Calcium signaling to nucleus via store-operated system during cell cycle in retinal neuroepithelium

Sugioka, Miho; Yamashita, Masayuki

doi:10.1016/s0168-0102(03)00004-x

Cited by 20 publications

(26 citation statements)

References 57 publications

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“…The overall reduction of I CRAC and relative low abundance of MagNuM in mitotic cells indicates that Ca 2+ influx plays a minor role during mitosis. This is in agreement with the observation that changes in intracellular Ca 2+ levels during mitosis are predominantly due to InsP 3 -induced Ca 2+ release but not influx [13,19,57].…”

Section: Discussionsupporting

confidence: 92%

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

et al. 2007

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Calcium signaling is a central mechanism for numerous cellular functions and particularly relevant for immune cell proliferation. However, the role of calcium influx in mitotic cell cycle progression is largely unknown. We here report that proliferating rat mast cells RBL-2H3 tightly control their major store-operated calcium influx pathway, I CRAC , during cell cycle progression. While I CRAC is maintained at control levels during the first gap phase (G1), the current is significantly upregulated in preparation for and during chromatin duplication. However, mitosis strongly suppresses I CRAC . Non-proliferating cells deprived of growth hormones strongly down-regulate I CRAC while increasing cell volume. We further show that the other known calcium (and magnesium) influx pathway in mast cells, the TRPM7-like magnesium-nucleotide-regulated metal (MagNuM) current, is largely uncoupled from cell cycle regulation except in G1. Taken together, our results demonstrate that both store-operated calcium influx via I CRAC and MagNuM are regulated at crucial checkpoints during cell cycle progression.

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Section: Discussionsupporting

confidence: 92%

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

et al. 2007

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“…In these cells, T cell receptor stimulation induces sustained SOCE through the Ca 2þ release-activated current (CRAC) resulting in sustained activation of the nuclear factor of activated T cells (NFAT) that promotes proliferation (Lewis, 2001). Many observations in this and other cell models relate SOCE and cell proliferation: (1) entry in cell cycle is preceded by SOC activation (Sugioka and Yamashita, 2003); (2) growth factor stimulation of cell proliferation is accompanied by increased activity and/or expression of transient receptor potential (TRP) channels that are related to SOCE (Golovina et al, 2001); (3) SOCE inhibition by different means (Ca 2þ removal, inorganic channel blockers, and CRAC antagonists) abolishes tumor cell proliferation (Weiss et al, 2001;Zitt et al, 2004). Two decades after the discovery SOCE (Putney, 1986) the link between emptying of intracellular Ca 2þ stores and the increased Ca 2þ influx is still unknown (Parekh and Putney, 2005).…”

mentioning

confidence: 88%

Dysregulated calcium homeostasis and oxidative stress in chronic myeloid leukemia (CML) cells

Ciarcia

d’Angelo

Pacilio

et al. 2010

Journal Cellular Physiology

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Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder caused by the oncogenic activity of the Bcr-Abl protein, a deregulated tyrosine kinase. Calcium may act directly on cellular enzymes and in conjunction with other cellular metabolites, such as cyclic nucleotides, to regulate cell functions. Alteration in the ionized calcium concentration in the cytosol has been implicated in the initiation of secretion, contraction, and cell proliferation as well as the production of reactive oxygen species (ROS) has been correlates with normal cell proliferation through activation of growth-related signaling pathways. In this study we evaluated in peripheral blood leukocytes from CML patients the role of the balance between intracellular calcium and oxidative stress in CML disease in order to identify possible therapeutic targets in patients affected by this pathology. Our results demonstrated that peripheral blood mononuclear cells derived from CML patients displayed decreased intracellular calcium [Ca(2+)](i) fluxes both after InsP(3) as well as ATP and ionomycin (IONO) administration. CML cells showed lower levels of superoxide dismutase (SOD) activity and significantly higher malondialdehyde levels (MDA) than peripheral blood mononuclear cells derived from control patients. Finally we showed that resveratrol is able to down-regulate InsP3 and ATP effects on intracellular calcium [Ca(2+)](i) fluxes as well as the effects of ATP and IONO on oxidative stress in CML cells.

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“…Recently Sugioka and Yamashita [19] reported that the intracytoplasmic Ca ++ concentration in the matrix cells in the retina changes in a cyclic fashion synchronously with the mitotic cycle. Although the precise mechanism is not yet known, the upregulated cytoplasmic Ca ++ is either directly or indirectly related with the levels of protein tyrosine phosphorylation.…”

Section: Resultsmentioning

confidence: 99%

The Molecular Mechanism of Elevator Movement

Fujita

Yasuda

2003

Acta Histochem. Cytochem

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The elevator movement of the matrix cell is synchronous with the mitotic cycle. Its mechanism has been thought to be due to cyclic changes in cell adhesion to the neighboring cells and the basement membrane. The present study aims to analyze the cytoplasmic changes by means of immunohistochemical investigations of the distributions of the adhesion molecules, N-cadherin, a-catenin, bcatenin, F-actin, etc. It was found that the adherent junctions and junctions to ECM of the matrix cell disintegrate during mitosis, releasing the cell from the intercellular adhesions and the basement membrane. As a consequence, the mitotic matrix cell is rounded out and attracted to the ventricular surface where the junctional complexes remain unchanged during mitosis. After division, the daughter matrix cells recover their adhesion apparatuses and, extending their cytoplasmic processes, resume their downward elevator movement.

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Calcium signaling to nucleus via store-operated system during cell cycle in retinal neuroepithelium

Cited by 20 publications

References 57 publications

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

Cell cycle-dependent regulation of store-operated ICRAC and Mg2+-nucleotide-regulated MagNuM (TRPM7) currents

Dysregulated calcium homeostasis and oxidative stress in chronic myeloid leukemia (CML) cells

The Molecular Mechanism of Elevator Movement

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