Evidence of Estrogen Receptors in Normal Human Osteoblast-Like Cells

Eriksen, E F; Colvard, Douglas S.; Berg, NJ; Graham, Matthew M.; Mann, KG; Spelsberg, T. C.; Riggs, B. Lawrence

doi:10.1126/science.3388021

Cited by 1,154 publications

(250 citation statements)

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“…A wide distribution of ER␣-immunoreactions has been reported in primate dermal fibroblasts (Bentley et al, 1986); human fibroblasts; human endothelial cells (Brandi et al, 1993); mammary gland cells (for review, see Pelletier, 2000); chondrocytes in cows, pigs, and humans (Claassen et al, 2001); human osteoblasts (Eriksen et al, 1988); and human osteoclasts (Pensler et al, 1990), in addition to female reproductive tissues, indicating that estrogen has diverse effects on development, growth, and homeostasis (Clark et al, 1992). Although many epidemiological studies have reported a higher frequency of TMD in females than in males (Campbell et al, 1993; LeResche, 1997; Kapila and Xie, 1998), there has been controversy concerning the presence of ER␣ in the TMJ.…”

Section: Discussionmentioning

confidence: 99%

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Yamada¹,

Nozawa-Inoue²,

Kawano³

et al. 2003

Anat. Rec.

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Numerous epidemiological studies have pointed out a higher frequency of temporomandibular disorder (TMD) in women than in men, which indicates the involvement of a sex hormone, such as estrogen, in the pathogenesis of TMD. Although estrogen is known to play pivotal roles in osteoarthrosis or rheumatoid arthritis in systemic joints, there have been few reports about the role of estrogen in the temporomandibular joint (TMJ). The effect of estrogen is generally mediated by the estrogen receptors (ERs) ER␣ (the predominant type) and ER␤. In this study we examined the expression of ER␣ protein and mRNA in the TMJ of adult male rats by immunocytochemistry and in situ hybridization histochemistry. Intense ER␣ immunoreactivity was localized in the synovial lining cells, stromal cells in the articular disc, and chondrocytes in the TMJ. These ER␣-immunopositive synovial lining cells are characteristic of cytoplasmic processes identified with confocal and immunoelectron microscopy, which indicates that they are synovial type B cells. In situ hybridization histochemistry confirmed intense signals for ER␣ in the synovial lining cells and the sublining fibroblasts at mRNA levels. The nuclei of chondrocytes showed an intense immunoreaction for ER␣ in the maturative and hypertrophic layers of the articular cartilage. In addition to the nuclear localization of ER␣, a weak immunoreaction appeared in the cytoplasm of some ER␣-positive cells. These findings support the hypothesis that TMJ tissue-at least in the male rat-has the potential to be an estrogen target tissue. Anat Rec Part A 274A: 934 -941, 2003.

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Section: Discussionmentioning

confidence: 99%

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Yamada¹,

Nozawa-Inoue²,

Kawano³

et al. 2003

Anat. Rec.

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“…Demonstrations that cells of the osteoblastic lineage, which include osteoblasts and osteocytes in bone and osteoblast progenitor cells in sites such as the bone marrow stroma, express both a and p isoforms of the estrogen receptor [7,10,38] have suggested that many effects of E?. on bone are mediated through actions on these cells.…”

Section: Introductionmentioning

confidence: 99%

Estrogen regulation of growth and alkaline phosphatase expression by cultured human bone marrow stromal cells

Holzer

Einhorn

Majeska

2002

Journal Orthopaedic Research

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Estrogen has been reported to regulate the growth and differentiation of cultured murine osteoprogenitor cells in bone marrow stroma. This study tested the ability of 17P-estradiol (E2) to regulate growth and expression of alkaline phosphatase (ALP), an osteoblastic differentiation marker, in strains of normal human bone marrow stromal cells derived from different donors. In eight strains examined, E2 at 1 and 10 n M produced at most modest effectxs on growth and ALP activity. Growth inhibition, seen in 4 of the 8 strains, was more common than stimulation (2 of the 8 strains); the greatest observed E2 effect was a n inhibition of ca. 5 0 V~ E2 altered ALP activity less dramatically than cell growth. Differences from control in total ALP per culture were seen in only two strains; one was a reduction, one an increase. Colony forming assays were used to determine if E2 changed the proportion of ALPexpressing cells in marrow stromal cell cultures. In contrast to growth experiments, ALP expression under colony forming conditions (200 cells per 35 mm-diameter well) was dependent on the type of serum supplementation used. Under permissive conditions using medium supplemented with 10% charcoal-treated fetal bovine serum, 10 n M E2 increased the number of ALP-positive colonies (cfu-ap) but not the total number of colonies formed (cfu-f). When cells cultured in the presence or absence of 10 nM E2 were replated at colony forming densities, significantly higher proportions of cfu-ap were found in 2 of 6 strains examined, while pretreatment with E2 affected the number of cfu-f in only 1 of the 6 strains. Similar results were obtained when colony formation was carried out in the presence of dexamethasone and ascorbate, although these agents themselves increased the formation of both cfu-f and cfu-ap. These results show that the direct effects of E2 on human marrow stromal cells are small and vary depending on the cell strain and on the experimental conditions; however, the E2 actions observed in this study were consistent with reports that E2 exerts direct actions on osteoblasts and osteoblast progenitor cells that favor rather than suppress their phenotypic expression.

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“…Vários trabalhos não evidenciam a presença de receptores de E2 nos osteoclastos (13), mas sim nos osteoblastos (14) e em células do estroma da medula óssea (15). Assim, o aumento da reabsorção óssea conseqüente à carência estrogênica pode ser secundário a um aumento da secreção pelos osteoblastos ou pelas células do estroma da medula óssea de fatores capazes de estimular osteoclastos e/ou seus precursores, resultando em aumento da reabsorção óssea.…”

Section: Osteoporose Pós-menopausa (Tipo I)unclassified

Fisiopatologia da osteoporose involutiva

Ramalho

Lazaretti‐Castro

1999

Arq Bras Endocrinol Metab

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A diminuição da densidade mineral óssea (DMO) com a idade é um fenômeno universal, atingindo todas as raças e culturas, não patológico em si, mas que se constitui um substrato para o desenvolvimento da osteoporose (OP). Em 1941, Albright descreveu pela primeira vez a OP, e chamou atenção para deficiência de estrógeno (E2) como causa principal desta patologia. Isso foi confirmado em trabalhos posteriores, onde a reposição hormonal preveniu a perda óssea. Posteriormente, Riggs e Melton classificaram a OP involutiva em tipo I e tipo II. A OP tipo I, ou pós-menopáusica, ocorre nos 10 anos que se seguem à menopausa, sendo uma conseqüência da deficiência de E2. Porém, o mecanismo de ação do E2 no osso ainda é desconhecido. Vários trabalhos não evidenciaram receptores de E2 em osteoclastos, sugerindo que o efeito do E2 se faz de forma indireta via osteoblastos ou pelas células do estroma da medula óssea, através da liberação de mediadores. Dados recentes são controversos sobre o papel da interleucina 6 como mediadora do efeito estrogênico. A OP tipo II, ou senil, ocorreria após 65 anos. À partir dessa idade, outros fatores também seriam determinantes da OP, dentre eles o hiperparatiroidismo secundário. Recentemente, Riggs e Melton retornaram a teoria unitária do modelo de OP involutiva, colocando o E2 como fator etiológico central para ambas as fases de perda óssea. As discussões sobre as classificações da OP têm objetivos didáticos, mas demonstram também o caráter heterogêneo e multifatorial da doença. ABSTRACTThe decrease in bone mineral density (BMD) with age is a universal phenomenon that affects all races and cultures; non-pathological by itself but it is the background to development of osteoporosis (OP). In 1941, Albright described the postmenopausal OP, and discussed the special role of the estrogen (E2) lack. Others that prevented the OP with hormonal therapy confirmed this hypothesis. Later, Riggs and Melton proposed a classification of involutional OP on type I and type II. The type I OP appears in the first 10 years after menopause and is secondary to the deficit of E2. However, it is not clear the mechanisms of action of E2 on bone tissue: which are the mediators and also the target cells. There is no E2 receptors identified on osteoclast. Probably, the E2 effects are indirectly through osteoblast or by bone marrow stromal cells. The citokines, specially the interleucine 6 are candidate to be the mediators of E2 actions, but the data are still controversy in the literature. Type II or senile OP is defined to occur after 65 years old. In this age, others factors further than E2 deficiency determine the OP, and the secondary hyperparathyroidism play a special role. Recently, Riggs and Melton proposed a return to Albright's idea suggesting a unitary model of the involutional OP and placing the E2 as the central ethiological factor of bone loss. This distinction in OP type I or type II is theoretical, but shows the heterogeneous and multifactorial aspects of this disease. (Arq Bras Endocrinol Metab 1999; 43/6...

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Evidence of Estrogen Receptors in Normal Human Osteoblast-Like Cells

Cited by 1,154 publications

References 21 publications

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Estrogen regulation of growth and alkaline phosphatase expression by cultured human bone marrow stromal cells

Fisiopatologia da osteoporose involutiva

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