Store-operated Ca2+ entry controls ameloblast cell function and enamel development

Eckstein, Miriam; Vaeth, Martin; Fornai, Cinzia; Bromage, Timothy; Nurbaeva, Meerim K.; Sorge, Jessica L.; Coelho, Paulo G.; Idaghdour, Youssef; Feske, Stefan; Lacruz, Rodrigo S.

doi:10.1172/jci.insight.91166

Cited by 43 publications

(79 citation statements)

References 44 publications

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“…These mice were analyzed by our lab to study the effects of Stim1/2-deficiency in enamel cells and in the enamel crystals [11]. The main findings from the enamel included severe hypomineralization, diminished Ca 2+ content in the enamel, and increased wear [11]. At the cellular level, we found nearly abolished SOCE, altered redox system, including differences in glutathione metabolism, increased ROS, and lower mitochondrial membrane potential.…”

Section: Enamel Defects In Stim1- and Orai1-deficient Micementioning

confidence: 98%

“…The Stim1 fl/fl and Stim2 fl/fl mice originally reported by Oh-Hora et al [53] were crossed with K14-Cre mice in the Feske lab to generate Stim1/2 K14Cre mice [54] lacking both Stim1/2 genes in keratin 14 derived tissues including ameloblasts. These mice were analyzed by our lab to study the effects of Stim1/2-deficiency in enamel cells and in the enamel crystals [11]. The main findings from the enamel included severe hypomineralization, diminished Ca 2+ content in the enamel, and increased wear [11].…”

Section: Enamel Defects In Stim1- and Orai1-deficient Micementioning

confidence: 99%

“…This elegant system that monitors the refilling of intracellular Ca 2+ stores also participating in Ca 2+ signaling has provided clarity regarding the pathway for Ca 2+ influx in enamel cells, which had been unresolved. Yet, it also poses new challenges as the data emerging from recent studies implicate CRAC channels in multiple functions of the enamel cells that have been thus far unrecognized [11]. Here, we review CRAC channelopathy in enamel and its impact on dental disease.…”

Section: Introductionmentioning

confidence: 99%

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CRAC channels in dental enamel cells

Eckstein

Lacruz

2018

Cell Calcium

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Enamel mineralization relies on Ca availability provided by Ca release activated Ca (CRAC) channels. CRAC channels are modulated by the endoplasmic reticulum Ca sensor STIM1 which gates the pore subunit of the channel known as ORAI1, found the in plasma membrane, to enable sustained Ca influx. Mutations in the STIM1 and ORAI1 genes result in CRAC channelopathy, an ensemble of diseases including immunodeficiency, muscular hypotonia, ectodermal dysplasia with defects in sweat gland function and abnormal enamel mineralization similar to amelogenesis imperfecta (AI). In some reports, the chief medical complain has been the patient's dental health, highlighting the direct and important link between CRAC channels and enamel. The reported enamel defects are apparent in both the deciduous and in permanent teeth and often require extensive dental treatment to provide the patient with a functional dentition. Among the dental phenotypes observed in the patients, discoloration, increased wear, hypoplasias (thinning of enamel) and chipping has been reported. These findings are not universal in all patients. Here we review the mutations in STIM1 and ORAI1 causing AI-like phenotype, and evaluate the enamel defects in CRAC channel deficient mice. We also provide a brief overview of the role of CRAC channels in other mineralizing systems such as dentine and bone.

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Section: Enamel Defects In Stim1- and Orai1-deficient Micementioning

confidence: 98%

Section: Enamel Defects In Stim1- and Orai1-deficient Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CRAC channels in dental enamel cells

Eckstein

Lacruz

2018

Cell Calcium

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“…Ameloblasts at this stage will lose and reform this ruffled-border in alternating waves of ruffled-ended to smooth-ended morphology a number of times (Fig 1). The mechanisms and signals triggering these waves are poorly understood but recent evidence suggests that changes in [Ca 2+ ]cyt or extracellular pH might be associated with the modulation from RA to SA [22, 23]. At the end of the maturation stage, ameloblasts reduce their height and regress forming a layer of epithelial cells around the enamel that is lost during eruption [1] .…”

Section: Life and Death Of A Very Tall Cellmentioning

confidence: 99%

“…These interactions can be transformative for enamel biologists and will certainly broaden the scope of cell physiology. As these studies develop, and there are already some good recent examples [22, 74], ameloblasts will become a wider target in the study of general cell physiology.…”

Section: The Futurementioning

confidence: 99%

Enamel: Molecular identity of its transepithelial ion transport system

Lacruz

2017

Cell Calcium

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Enamel is the most calcified tissue in vertebrates. It differs from bone in a number of characteristics including its origin from ectodermal epithelium, lack of remodeling capacity by the enamel forming cells, and absence of collagen. The enamel-forming cells known as ameloblasts, choreograph first the synthesis of a unique protein-rich matrix, followed by the mineralization of this matrix into a tissue that is ~95% mineral. To do this, ameloblasts arrange the coordinated movement of ions across a cell barrier while removing matrix proteins and monitoring extracellular pH using a variety of buffering systems to enable the growth of carbonated apatite crystals. Although our knowledge of these processes and the molecular identity of the proteins involved in transepithelial ion transport has increased in the last decade, it remains limited compared to other cells. Here we present an overview of the evolution and development of enamel, its differences with bone, and describe the ion transport systems associated with ameloblasts.

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