Biochemical effects of 17β-estradiol on UMR106 cells

Bankson, Daniel D.; Rifai, Nader; Williams, Mary Elizabeth; Silverman, Lawrence M.; Gray, T K

doi:10.1016/0169-6009(89)90023-8

Cited by 35 publications

(16 citation statements)

References 19 publications

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“…UMR-106 cell line is a well-characterized osteoblastic cell model, which expresses many phenotypic characteristics of normal osteoblasts (Forrest et al, 1985). Incubation of UMR-106 cells in serum-free medium containing 0.1 M E 2 led to increase of ALP activity, similar as previous reports (Gray et al, 1987;Bankson et al, 1989), thus validating our assay conditions suitable for bioactivity-guided isolation. Our result demonstrated that the crude ethanolic extract of TSZ could significantly increase the ALP activity in UMR-106 cells, indicating the existence of antiosteoporotic constituents in TSZ.…”

Section: Discussionsupporting

confidence: 86%

Antiosteoporotic compounds from seeds of Cuscuta chinensis

Yang

Chen

Wang

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionsupporting

confidence: 86%

Antiosteoporotic compounds from seeds of Cuscuta chinensis

Yang

Chen

Wang

et al. 2011

Journal of Ethnopharmacology

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“…For example, we recently reported that estrogen-induced bone formation is partially suppressed by inhibition of prostaglandin and nitric oxide synthesis. (14,15) Though growth factors such as TGF-␤1 and IGF-1 were also predicted to play a role in this response based on results of studies with isolated osteoblasts, (23)(24)(25)(26)(27) our preliminary findings suggested that if anything, expression of these factors tended to fall after estrogen administration. Interestingly, administration of diethylstilbestrol (DES) has also been reported to suppress IGF-I expression in rat bones.…”

Section: Estrogen Stimulates Bmp-6 Expressionmentioning

confidence: 92%

“…(17) For example, bone morphogenetic proteins (BMPs) are known to induce endochondral bone formation in vivo when administered as recombinant proteins (18,19) and are thought to play important roles in skeletal development and fracture repair. (20,21) Previous studies have reported that estrogen stimulates the release of osteogenic growth factors from osteoblasts in vitro, including BMPs, (22) insulin-like growth factor I (IGF-I), (23)(24)(25) and transforming growth factor-␤ (TGF-␤). (25)(26)(27) However, whether these serve as autocrine or paracrine mediators of estrogen's stimulatory action on bone formation in vivo has not previously been addressed.…”

mentioning

confidence: 99%

Increased Bone Morphogenetic Protein-6 Expression in Mouse Long Bones After Estrogen Administration

Plant

Tobias

2002

Journal of Bone and Mineral Research

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High-dose estrogen administration is known to induce new bone formation in mouse long bones. To study the role of regulatory proteins in this response, we examined associated changes in femoral messenger RNA (mRNA) for candidate factors. 17␤-estradiol (E 2 ) 0.5 mg was administered to intact female mice by weekly injection, and Northern blot analysis was performed 1, 2, 4, 8, 12, and 16 days after the first injection. In contrast to other factors, an increase was observed in mRNA for bone morphogenetic protein-6 (BMP-6), which reached significance at day 8 and subsequent time-points. Estrogen-induced changes in BMP-6 protein expression were assessed by immunocytochemistry in longitudinal femoral sections. In untreated animals, BMP-6 was expressed by a significant proportion of growth plate chondrocytes and a subpopulation of bone marrow cells. In contrast, osteoblasts were consistently BMP-6 negative. From as early as 4 days after starting estrogen, clusters of slightly elongated BMP-6 -positive cells were observed within the marrow cavity; the majority were close to active bone formation surfaces. Double immunolabeling studies revealed that only approximately 10% of BMP-6 -positive bone marrow cells co-expressed the osteoblast transcription factor Cbfa1 suggesting that they are largely distinct from the osteoblast precursor population generated concurrently. BMP-6 -positive cells expressed neither leukocyte nor erythroid markers (CD45 and TER-119, respectively), consistent with a stromal origin. We conclude that estrogen-induced osteogenesis in female mice is associated with increased levels of BMP-6 mRNA in mouse femurs, which seems to reflect the emergence of clusters of BMP-6 positive stromal cells adjacent to active bone formation surfaces. These findings raise the possibility that BMP-6 serves as a paracrine mediator of estrogen's osteogenic action in mice. (J Bone Miner Res 2002;17:782-790)

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“…It is known that estrogen as well as androgen influence osteoblastic cell functions through cell proliferation, alkaline phosphatase production and the expression of mRNA of insulin-like growth factor I (IGF-I) [25,26]. Hirato et al reported that 3fl-HSD activity in the fetal adrenal gland was strongly inhibited by estrogen [24].…”

Section: Discussionmentioning

confidence: 99%

3.BETA.-Hydroxysteroid Dehydrogenase Activity in Human Osteoblast-Like Cells.

et al. 1997

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Abstract. This paper describes for the first time the presence of 3/3-hydroxysteroid dehydrogenase (3/3-HSD) activity in osteoblast-like cells and investigates its characteristics. 313-HSD activity was detected by the formation of androstenedione from [3H]dehydroepiandrosterone (DHEA) in whole cell assays of human osteoblast-like cells, HOS and MG-63. The radiolabeled product, androstenedione, was purified by thin-layer chromatography and identified by recrystallization on admixture with authentic androstenedione to show constant specific activities. The apparent Michaelis constant (Km) for DHEA in HOS was found to be 9.9 µM and that in MG-63 was 80.4 µM. The expression of the 3f3-HSD messenger ribonucleic acid in HOS and MG-63 was demonstrated through a reverse transcriptionpolymerase chain reaction. The PCR products were confirmed by Southern blot analysis. The existence of 3/-HSD in osteoblast-like cells indicates that these cells convert i5 androgens into more biologically active 04 3-keto steroids. These results, together with the demonstration of other steroid converting enzyme systems, suggest that the osteoblast cells play an important role in facilitating hormonal action in bone tissue.

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Biochemical effects of 17β-estradiol on UMR106 cells

Cited by 35 publications

References 19 publications

Antiosteoporotic compounds from seeds of Cuscuta chinensis

Antiosteoporotic compounds from seeds of Cuscuta chinensis

Increased Bone Morphogenetic Protein-6 Expression in Mouse Long Bones After Estrogen Administration

3.BETA.-Hydroxysteroid Dehydrogenase Activity in Human Osteoblast-Like Cells.

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