Role of Extracellular Calcium Control, Calcium Sensing, and Regulation of Calcium Regulating Hormones in Heart Failure~!2009-09-29~!2009-11-30~!2010-06-14~!

2010 ◽  
Vol 3 (2) ◽  
pp. 16-24
Author(s):  
R. Schreckenberg ◽  
S. Wenzel ◽  
K.-D. Schluter
Keyword(s):  
Heart Failure ◽  
Extracellular Calcium ◽  
Calcium Sensing

Expression of extracellular calcium-sensing receptor in human osteoblastic MG-63 cell line

2001 ◽  
Vol 280 (2) ◽  
pp. C382-C393 ◽  
Author(s):  
Toru Yamaguchi ◽  
Naibedya Chattopadhyay ◽  
Olga Kifor ◽  
Chianping Ye ◽  
Peter M. Vassilev ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Northern Blot Analysis ◽  
Pcr Primers ◽  
Extracellular Calcium ◽  
Calcium Sensing Receptor ◽  
Patch Clamp Technique ◽  
Calcium Sensing ◽  
Specific Affinity

We have previously shown the expression of the extracellular calcium (Cao 2+)-sensing receptor (CaR) in osteoblast-like cell lines, and others have documented its expression in sections of murine, bovine, and rat bone. The existence of the CaR in osteoblasts remains controversial, however, since some studies have failed to document its expression in the same osteoblast-like cell lines. The goals of the present study were twofold. 1) We sought to determine whether the CaR is expressed in the human osteoblast-like cell line, MG-63, which has recently been reported by others not to express this receptor. 2) We investigated whether the CaR, if present in MG-63 cells, is functionally active, since most previous studies have not proven the role of the CaR in mediating known actions of Cao 2+ on osteoblast-like cells. We used immunocytochemistry and Western blotting with the specific, affinity-purified anti-CaR antiserum 4637 as well as Northern blot analysis and RT-PCR using a riboprobe and PCR primers specific for the human CaR, respectively, to show readily detectable CaR protein and mRNA expression in MG-63 cells. Finally, we employed the patch-clamp technique to show that an elevation in Cao 2+ as well as the specific, allosteric CaR activator NPS R-467 (0.5 μM), but not its less active stereoisomer NPS S-467 (0.5 μM), activate an outward K+ channel in MG-63 cells, strongly suggesting that the CaR in MG-63 cells is not only expressed but is functionally active.

276 Does TRP channel play a role of extracellular calcium sensing in urethral smooth muscle?

2016 ◽  
Vol 15 (3) ◽  
pp. e276
Author(s):  
S. Kajioka ◽  
M. Hayashi ◽  
T. Maki ◽  
R. Takahashi ◽  
M. Etoh
Keyword(s):  
Smooth Muscle ◽  
Extracellular Calcium ◽  
Trp Channel ◽  
Calcium Sensing ◽  
Urethral Smooth Muscle

Epidermal Keratinocyte Differentiation is Disrupted in Mice Lacking The Full Length Extracellular Calcium-Sensing Receptor

1997 ◽  
Vol 3 (S2) ◽  
pp. 185-186
Author(s):  
László G. Kömüves ◽  
Jonathan D. Harris ◽  
Chrystal Ho ◽  
Daniel D. Bikle
Keyword(s):  
In Situ Hybridization ◽  
Knockout Mice ◽  
Ion Homeostasis ◽  
Extracellular Calcium ◽  
Full Length ◽  
Keratinocyte Differentiation ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing

The importance of the extracellular calcium-sensing receptor (CaR) in the stringent control of extracellular Ca2+ concentration is well established. However, the presence of CaR in tissues not directly involved in regulating mineral ion homeostasis suggests a role for CaR in local regulation of cellular functions. Although extracellular Ca2+ regulates the differentiation of keratinocytes, the role of CaR in the epidermis is not established. In this work using knockout mice lacking full length CaR, we sought to determine the role of CaR in epidermal differentiation.Dorsal skin of Casr−/− knockout mice lacking full length CaR, and Casr+/+ (wild type) control mice, aged 4 to 7 days after birth was fixed in 4% formaldehyde in PBS, and in 2.5% glutaraldehyde and 2% formaldehyde in 0.1 M cacodylate buffer. The samples were embedded in paraffin (for immunohistochemistry and for in situ hybridization) or in Spurr’s or LR White resins. Digoxigenin labeled antisense and sense RNA probes for loricrin and filaggrin were used for in situ hybridization.

scholarly journals Role of the Calcium-Sensing Receptor in Cardiomyocyte Apoptosis via the Sarcoplasmic Reticulum and Mitochondrial Death Pathway in Cardiac Hypertrophy and Heart Failure

2013 ◽  
Vol 31 (4-5) ◽  
pp. 728-743 ◽  
Author(s):  
Fang-Hao Lu ◽  
Song-Bin Fu ◽  
Xiaoning Leng ◽  
Xinying Zhang ◽  
Shiyun Dong ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Cardiomyocyte Apoptosis ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
Mitochondrial Death Pathway

scholarly journals The Role of Calcium in Inflammation-Associated Bone Resorption

Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 69 ◽  
Author(s):  
Gordon L. Klein
Keyword(s):  
Bone Resorption ◽  
Inflammatory Response ◽  
Calcium Concentration ◽  
Burn Injury ◽  
Extracellular Calcium ◽  
Systemic Inflammatory Response ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
Injury Model

The aim of this mini-review is to discuss the role of calcium in the process of cytokine-mediated bone resorption in an effort to understand the role circulating calcium may play in the resorption of bone. The liberation of calcium and possibly phosphorus and magnesium by bone resorption may sustain and intensify the inflammatory response. We used a burn injury setting in humans and a burn injury model in animals in order to examine the effects on the bone of the systemic inflammatory response and identified the parathyroid calcium-sensing receptor as the mediator of increasing bone resorption, hence higher interleukin (IL)-1 production, and decreasing bone resorption, hence the lowering of circulating ionized calcium concentration. Thus, extracellular calcium, by means of the parathyroid calcium-sensing receptor, is able to modulate inflammation-mediated resorption.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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