Intracellular Ca2+ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Clementi, Emilio; Martino, Gianvito; Grimaldi, Luigi M. E.; Brambilla, Elena; Meldolesi, Jacopo

doi:10.1002/eji.1830240619

Cited by 31 publications

(16 citation statements)

References 31 publications

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“…Decreased Ca 2ϩ influx across the plasma membrane, after release of an unchanged IP 3 pool, was demonstrated in these 2 experimental models. Similar changes in Ca 2ϩ pools and binding proteins have been reported in other in vitro and in vivo studies (16). The spatial distribution of the intracellular Ca 2ϩ stores and the magnitude of the [Ca 2ϩ ] i signal after TCR activation described in these reports are similar to those presented here in SF T cells, supporting a role for ER Ca 2ϩ pools in the control of SF T cell signaling.…”

Section: Discussionsupporting

confidence: 77%

“…The Ca 2ϩ released from the ER, which is partly dependent on the magnitude of the initiating stimulus, is termed the "IP 3 pool" (15,16). A second Ca 2ϩ pool is released from the ER by thapsigargin, an inhibitor of the Ca 2ϩ ATPase pump which is responsible for Ca 2ϩ reuptake into the ER (17) (the "thapsigargin pool").…”

Section: Conclusion We Found Abnormalities In the Magnitude Patternmentioning

confidence: 99%

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Dysregulated intracellular Ca2 stores and Ca2 signaling in synovial fluid T lymphocytes from patients with chronic inflammatory arthritis

Carruthers

Arrol

Bacon

et al. 2000

Arthritis & Rheumatism

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We found abnormalities in the magnitude, pattern, and spatial distribution of [Ca2+]i signaling in T cells from SF of patients with chronic inflammatory arthritis. A reduction in the number of responding SF T cells may partly explain some of our observations. However, we propose that the observed redistribution of SF Ca2+ stores may underlie the altered [Ca2+]i signaling, thus making these cells hyporesponsive to mitogen. The inflammatory environment of the joint and the late stage of differentiation of SF T cells are both likely to contribute to these changes in [Ca2+]i signaling, resulting in aberrant T cell function and promotion of disease chronicity.

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Section: Discussionsupporting

confidence: 77%

Section: Conclusion We Found Abnormalities In the Magnitude Patternmentioning

confidence: 99%

Dysregulated intracellular Ca2 stores and Ca2 signaling in synovial fluid T lymphocytes from patients with chronic inflammatory arthritis

Carruthers

Arrol

Bacon

et al. 2000

Arthritis & Rheumatism

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“…So far, however, this notion is based on circumstantial evidence (6,7,21,22 45 Ca 2ϩ experiments were performed as described in the legend of Fig. 3.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Calreticulin Increases Intracellular Ca2+ Storage and Decreases Store-operated Ca2+ Influx

Méry

Mesaeli

Michalak

et al. 1996

Journal of Biological Chemistry

255

213

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concentration within intracellular stores is not known, nor is the biochemical machinery that mediates the signaling from Ca 2ϩ stores to the plasma membrane.In this study, we demonstrate that overexpression of calreticulin in L fibroblasts leads to an increase in the Ca 2ϩ content of thapsigargin-sensitive Ca 2ϩ stores and to a decrease in store-operated Ca 2ϩ influx. EXPERIMENTAL PROCEDURESMaterials-Thapsigargin and Geneticin were obtained from Life Technologies (Basel, Switzerland); monensin, ionomycin, and DTPA were obtained from Sigma. 45 Ca 2ϩ was purchased from Du Pont de Nemours/New England Nuclear Inc. (Dreieich, Germany), and fura-2/AM was from Molecular Probes, Inc. (Eugene, OR). Dulbecco's modified Eagle's culture medium and fetal calf serum were obtained from Gibco (Paisley, Scotland). Restriction endonucleases and DNA-modifying enzymes were purchased from Boehringer Mannheim, Life Technologies, Inc., and Bio/Can Scientific. Mouse L fibroblasts were a generous gift of D. Kobasa (Department of Biochemistry, University of Alberta). All other chemicals were of the highest grade available and were obtained from Fluka (Buchs, Switzerland) or Sigma. The medium referred to as "Ca 2ϩ -free medium" contained 138 mM NaCl, 6 mM KCl, 1 mM MgCl 2 , 20 mM glucose, and 20 mM HEPES, pH 7.4. The medium referred to as "Ca 2ϩ medium" contained, in addition, 1.0 mM CaCl 2 . When drugs were added as dimethyl sulfoxide solutions, final concentrations of dimethyl sulfoxide in the recording medium did not exceed 0.25%.Plasmid Construction-To construct pRCR calreticulin expression vector, the DraI/SmaI restriction DNA fragment (nucleotides 20 -1653) of pcDx-CRT (GenBank accession number J05138) (4) was first inserted into SmaI-digested pSVL vector (Pharmacia Biotech Inc.) to generate pSVL-CRT (pSCR-1) calreticulin expression vector. Next, the XhoI/SstI DNA restriction fragment, containing cDNA encoding full-length calreticulin, was excised from pSCR-1 vector and inserted into XhoI/SstI restriction sites of pRc/CMV vector (Invitrogen) to generate pRCR. * This work was supported by Swiss National Foundation Grant 32 30161.90 and by grants from the Medical Research Council of Canada, the Carlos and Elsie de Reuter Foundation, the Sandoz Foundation, the Ernst and Lucie Schmidheiny Foundation, the Société Académique de Genève, the Helmut Horten Foundation, and the Zyma Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.§ To whom correspondence should be addressed.

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“…It has been shown earlier that lymphocyte activation produces modifications of the calcium storage and release characteristics of the cell (38) and that SERCA enzyme activity is involved in the control of cell proliferation and of lymphocyte activation (39 -42). However, the role and the modulation of the expression of the various SERCA isoforms, coexpressed in the cell, have not been previously investigated.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Endoplasmic Reticulum Calcium Pump Expression during T Lymphocyte Activation

Launay

Bobe

Lacabaratz

et al. 1997

Journal of Biological Chemistry

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Calcium mobilization from intracellular storage organelles is a key component of the second messenger system inducing cell activation. Calcium transport ATPases associated with intracellular calcium storage organelles play a major role in controlling this process by accumulating calcium from the cytosol into intracellular calcium pools. In this study the modulation of the expression of the sarco-endoplasmic reticulum calcium transport ATPase (SERCA) isoenzymes has been studied in lymphocytes undergoing phorbol myristate acetate and ionomycin-induced activation. In several T lymphocyte cell lines a combined treatment by the two drugs resulted in an approximately 90% decrease of the expression of the calcium pump isoform recognized by the PLIM430 isoform-specific antibody, whereas the expression of the SERCA 2b isoform was increased approximately 2-fold. Phorbol ester or ionomycin applied separately was ineffective. In Jurkat T cells the downmodulation of expression of the SERCA isoform recognized by the PLIM430 antibody appeared concomitantly with the induction of interleukin-2 expression and could be inhibited by the immunosuppressant drug cyclosporine-A. These data indicate that T cell activation induces a selective and cyclosporine-A-sensitive modulation of the expression of the SERCA calcium pump isoforms. This reflects a profound reorganization of the calcium homeostasis of T cells undergoing activation and may open new avenues in the understanding of the plasticity of the calcium homeostasis of differentiating cells and in the pharmacological modulation of lymphocyte function.Calcium as a second messenger is a key component of the cellular signaling network controlling lymphocyte function (Refs. 1-3 and references therein). Activation of the T cell receptor complex and associated coreceptors by antigen presenting cells leads to the formation of two second messengers, diacylglycerol and inositol 1,4,5-trisphosphate (IP 3 ).1 The formation of diacylglycerol results in the activation of various cellular protein kinase C isoenzymes, and the binding of IP 3 to its receptor induces the release of calcium into the cytosol from intracellular calcium storage organelles (1-3). Calcium mobilization from the endoplasmic reticulum also provokes a calcium influx across the plasma membrane (4 -8). These events lead to the activation of several inducible transcription factors such as NFB, NFAT, or AP-1 (9). The induction of the transcription of activation-associated genes, e.g. the gene coding for IL-2 (9, 10), or the ␣ chain of the IL-2 receptor (11) leads to a profound reorganization of the structure and function of the cell, resulting in an activated phenotype. Endoplasmic reticulum associated calcium pumps (SERCA enzymes) accumulate calcium ions from the cytosol by ATP-dependent active transport into endoplasmic reticulum-associated calcium storage organelles (8). Because the increase of cytosolic calcium concentration, as well as the depletion of intracellular calcium pools, generate several activatory signals (5-8), ...

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Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Cited by 31 publications

References 31 publications

Dysregulated intracellular Ca2 stores and Ca2 signaling in synovial fluid T lymphocytes from patients with chronic inflammatory arthritis

Dysregulated intracellular Ca2 stores and Ca2 signaling in synovial fluid T lymphocytes from patients with chronic inflammatory arthritis

Overexpression of Calreticulin Increases Intracellular Ca2+ Storage and Decreases Store-operated Ca2+ Influx

Modulation of Endoplasmic Reticulum Calcium Pump Expression during T Lymphocyte Activation

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