Extracellular calcium sensing in rat aortic vascular smooth muscle cells

Smajilovic, Sanela; Hansen, Jakob Lerche; Christoffersen, Tue E. H.; Lewin, Ewa; Sheikh, Søren Paludan; Terwilliger, Ernest F.; Brown, Edward M.; Haunsø, Stig; Tfelt-Hansen, Jacob

doi:10.1016/j.bbrc.2006.07.192

Cited by 103 publications

(90 citation statements)

References 49 publications

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“…55 The CaR was shown previously to stimulate NO production in other cells. 56,57 The CaR was also found in VSMCs from the gerbilline spiral modiolar artery, 58 from rat aorta, 7 and from human aorta. 59 However, it should be noted that some investigators have been unable to demonstrate the presence of the CaR in aortic VSMCs.…”

Section: Expression Of the Car In The Cardiovascular Tissuesmentioning

confidence: 88%

“…5 Recently, the CaR has also been detected in endothelial cells and vascular smooth muscle cells (VSMCs) and shown to induce hyperpolarization of the smooth muscle cells. 6,7 Furthermore, several novel studies reported the CaR as a possible regulator of blood pressure. 8 -10 In this review, we summarize the status of research concerning possible roles of the CaR in blood pressure regulation and discuss possible mechanisms for its actions.…”

mentioning

confidence: 99%

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Novel Role of the Calcium-Sensing Receptor in Blood Pressure Modulation

Smajilovic

Tfelt-Hansen

2008

Hypertension

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Section: Expression Of the Car In The Cardiovascular Tissuesmentioning

confidence: 88%

mentioning

confidence: 99%

Novel Role of the Calcium-Sensing Receptor in Blood Pressure Modulation

Smajilovic

Tfelt-Hansen

2008

Hypertension

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“…Moreover, calcimimetics may directly affect the calcification process in vascular smooth muscle cells as the calcium sensing receptor is present in this cell type. 112,113 Also important to notice is that administration of daily doses of cinacalcet initially lowers serum PTH levels with an increase of these values toward predose concentrations after 12 to 24 hours thereby inducing oscillating serum PTH levels. 114 Daily intermittent decreases in serum PTH levels increase bone volume and density and thus have an anaboliclike effect on bone, 115 which may also reduce the risk for vascular calcification.…”

Section: Calcimimeticsmentioning

confidence: 99%

Vascular Calcification in Chronic Renal Failure

Neven

D’Haese

2011

Circulation Research

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Accelerated atherosclerotic plaque calcification and extensive medial calcifications are common and highly detrimental complications of chronic kidney disease. Valid murine models have been developed to investigate both pathologically distinguishable complications, which allow for better insight into the cellular mechanisms underlying these vascular pathologies and evaluation of compounds that might prevent or retard the onset or progression of vascular calcification. This review describes various experimental models that have been used for the study of arterial intimal and/or medial calcification and discusses the extent to which this experimental research has contributed to our current understanding of vascular calcification, particularly in the setting of chronic renal failure. (Circ Res. 2011;108:249-264.) Key Words: animal models Ⅲ vascular calcification Ⅲ chronic renal failure C ardiovascular disease is the main cause of morbidity and mortality in patients with chronic kidney disease (CKD), accounting for approximately 50% of all deaths in patients on dialysis and in recipients of renal transplants. 1 A large-scale prospective population-based study showed that renal function was inversely associated with cardiovascular and allcause mortality. 2 Vascular calcification is the major cause of cardiovascular disease in patients with CKD as it contributes to myocardial ischemia, impaired myocardial function, valvular insufficiency, arrhythmias and stroke and is shown to be a strong independent predictor of mortality in the general 3,4 as well as in the dialysis population. [5][6][7] In patients with endstage renal disease, the risk of death increases with the number of vascular sites affected by calcification in the aorta and the carotid and femoral arteries. 5 The high prevalence of vascular calcification is already reported in early stages of CKD 8,9 and in young dialysis patients. 10,11 Atherosclerotic plaque burden in the intimal layer is higher and these lesions are also more heavily calcified in CKD patients compared to the normal population. 12-14 Although intimal calcification is associated with cardiovascular mortality, 6 it remains controversial whether calcification of advanced atherosclerotic lesions stabilizes plaque vulnerability [15][16][17] or rather contributes to rupture of the fibrous cap, 18,19 leading to thrombotic events and myocardial infarction. Interestingly, Ehara et al 20 nicely showed that the pattern of calcification in the intimal plaque is of importance: small, frequent, spotty calcifications are more often found in patients with an acute myocardial infarction or with unstable angina pectoris, whereas the presence of extensive calcifications was highest in those with stable angina pectoris. Recent investigations add new insights to this observation and indicate that, in contrast to spacious calcified areas, sparse microcalcifications produce local stress, 21 activate macrophages to secrete inflammatory mediators 22 and induce apoptosis of vascular smooth muscle cells, 23...

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“…In previous studies, NPS R-467 was used at concentrations ranging between 1 and 10 mM and it was observed that maximal increase in intracellular Ca 2C concentration occurred after incubation with 1 and 5 mM NPS R-467 , Mun et al 2004. The effects of NPS 2390 were tested at the concentration of 10 mM , Smajilovich et al 2006. Control group oocytes were cultured in the absence of these substances.…”

Section: Functional Role Of Casr In Mammalian Oocytesmentioning

confidence: 99%

The extracellular calcium-sensing receptor is expressed in the cumulus–oocyte complex in mammals and modulates oocyte meiotic maturation

Santis¹,

Casavola²,

Reshkin³

et al. 2009

Reproduction

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The extracellular calcium-sensing receptor (CASR) plays an important role in cells involved in calcium (Ca 2C ) homeostasis by directly sensing changes in the extracellular Ca 2C ion concentration. We previously reported the localization and quantitative expression of CASR protein in human oocytes. In this study, we examined the expression and the functional role of CASR during oocyte meiotic maturation in a large mammal animal model, the horse. As in humans, CASR protein was found to be expressed in equine oocytes and cumulus cells. Western-blot analysis revealed a single 130 kDa band in denuded oocytes and a doublet of 130-120 kDa in cumulus cells. CASR labeling was observed by confocal microscopy in cumulus cells and in oocytes on the plasma membrane and within the cytoplasm at all examined stages of meiosis. Functionally, the CASR allosteric effector NPS R-467, in the presence of 2.92 mM external Ca 2C , increased oocyte maturation rate in a dose-dependent manner and its stimulatory effect was attenuated by pre-treatment with the CASR antagonist NPS 2390. NPS R-467 had no effect in suboptimal external Ca 2C (0.5 mM), indicating that it requires higher external Ca 2C to promote oocyte maturation. In oocytes treated with NPS R-467, CASR staining increased at the plasmalemma and was reduced in the cytosol. Moreover, NPS R-467 increased the activity of MAPK, also called ERK, in cumulus cells and oocytes. These results provide evidence of a novel signal transduction pathway modulating oocyte meiotic maturation in mammals in addition to the well-known systemic hormones.

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Extracellular calcium sensing in rat aortic vascular smooth muscle cells

Cited by 103 publications

References 49 publications

Novel Role of the Calcium-Sensing Receptor in Blood Pressure Modulation

Novel Role of the Calcium-Sensing Receptor in Blood Pressure Modulation

Vascular Calcification in Chronic Renal Failure

The extracellular calcium-sensing receptor is expressed in the cumulus–oocyte complex in mammals and modulates oocyte meiotic maturation

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