Biological actions and mechanism of action of calbindin in the process of apoptosis

Christakos, Sylvia; Liu, Yan

doi:10.1016/j.jsbmb.2004.03.007

Cited by 57 publications

(32 citation statements)

References 15 publications

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“…Therefore, some antiapoptotic mechanisms in germ cells must be 'turned on' to limit apoptosis. Among the various apoptotic molecules, CB has been suggested to protect different cell types against apoptotic cell death induced by both calcium-independent and calcium-dependent pathways (Christakos & Liu 2004). In our study, we have demonstrated that CB is overexpressed in Rb heterozygous testis, with maximal expression in metaphase spermatocytes.…”

Section: Discussionsupporting

confidence: 53%

“…CB expression is low in both mice and chick testes and is vitamin D independent and dependent respectively (Walters et al 1991, Inpanbutr et al 1996. Christakos & Liu (2004) showed that CB has a major role in different cell types in protecting against cell death by preventing calcium-mediated mitochondrial damage and the subsequent release of cytochrome c.…”

Section: Introductionmentioning

confidence: 99%

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A mitochondrial mechanism is involved in apoptosis of Robertsonian mouse male germ cells

et al. 2008

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The aim of this study was to determine whether the intrinsic mechanism of apoptosis is involved in the death of germ cells in Robertsonian (Rb) heterozygous adult male mice. Testes from 5-month-old Rb heterozygous CD1!Milano II mice were obtained and compared with those from homozygous CD1 (2nZ40) and Milano II (2nZ24) mice. For histological evaluation of apoptosis, TUNEL labelling and immunohistochemistry were used to localise Bax and cytochrome c. Expression of calbindin D 28k (CB), an anti-apoptotic molecule, was also analysed by immunohistochemistry and immunoblotting. Testicular ultrastructure was visualised by electron microscopy. Morphology and cell associations were abnormal in the Rb heterozygous seminiferous epithelium. An intense apoptotic process was observed in tubules at stage XII, mainly in metaphase spermatocytes. Metaphase spermatocytes also showed Bax and cytochrome c redistributions. Mitochondria relocated close to the paranuclear region of spermatocytes. CB was mainly expressed in metaphase spermatocytes, but also in pachytene spermatocytes, spermatids and Sertoli cells at stage XII. The co-localisation of CB and TUNEL labelling was very limited. Sixty per cent of metaphase spermatocytes were apoptotic and calbindin negative, while 40% were calbindin positive without signs of apoptosis. Ten per cent of the Bax-and cytochrome c-positive cells were also calbindin positive. These data suggest that apoptosis of the germ cells in heterozygous mice occurs, at least in part, through a mitochondrial-dependent mechanism. Calbindin overexpression might prevent or reduce the apoptosis of germ cells caused by Rb heterozygosity, which could partially explain the subfertility of these mice. Reproduction (2008) 135 797-804

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

A mitochondrial mechanism is involved in apoptosis of Robertsonian mouse male germ cells

et al. 2008

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“…Although Са 2+ sensors regulate the activities of ion channels and enzymes, Са 2+ buffers modulate the amplitude and kinetics of free Са 2+ transients and maintain Са 2+ homeostasis. For example, Са 2+ buffers keep the concentration of free Са 2+ below the levels that would induce cell death (Christakos and Liu, 2004;D'Orlando et al, 2001;Kook et al, 2014). Because the affinity of tescalcin for Ca 2+ is in the micromolar range (Gutierrez-Ford et al, 2003), it is thought to be a Са 2+ -sensor.…”

Section: +mentioning

confidence: 99%

Emerging roles of the single EF-hand Ca2+ sensor tescalcin in the regulation of gene expression, cell growth and differentiation

Kolobynina

Solovyova

Levay

et al. 2016

Journal of Cell Science

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Tescalcin (TESC, also known as calcineurin-homologous protein 3, CHP3) is a 24-kDa EF-hand Ca2+-binding protein that has recently emerged as a regulator of cell differentiation and growth. The TESC gene has also been linked to human brain abnormalities, and high expression of tescalcin has been found in several cancers. The expression level of tescalcin changes dramatically during development and upon signal-induced cell differentiation. Recent studies have shown that tescalcin is not only subjected to up- or down-regulation, but also has an active role in pathways that drive cell growth and differentiation programs. At the molecular level, there is compelling experimental evidence showing that tescalcin can directly interact with and regulate the activities of the Na+/H+ exchanger NHE1, subunit 4 of the COP9 signalosome (CSN4) and protein kinase glycogen-synthase kinase 3 (GSK3). In hematopoetic precursor cells, tescalcin has been shown to couple activation of the extracellular signal-regulated kinase (ERK) cascade to the expression of transcription factors that control cell differentiation. The purpose of this Commentary is to summarize recent efforts that have served to characterize the biochemical, genetic and physiological attributes of tescalcin, and its unique role in the regulation of various cellular functions.

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“…CALB1 inhibits the activity of caspase-3, a downstream effector of multiple apoptotic signaling pathways, and that inhibition results in an inhibition of apoptosis in osteoblastic cells (21,37). CALB1 may also protect against apoptosis in dopaminergic neurons through activation of the phosphoinositide 3 (PI3) kinase-Akt signaling pathway (38).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

2017

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Abstract. Osteosarcoma is the most common type of primary malignant bone tumor and has a high propensity to metastasize to the lungs and bones. Calbindin 1 (CALB1) is a constituent Ca 2+ binding protein, which can prevent apoptotic death in several cell types induced through various pro-apoptotic signaling pathways. To investigate whether CALB1 is implicated in the tumor growth of human osteosarcoma, two different short hairpin RNAs (shRNAs) against CALB1 were used for CALB1-knockdown in osteosarcoma U2OS cells. The U2OS cells were divided into three groups: Two groups with CALB1 knockdown (CALB1-shRNA 1 and CALB1-shRNA 2) and one control group (Con-shRNA). Reverse transcription-quantitative polymerase chain reaction and western blot analysis confirmed that the CALB1-shRNA 1-and 2-infected cells exhibited significantly lower levels of CALB1 gene and protein expression compared with the Con-shRNA group. The proliferation and colony formation abilities were significantly inhibited in CALB1-deficient U2OS cells compared with the control, as measured using an MTT assay and crystal violet staining. Flow cytometry revealed that the number of CALB1-shRNA 2-injected cells was increased in the G 0 /G 1 and G 2 /M phases, but decreased in the S phase, compared with the control group. The assessment of apoptosis and necrosis using Annexin V/7-aminoactinomycin D demonstrated that there was a significantly higher percentage of necrotic, early apoptotic, and late apoptotic cells, but a significantly lower percentage of viable cells in U2OS cells with CALB1-knockdown compared with the control group. In conclusion, CALB1 contributes to protecting osteosarcoma cells from apoptosis and provides a potential novel target for gene therapy to treat patients with osteosarcoma.

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Biological actions and mechanism of action of calbindin in the process of apoptosis

Cited by 57 publications

References 15 publications

A mitochondrial mechanism is involved in apoptosis of Robertsonian mouse male germ cells

A mitochondrial mechanism is involved in apoptosis of Robertsonian mouse male germ cells

Emerging roles of the single EF-hand Ca2+ sensor tescalcin in the regulation of gene expression, cell growth and differentiation

Downregulation of calbindin 1, a calcium-binding protein, reduces the proliferation of osteosarcoma cells

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