Increased Fat Due to Estrogen Deficiency Induces Bone Loss by Elevating Monocyte Chemoattractant Protein-1 (MCP-1) Production

Kim, Youn-Young; Kim, Song Hee; Oh, So-Ra; Sul, Ok-Joo; Lee, Hyeyoung; Kim, Hyun-Ju; Kim, Shin‐Yoon; Choi, Hye-Seon

doi:10.1007/s10059-010-0027-x

Cited by 20 publications

(21 citation statements)

References 39 publications

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“…The lack of MCP-1 attenuated the influx of blood CD11c cells, which were significantly elevated by OVX, thus partly explaining the increase of CD11c cells in AT of OVX mice. Previously we have demonstrated that OVX increased serum MCP-1 [20]. OVX also resulted in increase of M-CSF compared with sham surgery, whereas the absence of MCP-1 reduced it.…”

Section: Discussionmentioning

confidence: 77%

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Monocyte Chemoattractant Protein-1 Deficiency Attenuates Oxidative Stress and Protects against Ovariectomy-Induced Chronic Inflammation in Mice

et al. 2013

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BackgroundLoss of ovarian function is highly associated with an elevated risk of metabolic disease. Monocyte chemoattractant protein-1 (MCP-1, C-C chemokine ligand 2) plays critical roles in the development of inflammation, but its role in ovariectomy (OVX)-induced metabolic disturbance has not been known.Methodology and Principal FindingsWe investigated the role of MCP-1 in OVX-induced metabolic perturbation using MCP-1-knockout mice. OVX increased fat mass, serum levels of MCP-1, macrophage-colony stimulating factor (M-CSF), and reactive oxygen species (ROS), whereas MCP-1 deficiency attenuated these. OVX-induced increases of visceral fat resulted in elevated levels of highly inflammatory CD11c-expressing cells as well as other immune cells in adipose tissue, whereas a lack of MCP-1 significantly reduced all of these levels. MCP-1 deficiency attenuated activation of phospholipase Cγ2, transforming oncogene from Ak strain, and extracellular signal-regulated kinase as well as generation of ROS, which is required for up-regulating CD11c expression upon M-CSF stimulation in bone marrow-derived macrophages.Conclusions/SignificanceOur data suggested that MCP-1 plays a key role in developing metabolic perturbation caused by a loss of ovarian functions through elevating CD11c expression via ROS generation.

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Section: Discussionmentioning

confidence: 77%

“…In previous studies, we demonstrated that OVX increases serum MCP-1 level [20]. To investigate whether MCP-1 contributes to OVX-induced metabolic dysfunction, we analyzed MCP-1-knockout (KO) mice, compared with wild type (WT) mice.…”

Section: Resultsmentioning

confidence: 99%

Monocyte Chemoattractant Protein-1 Deficiency Attenuates Oxidative Stress and Protects against Ovariectomy-Induced Chronic Inflammation in Mice

et al. 2013

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“…The average daily intake of food was not different between SHAM and OVX groups, indicating that lipid accumulation in OVX mice was not a result of hyperphagy. But probably a result of alterations in fatty acid metabolism, as an activated hepatic fatty acid synthesis and impaired fatty acid oxidation (Kumagai et al 1993;Sanyal et al 2001;Kim et al 2010). Body weight gain and adiposity were reduced with both the treatments and the levels of glucose, total cholesterol, LDL-cholesterol and VLDLcholesterol were decreased in OVX mice treated with UDCA, or HRT.…”

Section: Discussionmentioning

confidence: 99%

Use of Ursodeoxycholic Acid on Post-menopausal Obesity, Hepatic steatosis and Plasma Profile as an Alternative Treatment for Hormone Replacement Therapy

Franzoni

Amorim

Silva

et al. 2015

Braz. arch. biol. technol.

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“…Observed in our study, the concentrations of TRAP significantly increased from week 8 to week 12, indicating that the osteoclastogenesis might be activated by corticosteroids. MCP-1 also plays a very important role in activating and aggregating the monocytes/macrophages [37]. Moreover, steroid-induced osteonecrosis arose from the aberrant immune response and the imbalance of bone metabolism.…”

Section: Discussionmentioning

confidence: 99%

Immune response associated with Toll-like receptor 4 signaling pathway leads to steroid-induced femoral head osteonecrosis

Tian

Wen

Dang

et al. 2014

BMC Musculoskelet Disord

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BackgroundFemoral head osteonecrosis is frequently observed in patients treated with excessive corticosteroids. The objective of the current study was to establish a rat model to investigate the disruption of immune response in steroid-induced femoral head osteonecrosis via Toll-like receptor 4 (TLR4) signaling pathway.MethodsMale SD rats were divided into the treatment group (group A) and the model group (group B) consisting of 24 rats each, and were injected intramuscularly with 20 mg/kg methylprednisolone (MP) for 8 weeks, once a week. The rats in group A were injected intravenously with 7.5 mg/kg TAK242 before each MP administration. A control group (group N) consisted of 12 rats were received saline injection. All animals were sacrificed 8, 10 and 12 weeks from the first MP injection, respectively. Histopathological analysis was performed and the concentration of tartrate-resistant acid phosphatase (TRAP) in serum was tested. The signaling molecules including TLR4, MyD88, NF-κB p65 and MCP-1 were detected by immunohistochemistry, quantitative real-time PCR and Western blot.ResultsFemoral head osteonecrosis was observed in the model rats, and the concentration of TRAP and positive staining of all signaling molecules increased significantly in group B compared with that in group A and group N. Compare with the control group, the mRNA expressions and protein levels of all signaling molecules were enhanced significantly in group B, but no significant in group A.ConclusionsCorticosteroids can induce femoral head osteonecrosis by disturbing the immune response via TLR4 signaling pathway. These findings suggest that the disruption of immune response play a role in the pathogenesis of osteonecrosis.

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Increased Fat Due to Estrogen Deficiency Induces Bone Loss by Elevating Monocyte Chemoattractant Protein-1 (MCP-1) Production

Cited by 20 publications

References 39 publications

Monocyte Chemoattractant Protein-1 Deficiency Attenuates Oxidative Stress and Protects against Ovariectomy-Induced Chronic Inflammation in Mice

Monocyte Chemoattractant Protein-1 Deficiency Attenuates Oxidative Stress and Protects against Ovariectomy-Induced Chronic Inflammation in Mice

Use of Ursodeoxycholic Acid on Post-menopausal Obesity, Hepatic steatosis and Plasma Profile as an Alternative Treatment for Hormone Replacement Therapy

Immune response associated with Toll-like receptor 4 signaling pathway leads to steroid-induced femoral head osteonecrosis

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