Microarray analysis of changes in bone cell gene expression early after cadmium gavage in mice

Regunathan, Akhila; Glesne, David; Wilson, Allison K.; Song, Jongwoo; Nicolae, Dan L.; Flores, Tony; Bhattacharyya, Maryka H.

doi:10.1016/s0041-008x(03)00163-7

Cited by 57 publications

(30 citation statements)

References 78 publications

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“…It has been shown that Cd may inhibit cell proliferation, differentiation and mineralization in osteoblasts (Chen et al, 2007). Regunathan et al (2003) reported that genes for bone formation showed little or no response to low level of Cd exposure and Cd might stimulate bone demineralization involving osteoclast activation. We speculated that osteoclasts may be the important target cells for Cd toxicity, in particular at low level of exposure.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, several organ culture systems also indicate that Cd stimulates bone resorption (Suzuki et al, 1989(Suzuki et al, , 1990Miyahara et al, 1992Miyahara et al, , 2001Wang et al, 1994). Microarray analysis shows that bone demineralization stimulated by Cd is related with osteoclast activation (Regunathan et al, 2003). Our previous studies in vitro showed that osteoclasts might be the target cells for low level of Cd exposure (Chen et al, 2009a).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Environmental level of cadmium exposure stimulates osteoclasts formation in male rats

Chen

Wang

Xu-fang

et al. 2013

Food and Chemical Toxicology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Environmental level of cadmium exposure stimulates osteoclasts formation in male rats

Chen

Wang

Xu-fang

et al. 2013

Food and Chemical Toxicology

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“…Cyr61 mRNA has been detected in human osteoblasts (Schutze et al 1998, Lechner et al 2000, and is up-regulated by cytokines such as tumor necrosis factor (TNF)-and interleukin (IL)-1 , which are important stimulators of bone resorption (Schutze et al 1998). Interestingly, Cyr61 was the most up-regulated gene in a microarray analysis of mice fed with cadmium, an in vivo model for cadmiuminduced osteoporosis (Regunathan et al 2003). It is possible that osteoblast-derived Cyr61 contributes to the increased bone resorption observed in the initial phase of GC-induced osteoporosis.…”

Section: Cysteine-rich Protein 61 (Cyr61)mentioning

confidence: 99%

Gene expression profiling of glucocorticoid-inhibited osteoblasts

Leclerc

Luppen²,

Ho³

et al. 2004

Journal of Molecular Endocrinology

108

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Glucocorticoid (GC) treatment for the management of autoimmune and inflammatory diseases is associated with decreased bone formation and increased risk for fracture. In MC3T3-E1 cell cultures, 0·1 -1 µM dexamethasone (DEX) arrests development of the osteoblast phenotype when administration commences at a commitment stage around the time of confluency. To gain new insights into GC-induced osteoporosis, we performed microarray-based gene expression analysis of GC-arrested MC3T3-E1 cultures, 2·5 days after the administration of DEX. Of the .12 000 transcripts interrogated, 74 were up-regulated and 17 were down-regulated by at least 2·5-fold (P¯0·05). Some of these genes, such as Mmp13, Serum/GC-regulated kinase and Tieg, have previously been reported as GC-responsive. Others are shown here for the first time to respond to GCs. DEX strongly repressed Krox20/Egr2 at both the mRNA and the protein level. This is especially significant because mice lacking this transcription factor develop osteoporosis. The data also suggest that the bone morphogenetic protein (BMP) pathway, which is involved in regulating bone mass, and other pathways that influence BMP signaling, are abrogated by GCs: (i) DEX increased the mRNA levels of the BMP antagonists Follistatin and Dan; (ii) DEX increased the levels of p21 Rasgap3 and Ptpn16/MKP-1 mRNAs, negative regulators of the MAP kinase pathway; and (iii) DEX decreased Cox mRNA levels. DEX also increased thrombospondin mRNA levels, which negatively regulate bone mass in vivo, as well as the adipocytic marker Fkbp51. These and other observations disclose novel gene targets, whose regulation by GCs in osteoblasts may shed light on and provide new therapeutic approaches to osteoporosis.

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“…Cd has been related with iron transporters, not only divalent-metal transporter-1 but also Tfrc (Leazer et al, 2002;Regunathan et al, 2003). Therefore, Tfrc might influence Cd transport into the neonatal brain.…”

Section: Resultsmentioning

confidence: 99%

Microarray analysis of neonatal brain exposed to cadmium during gestation and lactation

et al. 2013

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-DNA microarray containing 30,000 genes was used to monitor the transcriptional response of the neonatal brain after cadmium (Cd) exposure. C57BL/6J pregnant mice were exposed to Cd (10 ppm) during gestation and lactation via drinking water. In a comparison between the Cd-exposed neonatal brain and control, three genes including transferrin receptor (Tfrc) were up-regulated and one gene was down-regulated.

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Microarray analysis of changes in bone cell gene expression early after cadmium gavage in mice

Cited by 57 publications

References 78 publications

Environmental level of cadmium exposure stimulates osteoclasts formation in male rats

Environmental level of cadmium exposure stimulates osteoclasts formation in male rats

Gene expression profiling of glucocorticoid-inhibited osteoblasts

Microarray analysis of neonatal brain exposed to cadmium during gestation and lactation

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