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Scientific paper - Original scientific paper
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, no. 3, 2010, pp. 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 and Ana Marušić. "Fas receptor is required for estrogen deficiency-induced bone loss in mice." Laboratory Investigation 90, no. 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), pp. 402-413. doi: 10.1038/labinvest.2009.144

Kovačić N, Grčević D, Katavić V, Lukić IK, Grubišić V, Mihovilović K, and sur.. Fas receptor is required for estrogen deficiency-induced bone loss in mice. Laboratory Investigation [Internet]. 2010 March [cited 2024 April 10];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, no. 3, pp. 402-413, March 2010. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:105:601792. [Accessed: 10 April 2024]

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Metadata
Title (english)Fas receptor is required for estrogen deficiency-induced bone loss in mice
AuthorNataša Kovačić
AuthorDanka Grčević
AuthorVedran Katavić
AuthorIvan Krešimir Lukić
AuthorVladimir Grubišić
AuthorKarlo Mihovilović
AuthorHrvoje Cvija
AuthorPeter Ian Croucher
AuthorAna Marušić
Author's institutionUniversity of Zagreb
School of Medicine
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
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.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionAccepted version
Journal titleLaboratory Investigation
Numberingvol. 90, no. 3, pp. 402-413
p-ISSN0023-6837
DOIhttps://doi.org/10.1038/labinvest.2009.144
URN:NBNurn:nbn:hr:105:601792
Publication2010-03
Document URLhttps://doi.org/10.1038/labinvest.2009.144
Type of resourceText
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2024-03-28 11:49:12