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Fas receptor is required for estrogen deficiency-induced bone loss in mice
Laboratory Investigation, 90 (2010), 3; 402-413. https://doi.org/10.1038/labinvest.2009.144
Kovačić, Nataša; Grčević, Danka; Katavić, Vedran; Lukić, Ivan Krešimir; Grubišić, Vladimir; Mihovilović, Karlo; Cvija, Hrvoje; Croucher, Peter Ian; Marušić, Ana

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Kovačić, N., Grčević, D., Katavić, V., Lukić, I. K., Grubišić, V., Mihovilović, K. ... Marušić, A. (2010). Fas receptor is required for estrogen deficiency-induced bone loss in mice. Laboratory Investigation, 90. (3), 402-413. doi: 10.1038/labinvest.2009.144

Kovačić, Nataša, et al. "Fas receptor is required for estrogen deficiency-induced bone loss in mice." Laboratory Investigation, vol. 90, br. 3, 2010, str. 402-413. https://doi.org/10.1038/labinvest.2009.144

Kovačić, Nataša, Danka Grčević, Vedran Katavić, Ivan Krešimir Lukić, Vladimir Grubišić, Karlo Mihovilović, Hrvoje Cvija, Peter Ian Croucher i Ana Marušić. "Fas receptor is required for estrogen deficiency-induced bone loss in mice." Laboratory Investigation 90, br. 3 (2010): 402-413. https://doi.org/10.1038/labinvest.2009.144

Kovačić, N., et al. (2010) 'Fas receptor is required for estrogen deficiency-induced bone loss in mice', Laboratory Investigation, 90(3), str. 402-413. doi: 10.1038/labinvest.2009.144

Kovačić N, Grčević D, Katavić V, Lukić IK, Grubišić V, Mihovilović K, i sur.. Fas receptor is required for estrogen deficiency-induced bone loss in mice. Laboratory Investigation [Internet]. 03.2010. [pristupljeno 14.04.2024.];90(3):402-413. doi: 10.1038/labinvest.2009.144

N. Kovačić, et al., "Fas receptor is required for estrogen deficiency-induced bone loss in mice", Laboratory Investigation, vol. 90, br. 3, str. 402-413, Ožujak 2010. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:105:601792. [Citirano: 14.04.2024.]

Za citiranje koristite ovu mrežnu adresu: https://urn.nsk.hr/urn:nbn:hr:105:601792
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Podaci o radu
Naslov (engleski)Fas receptor is required for estrogen deficiency-induced bone loss in mice
AutorNataša Kovačić
AutorDanka Grčević
AutorVedran Katavić
AutorIvan Krešimir Lukić
AutorVladimir Grubišić
AutorKarlo Mihovilović
AutorHrvoje Cvija
AutorPeter Ian Croucher
AutorAna Marušić
Autorova ustanovaSveučilište u Zagrebu
Medicinski fakultet
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Sažetak (engleski)
Bone mass is determined by bone cell differentiation, activity, and death, which mainly occur through apoptosis. Apoptosis can be triggered by death receptor Fas (CD95), expressed on osteoblasts and osteoclasts and may be regulated by estrogen. We have previously shown that signaling through Fas inhibits osteoblast differentiation. In this study we analyzed Fas as a possible mediator of bone loss induced by estrogen withdrawal. At 4 weeks after ovariectomy (OVX), Fas gene expression was greater in osteoblasts and lower in osteoclasts in ovariectomized C57BL/6J (wild type (wt)) mice compared with sham-operated animals. OVX was unable to induce bone loss in mice with a gene knockout for Fas (Fas -/- mice). The number of osteoclasts increased in wt mice after OVX, whereas it remained unchanged in Fas -/- mice. OVX induced greater stimulation of osteoblastogenesis in Fas -/- than in wt mice, with higher expression of osteoblast-specific genes. Direct effects on bone cell differentiation and apoptosis in vivo were confirmed in vitro, in which addition of estradiol decreased Fas expression and partially abrogated the apoptotic and differentiation-inhibitory effect of Fas in osteoblast lineage cells, while having no effect on Fas-induced apoptosis in osteoclast lineage cells. In conclusion, the Fas receptor has an important role in the pathogenesis of postmenopausal osteoporosis by mediating apoptosis and inhibiting differentiation of osteoblast lineage cells. Modulation of Fas effects on bone cells may be used as a therapeutic target in the treatment of osteoresorptive disorders.
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran
Verzija publikacijeZavršna verzija rukopisa prihvaćena za objavljivanje (postprint)
Naslov časopisaLaboratory Investigation
Brojčani podacivol. 90, br. 3, str. 402-413
p-ISSN0023-6837
DOIhttps://doi.org/10.1038/labinvest.2009.144
URN:NBNurn:nbn:hr:105:601792
Datum objave publikacije2010-03
URL dokumentahttps://doi.org/10.1038/labinvest.2009.144
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
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Datum i vrijeme pohrane2024-03-28 11:49:12