasL deficiency causes an increase in the expression of Tgfb ligands and stimulation by FasL reduces Tgfb expression in osteoblastic cells. The candidates mediating the effect comprise Prrx1 for Tgfb3 and Mef2c for Tgfb1/2. These results indicate FasL as a novel cytokine interfering with Tgfb signaling and thus the complex osteogenic network. The emerging non-apoptotic functions of FasL in bone development and maintenance should also be considered in treatment strategies such as the anti-osteoporotic factor.
ER -
KRATOCHVILOVA, Adela, Lucia KNOPFOVÁ, Janka GREGORKOVA, Reinhard GRUBER, Eva JANECKOVA, Yang CHAI and Eva MATALOVA. FasL impacts Tgfb signaling in osteoblastic cells. \textit{Cells \&{} Development}. Elsevier B.V., 2024, vol.~179, September 2024, p.~1-6. ISSN~2667-2901. Available from: https://dx.doi.org/10.1016/j.cdev.2024.203929.
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