Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

Chalmers, J. P.; Lin, Shuo-Yen J.; Martino, Tami A.; Arab, Sara; Liu, Peter; Husain, Mansoor; Sole, Michael J.; Belsham, Denise D.

doi:10.1677/jme-08-0050

Cited by 27 publications

(19 citation statements)

References 39 publications

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“…Since the establishment of the MOVAS-1 cell line (28), these cells have been utilised in vascular studies that have investigated the cell cycle (28), neuroendocrine peptide expression profiles (29), circadian rhythms (30) and signal transduction responses (31). However, to date, no published studies have employed the MOVAS-1 cell line to investigate vascular calcification.…”

Section: Discussionmentioning

confidence: 99%

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MOVAS-1 cell line: A new in vitro model of vascular calcification

Mackenzie

Zhu²,

Longley³

et al. 2011

Int J Mol Med

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Abstract. Vascular calcification has severe clinical consequences in a number of diseases, including diabetes, atherosclerosis and end-stage renal disease. The in vitro calcification of primary mouse, human and bovine vascular smooth muscle cells (VSMCs) is commonly employed to examine the mechanisms of vascular calcification. However, to date, no published studies have utilised a murine cell line to investigate this process. In the present study, we aimed to determine whether the mouse VSMC line MOVAS-1 can calcify in vitro. We established that the calcification of MOVAS-1 cells can be induced in the presence of calcifying medium (containing β-glycerophosphate and ascorbic acid), as detected by Alizarin Red and von Kossa staining, and quantification of calcium deposition and alkaline phosphatase activity. We also showed that the time course of MOVAS-1 calcification is comparable to that of the primary murine aortic VSMCs, establishing the MOVAS-1 cells as a feasible and relevant model. Significant increases in the mRNA expression profile of key genes associated with vascular calcification (Ocn, Akp2 and PiT-1) were observed in MOVAS-1 cells cultured under calcifying conditions, with similar changes in expression in murine aortic VSMCs. Furthermore, a significant reduction in calcification was observed in MOVAS-1 cells following treatment with levamisole and etidronate, known inhibitors of calcification. In conclusion, we demonstrated that the MOVAS-1 line is a reliable, convenient and economical system in which to investigate vascular calcification in vitro, and will make a useful contribution to increasing our understanding of this pathological process.

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Section: Discussionmentioning

confidence: 99%

“…This cell line exhibits a smooth muscle cell-specific phenotype, and has been employed to investigate the VSMC cell cycle (28); neuroendocrine peptide expression profiles (29); vascular circadian rhythms (30) and signal transduction responses to cytokines (31).…”

Section: Introductionmentioning

confidence: 99%

MOVAS-1 cell line: A new in vitro model of vascular calcification

Mackenzie

Zhu²,

Longley³

et al. 2011

Int J Mol Med

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“…Galanin immunoreactivity has been localized in all major regions of the heart in rats and other mammalian species (Xu et al, 1995b) and GAL mRNA has been detected in mouse cardiovascular cells (Chalmers et al, 2008). After myocardial infarction and after ischemiareperfusion in rodents, galanin content was elevated in the left ventricle (Habecker et al, 2005;Ewert et al, 2008;Alston et al, 2011), indicating a role for galanin in the response of the heart to injury.…”

Section: Heart and Central Cardiovascular Controlmentioning

confidence: 99%

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

et al. 2014

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“…MOVAS-1 cells were kindly provided by Dr. Husain at the University of Toronto and cultured in DMEM containing 10% FBS with either 3.0 mM phosphate or 5.0 mM glycerophosphate ( 24,25 ).…”

Section: Cell Culture Studiesmentioning

confidence: 99%

Activating transcription factor 4 regulates stearate-induced vascular calcification

Masuda

Ting

Levi

et al. 2012

Journal of Lipid Research

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terol, and oxidized phospholipids), and hormonal factors (tumor necrosis factor-␣ , bone morphogenetic protein-2, matrix gla protein, osteocalcin, fi broblast growth factors, and Klotho) in the pathogenesis of vascular calcifi cation (3)(4)(5)(6)(7)(8)(9)(10).Recently, we reported that bile acid nuclear receptor, farnesoid X receptor (FXR), and oxysterol nuclear receptor, liver X receptor (LXR), elicit opposite effects on vascular calcifi cation ( 11-13 ). We found that FXR activation attenuated CKD-dependent atherosclerotic calcifi cation in ApoE Ϫ / Ϫ mice with 5/6 nephrectomy. FXR activation by either VP16-FXR overexpression or INT-747 (an FXR-specifi c agonist) treatment attenuated mineralization of vascular smooth muscle cells (VSMCs) in culture. Conversely, FXR inhibition by FXR shRNA and the dominant negative (DN) form of FXR augmented vascular calcifi cation ( 11 ). In contrast to FXR, LXR activation by LXR agonists and adenovirus-mediated LXR overexpression by VP16-LXR ␣ and VP16-LXR ␤ promoted mineralization of VSMCs. Conversely, LXR inhibition by dominant negative forms of LXR ␣ and LXR ␤ attenuated vascular calcifi cation in VSMCs ( 12 ). The regulation of mineralization by FXR and LXR agonists was highly correlated with changes in lipid accumulation, fatty acid synthesis, and the expression of sterol regulatory element binding protein-1 (SREBP-1). The rate of lipogenesis in VSMCs through the SREBP-1c-dependent pathway was reduced by FXR activation but increased by LXR activation ( 11,12 ). SREBP-1c overexpression promoted mineralization in VSMCs, whereas SREBP-1c DN inhibited alkaline phosphatase activity and mineralization induced by LXR agonists. LXR and SREBP-1c activations increased, whereas FXR activation decreased saturated and monounsaturated fatty acids derived from lipogenesis. Furthermore, we found that stearate markedly Abstract Previously, we reported that stearate, a saturated fatty acid, promotes osteoblastic differentiation and mineralization of vascular smooth muscle cells (VSMC). In this study, we examined the molecular mechanisms by which stearate promotes vascular calcifi cation. ATF4 is a pivotal transcription factor in osteoblastogenesis and endoplasmic reticulum ( Cardiovascular disease, such as vascular calcifi cation, is the leading cause of death in patients with chronic kidney disease, accounting for over 50% of deaths ( 1, 2 ). Vascular calcifi cation is frequently observed in advanced atherosclerotic lesions and is a highly regulated process that recapitulates osteogenesis in bone formation. Recent in vivo and in vitro studies have implicated the involvement of numerous positive and negative regulators, including serum phosphate, several lipid-derived molecules (saturated fatty acids, oxys- University of Colorado Denver , Aurora, CO Abbreviations: ALP, alkaline phosphatase; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; eIF2 ␣ , ␣ -subunit of eukaryotic initiation factor 2; ER, endoplasmic reticulum; FXR, farnesoid X receptor; LXR, liver X recept...

show abstract

Diurnal profiling of neuroendocrine genes in murine heart, and shift in proopiomelanocortin gene expression with pressure-overload cardiac hypertrophy

Cited by 27 publications

References 39 publications

MOVAS-1 cell line: A new in vitro model of vascular calcification

MOVAS-1 cell line: A new in vitro model of vascular calcification

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

Activating transcription factor 4 regulates stearate-induced vascular calcification

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