Novel effect of estrogen on RANK and c-fms expression in RAW 264.7 cells

Galal, Nadia; El-Beialy, Waleed; Deyama, Yoshiaki; Yoshimura, Yoshitaka; Suzuki, Kuniaki; Totsuka, Yasunori

doi:10.3892/ijmm.20.1.97

Cited by 12 publications

(13 citation statements)

References 27 publications

(31 reference statements)

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“…Abubaker et al (29) found ER α immunoreactivity in the articular disc of human TMJs; however, Campbell et al (5) found no such immunoreactivity in the articular disc of a TMJ obtained from a TMD patient. In our previous study (30), with the use of Western blotting and PCR amplification, we were able to demonstrate the novel detection of ER ß and confirmed presence of ER α in RAW 264.7 cells (representing macrophage-like type A synovial linning cells). In this study we showed expression of ER α and ß in HFLS (synovial linning cells type B), thus exploring both kinds of synovial lining cells.…”

Section: Discussionmentioning

confidence: 99%

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Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Galal

Beialy²,

Deyama³

et al. 2008

Int J Mol Med

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Abstract. Several epidemiological studies have reported that temporomandibular disorder is more prevalent in women, which suggests the involvement of sex hormones, such as estrogen, in the pathogenesis of this disease. PCR amplification and Western blotting were employed to target the expression of estrogen receptors (ERs) in human fibroblast-like synovial and ATDC5 cells. The effect of estrogen was investigated through the expression of RANKL, osteoprotegerin (OPG), M-CSF/CSF-1 and c-fms. We showed expression of M-CSF/ CSF-1 and c-fms, with time-dependent increase in both after the addition of estrogen. Based on previous studies reporting that M-CSF/CSF-1 regulates the proliferation and differentiation of hemopoietic progenitor cells into mature macrophages, we put forward a new hypothesis based on the increased inflammation and tendency of females to suffer more from temporomandibular disorder (TMD) in the presence of external exacerbating factors. Detection of RANKL and OPG in ATDC5 and expression of both in HFLS was confirmed with complete disappearance of the RANKL band, and marked increase in the expression of OPG after 1 h from the addition of estrogen.

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Section: Discussionmentioning

confidence: 99%

“…In our previous study (30) we showed that estrogen increased expression of c-fms in macrophage-like cells. In the present study, we detected the expression of M-CSF/CSF-1 and c-fms in ATDC5 and HFLS cells and we further demonstrated increased expression of M-CSF/CSF-1 and c-fms via estrogen.…”

Section: Discussionmentioning

confidence: 99%

Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Galal

Beialy²,

Deyama³

et al. 2008

Int J Mol Med

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“…Previously, we reported the effects of estrogen on RaW 264.7 and hFls cells, regarding inflammation and bone resorption [15,16]. In the current study we investigated the expression of PMca isoforms in RaW 264.7 and hFls cells, as well as, the modulatory effect of 17β-estradiol on the expression levels of PMca isoforms.…”

Section: Western Blottingmentioning

confidence: 99%

“…another reported the effect of 17β-estradiol on sarcoplasmic reticulum Ca 2+ -atPase in h9c2 cells [14]; neither report assessed the direct effects of 17β-estradiol on PMCA, nor the relevantly affected PMca isoform. We investigated the effects of our previously reported optimal concentration of 10 -8 M 17β-estradiol [15,16] on hFls and RaW 264.7 cells. the specific ca 2+ -atPase activity in RaW 264.7 and hFls treated for 24 hours decreased to 62% and 94% respectively, compared to that of their control (100%) (Fig.…”

Section: Cell Homogenatementioning

confidence: 99%

Effects of Estrogen on PMCA 2 and 4 in Human Fibroblast-like Synovial Cells and Mouse Macrophage-like Cells

et al. 2010

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Abstract.We investigated the possible roles of estrogen on plasma membrane ca 2+ -ATPase (PMCA) in human fibroblastlike synovial cells (hFls) and mouse macrophage-like cells (RaW 264.7). Western blots revealed the expression of PMca 2 and 4 in both cells. In vitro treatments with 17β-estradiol for 24 hours resulted in a concentration dependent decrease in PMca expression. Moreover, ca 2+ -ATPase specific activity was similarly decreased with estrogen treatments. However, treatments for 1 hour in the presence or absence of cycloheximide demonstrated non-significant effects. These results suggest that estrogen has a modulatory role on ca 2+ homeostasis through decreasing PMca expression and abating their activity. correspondence to: kuniaki sUZUkI, hokkaido University, Graduate school of dental Medicine, kita-ku, kita 13, Nishi 7, sapporo 060-8586, hokkaido, Japan. e-mail: ksuzuki@den.hokudai.ac.jp *authors equally contributed to work The clAssic model of the estrogen action involves binding to intracellular steroid receptors. In the last decade, increasing body of evidence for the rapid nongenomic effects of the hormone has been demonstrated and its mechanisms of action were shown to include receptor and non-receptor-mediated pathways [1,2]. Fast responses with unique steroid specificity have been reported to occur in purified plasma membrane preparations [3]. Possible mechanism has been attributed to interaction with membrane lipids that then altered the function of membrane proteins. It was reported that steroids may have a direct effect on the protein-protein interaction and may also bind directly to protein molecules [4]. In the past years, estradiol, a lipophilic molecule that can easily cross plasma membranes and blood-brain barrier, has received considerably more attention. Numerous studies revealed that estrogens exert neuro-protective effect in the aged or injured brain, maintain intracellular calcium homeostasis and, at high hormone level, promote antioxidant activity [5][6][7][8].cytosolic ca 2+ regulates several cellular processes and its concentration is, in turn, finely regulated by various channels, pumps and exchangers. the plasma membrane ca 2+

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“…The effects of estrogen on osteoblasts include both direct effects resulting in increased bone formation, and an indirect effect, via an osteoblast-mediated interaction with preosteoclasts and osteoclasts, resulting in decreased bone resorption (Galal et al 2007). Estrogen exerts its indirect effect through products secreted by osteoblasts that include receptor activator of nuclear factor kB ligand (RANKL), colony-stimulating factor-1 (CSF1), and osteoprotegerin (OPG), which are important in differentiation and maturation of osteoclasts.…”

Section: Introductionmentioning

confidence: 99%

Ormeloxifene inhibits osteoclast differentiation in parallel to downregulating RANKL-induced ROS generation and suppressing the activation of ERK and JNK in murine RAW264.7 cells

Kharkwal

Chandra²,

Fatima³

et al. 2012

Journal of Molecular Endocrinology

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Ormeloxifene (Orm), a triphenylethylene compound, has been established as a selective estrogen receptor modulator (SERM) that suppresses the ovariectomy-induced bone resorption in rats. However, the precise mechanism underlying the bone-preserving action of Orm remains unclear. In this study, we evaluated the effect of Orm on osteoclast formation induced by receptor activator of nuclear factor kB ligand (RANKL) in the murine macrophage cell line RAW264.7. We also explored the mechanism of action of Orm by studying the RANKL-induced signaling pathways required for osteoclast differentiation. We found that Orm inhibited osteoclast formation from murine macrophage RAW264.7 cells induced by RANKL in a dose-dependent manner. Orm was able to abolish RANKL-induced reactive oxygen species (ROS) elevation and inhibited the transcriptional activation of two key RANKL-induced transcription factors namely activator protein-1 (AP-1) and NF-kB through mechanisms involving MAPKs. Activation of two MAPKs, i.e. ERK (MAPK1) and JNK (MAPK8), was alleviated by Orm effectively, which subsequently affected the activation of c-Jun and c-Fos, which are the essential components of the AP-1 transcription complex. Taken together, our results demonstrate that Orm potentially inhibits osteoclastogenesis by inhibiting ROS generation and thereby suppressing the activation of ERK1/2 (MAPK3/MAPK1) and JNK (MAPK8) and transcription factors (NF-kB and AP-1), which subsequently affect the regulation of osteoclastogenesis. These results provide a possible mechanism of action of Orm in regulating osteoclastogenesis, thereby supporting the beneficial bone-protective effects of this compound.

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Novel effect of estrogen on RANK and c-fms expression in RAW 264.7 cells

Cited by 12 publications

References 27 publications

Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Effects of Estrogen on PMCA 2 and 4 in Human Fibroblast-like Synovial Cells and Mouse Macrophage-like Cells

Ormeloxifene inhibits osteoclast differentiation in parallel to downregulating RANKL-induced ROS generation and suppressing the activation of ERK and JNK in murine RAW264.7 cells

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