scholarly journals Calcium-Sensing Receptor in Human Peripheral Blood T Lymphocytes Is Involved in the AMI Onset and Progression through the NF-κB Signaling Pathway

2016 ◽  
Vol 17 (9) ◽  
pp. 1397 ◽  
Author(s):  
Jing-Ya Zeng ◽  
Jing-Jing Du ◽  
Ying Pan ◽  
Jian Wu ◽  
Hai-Liang Bi ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Tai-yu Zhai ◽  
Bao-hong Cui ◽  
Lei Zou ◽  
Jing-ya Zeng ◽  
Song Gao ◽  
...  

The calcium-sensing receptors (CaSRs) play an important role in many tissues and organs that are involved in inflammatory reactions. Peripheral blood polymorphonuclear neutrophils (PMNs) are important inflammatory cells. However, the expression and functions of CaSR in peripheral blood PMNs are still not reported. In this study, we collected rat peripheral blood PMNs to observe the relationship between CaSR and PMNs. From the results, we found first that the CaSR protein was expressed in PMNs, and it increased after PMNs were activated with fMLP. In addition, CaSR activator cincalcet promoted the expression of CaSR and P-p65 (NF-κB signaling pathway protein) and Bcl-xl (antiapoptosis protein), and it increased the secretion of interleukin-6 (IL-6) and myeloperoxidase (MPO); meanwhile, it decreased proapoptosis protein Bax expression and the production of IL-10 and reactive oxygen species (ROS). At the same time, cincalcet also decreased the PMN apoptosis rate analyzed by flow cytometry. However, CaSR inhibitor NPS-2143 and NF-κB signaling pathway inhibitor PDTC reverse the results cited earlier. All of these results indicated that CaSR can regulate PMN functions and status to play a role in inflammation, which is probably through the NF-κB signaling pathway.


2002 ◽  
Vol 364 (1) ◽  
pp. 245-254 ◽  
Author(s):  
Alessandra GAMBERUCCI ◽  
Emanuele GIURISATO ◽  
Paola PIZZO ◽  
Maristella TASSI ◽  
Roberta GIUNTI ◽  
...  

In Jurkat and human peripheral blood T-lymphocytes, 1-oleoyl-2-acetyl-sn-glycerol (OAG), a membrane-permeant analogue of diacylglycerol, activated the influx of Ca2+, Ba2+ and Sr2+. OAG also caused plasma-membrane depolarization in Ca2+-free media that was recovered by the addition of bivalent cation, indicating the activation of Na+ influx. OAG-induced cation influx was (i) mimicked by the natural dacylglycerol 1-stearoyl-2-arachidonyl-sn-glycerol, (ii) not blocked by inhibiting protein kinase C or in the absence of phopholipase C activity and (iii) blocked by La3+ and Gd3+. Differently from OAG, both thapsigargin and phytohaemagglutinin activated a potent influx of Ca2+, but little influx of Ba2+ and Sr2+. Moreover, the influx of Ca2+ activated by thapsigargin and that activated by OAG were additive. Furthermore, several drugs (i.e. econazole, SKF96365, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, 2-aminoethoxy diphenylborate and calyculin-A), while inhibiting the influx of Ca2+ induced by both thapsigargin and phytohaemagglutinin, did not affect OAG-stimulated cation influx. Transient receptor potential (TRP) 3 and TRP6 proteins have been shown previously to be activated by diacylglycerol when expressed heterologously in animal cells [Hofmann, Obukhov, Schaefer, Harteneck, Gudermann and Schultz (1999) Nature (London) 397, 259–263]. In both Jurkat and peripheral blood T-lymphocytes, mRNA encoding TRP proteins 1, 3, 4 and 6 was detected by reverse transcriptase PCR, and the TRP6 protein was detected by Western blotting in a purified plasma-membrane fraction. We conclude that T-cells express a diacylglycerol-activated cation channel, unrelated to the channel involved in capacitative Ca2+ entry, and associated with the expression of TRP6 protein.


Blood ◽  
2003 ◽  
Vol 101 (1) ◽  
pp. 216-225 ◽  
Author(s):  
Anthony D. Cristillo ◽  
Mirtha J. Macri ◽  
Barbara E. Bierer

Abstract The chemokine superfamily consists of small (8-10 kDa) molecules that function to attract, selectively, different subsets of leukocytes. Binding of chemokines to their appropriate G-protein–coupled receptors is necessary for primary immune responses and for homing of leukocytes to lymphoid tissues. Here, we have characterized the signaling pathways in primary T lymphocytes that regulate chemokine gene induction using an RNase protection assay. Dependence on stimulation through the coreceptor CD28 and sensitivity to the calcineurin inhibitors cyclosporine and tacrolimus were studied using purified human peripheral blood lymphocytes. Lymphotactin (Ltn), macrophage inflammatory protein (MIP)–1α, and MIP-1β were all rapidly induced and sensitive to cyclosporine treatment. At later time points, the expression of MIP-1α and MIP-1β, but not of Ltn, was restored despite the inhibition of calcineurin activity. By contrast, the induction of interleukin-8 was delayed and was found to be cyclosporine insensitive. Calcineurin activity of IP-10 mRNA induction was contingent on the specific T-cell stimulation conditions, suggesting that IP-10 expression is modulated by calcineurin-dependent and -independent signaling pathways. Differential chemokine expression profiles result from the engagement of T-cell coreceptors and the requirement for, and the dependence on, calcineurin phosphatase activity.


Oncogene ◽  
1999 ◽  
Vol 18 (8) ◽  
pp. 1581-1588 ◽  
Author(s):  
Teresa Laín de Lera ◽  
Lola Folgueira ◽  
Angel G Martín ◽  
Catherine Dargemont ◽  
María-Antonia Pedraza ◽  
...  

PLoS ONE ◽  
2010 ◽  
Vol 5 (6) ◽  
pp. e11373 ◽  
Author(s):  
Matthew E. Brown ◽  
Elizabeth Rondon ◽  
Deepika Rajesh ◽  
Amanda Mack ◽  
Rachel Lewis ◽  
...  

1989 ◽  
pp. 551-553
Author(s):  
Frits Koning ◽  
Rafick P. Sekaly ◽  
Erwin Tschachler ◽  
Roberto Biassoni ◽  
Marvin S. Reitz ◽  
...  

1987 ◽  
Author(s):  
S Aydar ◽  
S Alataş ◽  
L Numanoğlu ◽  
A Sönmezdağ

Human peripheral blood T lymphacytes when cultered in the presence of mitogen Phytohemogglutinin (PHA) acquire the capacity to form E rosettes with sheep erythrocytes that are resistant to incubation at 37° C. Whereas human thymus lymphocytes form 37° C stable E rosettes. On the other hand, it is shown that the use of anticoagulants can prevent cancer metastases which brings forth the importance of explaining the relationship between the lymphocyte functions and anticoagulant action mecha-nismus. In order to investigate this relationship, we did a group af experiments with lymphocytes of normal children and of children with severe burn wounds. Peripheral blood lymphocytes were seperated by “Lymphoprep” centrifugation technique. The lymphocytes of normal children and patients with burn were divided in two groups: A-Activated lymphocytes: 1×106 /ml lymphocytes were cultured and activated by PHAfor 48 hours at 37° C in RPMI 1640. B-Non activated lymphocytes were in culture witout PHA. 1×10™6 M/ml warfarin sulfate was added to some of the cultures of each group prior to the culture conditions. At the end of the 48 hour incubation, heat stable rosette formation was determined by the method of Wauve and co-workers. Significantly elevated levels of heat stable rosette forming cells were found in the PHA activated culture treated with warfarin sulfate in normals and patients with burn. Although the blastic transformation of T lymphocytes was found to be depressed, heat stable rosette formation of warfarin sulfate treated lymphocytes abtained from burn patients was observed to be significantly elevated. It is concluded that warfarin sulfate increases the activity of T lymphocytes by interfering with the resynthesis of heai stable E receptors.


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