Modulation of survival in osteoblasts from postmenopausal women

García-Moreno, Carmen; Catalán, Marina P.; Ortíz, Alberto; Álvarez, Lara; Piedra, Concepción de la

doi:10.1016/j.bone.2004.02.021

Cited by 24 publications

(20 citation statements)

References 38 publications

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“…These results are supported by a recent publication of opposing effects of estrogen and androgen on apoptosis, here in T47D cells (22). Further, our in vitro analyses are consistent with multiple reports indicating that estrogen can reduce osteoblast apoptosis in some (12,27,65), but not all circumstances (11).…”

Section: Discussionsupporting

confidence: 92%

Section: Androgen the Ar And Bone Cellsmentioning

confidence: 99%

“…This work has resulted in submission of both an abstract and a peer-reviewed publication (11). (Please refer to Appendices 2 and 3).…”

mentioning

confidence: 99%

“…This reduction in osteoblast viability, which can be inhibited with AR antagonists, might be associated with enhanced apoptosis, even in settings of enhanced bone formation (K Wiren, unpublished). Androgens may also augment the osteoanabolic effects of mechanical strain in osteoblasts (see also Update) [11].Analysis of AR, ERa and ERß mRNA and protein expression during osteoblast differentiation in vitro show that all receptors display expression patterns dependent upon the stage of differentiation [12]. The levels of AR expression increase throughout osteoblast differentiation, with the highest AR levels seen in mature osteoblast/ osteocytic cultures, suggesting that androgen may predominantly affect mature osteoblasts.…”

mentioning

confidence: 99%

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Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality, and Bone Architecture

Wiren¹,

Jepsen²

2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. (From -To) REPORT DATE (DD-MM-YYYY) 01-12-2005 REPORT TYPE Annual DATES COVERED PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBEROregon Health and Science University Portland, OR 97239-0398 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTAndrogens have been shown to be important mediators of bone growth and remodeling independent of estrogen. A better understanding of the consequences of androgen action in bone is particularly important given increased anabolic steroid abuse. In addition, since bone architecture and bone material properties play important roles in stress fracture, analysis of this model represents a unique opportunity to characterize the consequences of androgen action in both genders on bone microarchitectural quality and the integrity of the skeleton in vivo. We genetically engineered transgenic mice in which androgen receptor (AR) overexpression is skeletally targeted to better understand the role of androgen signaling in bone. The central hypothesis of this proposal is that AR transactivation in the osteoblast lineage provides key regulatory signals that regulate the progression of osteoblast differentiation and osteogenesis, control the resorption of calcified bone, and modulate lineage determination in the marrow, to influence skeletal architecture and matrix quality. In the first year, we have successfully created the second line of AR-transgenic mice using the col2.3 promoter to drive AR expression. Ongoing analysis of studies (proposed in Specific Aim 1) suggest that AR transactivation (in young adults of col2.3 with col3.6 ARtransgenic animals) in mature osteoblasts is primarily responsible for mediating the effects of androgen on matrix quality and/or mineralization, while immature cells mediate effects of androgen on the periosteum and potentially body composition. Further, e...

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Section: Discussionsupporting

confidence: 92%

Section: Androgen the Ar And Bone Cellsmentioning

confidence: 99%

“…This work has resulted in submission of both an abstract and a peer-reviewed publication (11). (Please refer to Appendices 2 and 3).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality, and Bone Architecture

Wiren¹,

Jepsen²

2005

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“…These osteoblasts have increased expression of Fas mRNA and protein, as well as increased sensitivity to Fas ligand-induced cell death (Garcia-Moreno et al, 2004). Quickly it becomes clear that by modulating just osteoblast survival, the onset of osteoporosis can be pushed forward or back; one receptor can possibly directing an entire pathogenesis.…”

Section: Apoptosis: Regulation Of Remodelingmentioning

confidence: 99%

Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro

et al. 2011

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Comparative in vivo evaluation of porous and dense duplex titanium and hydroxyapatite coating with high roughnesses in different implantation environments

Borsari

Fini

Giavaresi

et al. 2008

J Biomedical Materials Res

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Ti (PG60) and Ti plus HA (HPG60) dense coatings with ultrahigh roughness (Ra: 74 +/- 8 microm and 53 +/- 18 microm, respectively) were compared to high Ti (Ti60) and Ti plus HA (HT60) high roughened porous coatings (Ra: 40 +/- 7 microm and 36 +/- 3 microm, respectively). Surfaces were implanted in cortical and trabecular bone of young adult (YOUNG), aged (AGED) and estrogen-deficient sheep (OVX) and analyzed by means of histology, histomorphometry and push-out tests 3 months after implantation. A significantly lower value in affinity index (AI) of PG60 when compared to TI60 (p < 0.01) was observed in cortical bone. In trabecular bone, lower values in AI were found in TI60 and PG60 when compared to their HA-coated surfaces (p < 0.0005). Bone ingrowth (BI) of TI60 and PG60 was significantly lower than that of the HA-coated surfaces in trabecular bone (p < 0.05). Significantly lower values in BI in OVX sheep in comparison to YOUNG sheep in both cortical and trabecular bone were observed (p < 0.05). Data showed that high roughness and Ti and HA-coated surfaces are suitable for aged and osteoporotic patients. HA coatings represent the most successful strategy in trabecular bone.

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Modulation of survival in osteoblasts from postmenopausal women

Cited by 24 publications

References 38 publications

Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality, and Bone Architecture

Enhanced Androgen Signaling with Androgen Receptor Overexpression in the Osteoblast Lineage Controls Skeletal Turnover, Matrix Quality, and Bone Architecture

Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro

Comparative in vivo evaluation of porous and dense duplex titanium and hydroxyapatite coating with high roughnesses in different implantation environments

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