Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels

Xu, Youjia; Li, Guangfei; Du, Bencai; Zhang, Peng; Xiao, Li; Sirois, Pierré; Li, Kai

doi:10.1016/j.regpep.2011.08.009

Cited by 31 publications

(22 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Established OB-6 [2] and hFOB1.19 [36] human osteoblastic cells were purchased from the Cell Bank of the Shanghai Institute of Biological Sciences (Shanghai, China). Cells were cultured as described previously [2,36].…”

Section: Cell Culturementioning

confidence: 99%

See 1 more Smart Citation

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Fan¹,

Zhang²,

Liu³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Dexamethasone (Dex) induces injuries to human osteoblasts. In this study, we tested the potential role of the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (Lnc-MALAT1) in this process. Materials: Two established human osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts were treated with Dex. Lnc-MALAT1 expression was analyzed by quantitative real-time polymerase chain reaction assay. Cell viability, apoptosis, and death were tested by the MTT assay, histone-DNA assay, and trypan blue staining assay, respectively. AMP-activated protein kinase (AMPK) signaling was evaluated by western blotting and AMPK activity assay. Results: Lnc-MALAT1 expression was downregulated by Dex treatment in the established osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts. The level of Lnc-MALAT1 was decreased in the necrotic femoral head tissues of Dex-administered patients. In osteoblastic cells and primary human osteoblasts, forced overexpression of Lnc-MALAT1 using a lentiviral vector (LV-MALAT1) inhibited Dex-induced cell viability reduction, cell death, and apoptosis. Conversely, transfection with Lnc-MALAT1 small interfering RNA aggravated Dex-induced cytotoxicity. Transfection with LV-MALAT1 downregulated Ppm1e (protein phosphatase, Mg^2+/ Mn²⁺-dependent 1e) expression to activate AMPK signaling. Treatment of osteoblasts with AMPKα1 short hairpin RNA or dominant negative mutation (T172A) abolished LV-MALAT1-induced protection against Dex-induced cytotoxicity. Furthermore, LV-MALAT1 induced an increase in nicotinamide adenine dinucleotide phosphate activity and activation of Nrf2 signaling. Dex-induced reactive oxygen species production was significantly attenuated by LV-MALAT1 transfection in osteoblastic cells and primary osteoblasts. Conclusion: Lnc-MALAT1 protects human osteoblasts from Dex-induced injuries, possibly via activation of Ppm1e-AMPK signaling.

show abstract

Section: Cell Culturementioning

confidence: 99%

“…Cells were cultured as described previously [2,36]. The primary human osteoblasts were provided by Dr. Ji [6] and cultured under previously described conditions [6,37].…”

Section: Cell Culturementioning

confidence: 99%

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Fan¹,

Zhang²,

Liu³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Hepcidin inhibits iron transport by binding to the iron export channel ferroportin that is located on the basolateral surface of gut enterocytes and the plasma membrane of reticuloendothelial cells (19,20). The first direct experimental evidence establishing the linkage between hepcidin and OP came from the study performed by Xu and colleagues (17) reporting that hepcidin was shown to be significantly capable of increasing intracellular calcium concentration in osteoblast cell line hFOB1.19. The study, albeit carried out in an in vitro cell culture system, sheds new light into the crucial role of iron homeostasis in bone metabolism (5).…”

Section: Discussionmentioning

confidence: 99%

“…It may also be associated with anemia and hemochromatosis, therefore a high concentration of iron in sera seems to be sufficiently necessary but insufficient condition to the judgment of onset of OP. Thirdly, hepcidin has been shown to be able to increase the intracellular calcium (17), the calcium concentration should have been detected.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Reduced hepcidin level features osteoporosis

Liu

Zhong

et al. 2018

Exp Ther Med

View full text Add to dashboard Cite

Osteoporosis (OP) is a common serious skeletal disorder marked by increased risk of bone fracture due to fragility. OP has been taken to be a disease linked with abnormal calcium metabolism that alone is obviously insufficient to explain the development of OP. Iron overload has been associated with the development of OP and increasing studies have suggested the association. However, direct evidence for this has not been clinically established. To this end, using the Roche biochemical autoanalyzer, we detected the concentration of iron, soluble transferrin receptor 2 (TFR2), and hepcidin, a key peptide regulating iron homeostasis, in the sera from patients with OP. It was shown that the iron and TFR2 concentration was markedly higher than that of healthy control; whereas the concentration of hepcidin was markedly lower than that in control. In addition, to pilot explore the underlying mechanism by which hepcidin was downregulated, we present that hepcidin can directly interact with TFR2 using immunoprecipitation. The present study first established the direct biochemical evidence for the involvement of hepcidin in the pathogenesis of OP, indicating that the upregulation of hepcidin could be used as a novel alternative therapeutic strategy in the management of OP.

show abstract

Osteoblast cell membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry for screening specific active components from traditional Chinese medicines

et al. 2017

View full text Add to dashboard Cite

A method using osteoblast membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry was developed to recognize and identify the specific active components from traditional Chinese medicines. Primary rat osteoblasts were used for the preparation of the stationary phase in the cell chromatography method. Retention components from the cell chromatography were collected and analyzed by liquid chromatography with time-of-flight mass spectrometry. This method was applied in screening active components from extracts of four traditional Chinese medicines. In total, 24 potentially active components with different structures were retained by osteoblast cell chromatography. There were five phenolic glucosides and one triterpenoid saponin from Curculigo orchioides Gaertn, two organic acids and ten flavonoids from Epimedium sagittatum Maxim, one phthalide compound and one organic acid from Angelica sinensis Diels, and two flavonoids and two saponins from Anemarrhena asphodeloides Bunge. Among those, four components (icariin, curculigoside, ferulaic acid, and timosaponin BII) were used for in vitro pharmacodynamics validation. They significantly increased the osteoblast proliferation, alkaline phosphatase activity, levels of bone gla protein and collagen type 1, and promoted mineralized nodule formation. The developed method was an effective screening method for finding active components from complex medicines that act on bone diseases.

show abstract

Hepcidin increases intracellular Ca2+ of osteoblast hFOB1.19 through L-type Ca2+ channels

Cited by 31 publications

References 13 publications

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Reduced hepcidin level features osteoporosis

Osteoblast cell membrane chromatography coupled with liquid chromatography and time-of-flight mass spectrometry for screening specific active components from traditional Chinese medicines

Contact Info

Product

Resources

About