Regulation of Ca2+ signals in a parotid cell line Par-C5
| Autor: | Xiuhua Sun, Robert Castro, J. Ricardo Martinez, Ann-Christin Mörk, Guo H. Zhang, Xiao-bing Liu |
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| Rok vydání: | 2001 |
| Předmět: |
Purinergic P2 Receptor Agonists
medicine.medical_specialty Thapsigargin Inositol 1 4 5-Trisphosphate Muscarinic Agonists Receptors Purinergic P2Y2 chemistry.chemical_compound Internal medicine Muscarinic acetylcholine receptor medicine Acinar cell Animals Parotid Gland Calcium Signaling Receptor General Dentistry Cell Line Transformed Analysis of Variance Phospholipase C Receptors Purinergic P2 Tumor Necrosis Factor-alpha Cell Biology General Medicine Receptors Adrenergic alpha Receptors Muscarinic Rats Cell biology Calcium Channel Agonists Endocrinology Otorhinolaryngology chemistry Ionomycin Calcium Adrenergic alpha-Agonists Acetylcholine Intracellular medicine.drug |
| Zdroj: | Archives of Oral Biology. 46:1141-1149 |
| ISSN: | 0003-9969 |
| DOI: | 10.1016/s0003-9969(01)00074-7 |
| Popis: | The Ca(2+) signaling system in an established immortalized rat parotid acinar cell line, Par-C5, was examined using the Ca(2+)-sensitive fluorescent indicator fura-2 and by measuring inositol 1,4,5-trisphosphate (IP(3)) formation. Agonist-induced increase in intracellular Ca(2+) ([Ca(2+)](i)) by mobilization of intracellular stores and influx across the cell membrane was stimulated by acetylcholine (ACh) and ATP, whereas noradrenaline-(NA)-induced a small [Ca(2+)](i) increase mediated primarily by release from intracellular Ca(2+) stores. [Ca(2+)](i) increase by ACh and ATP was mediated through the phosphoinositide signal pathway since both agonists significantly increased 1,4,5-IP(3) formation and Ca(2+) mobilization was abolished by the phospholipase C inhibitor U73122. In Ca(2+)-free medium, ACh or ATP discharged the IP(3)-sensitive Ca(2+) store and essentially abolished subsequent [Ca(2+)](i) response to thapsigargin (TG). Exposure to ionomycin and monensin after TG induced a further mobilization of Ca(2+), suggesting IP(3)-insensitive stores are present. Furthermore, depletion of IP(3)-sensitive Ca(2+) stores by TG, ACh and ATP enhanced plasmalemmal Ca(2+)-entry pathways. Exposure to tumor necrosis factor-alpha (TNF-alpha), a cytokine associated with lymphocyte invasion of salivary epithelial cells in autoimmune disorders, significantly reduced ACh-stimulated Ca(2+) mobilization. TNF-alpha inhibitory effect on Ca(2+) mobilization was not directly due to an interaction on muscarinic receptors since ACh-induced 1,4,5-IP(3) formation was not altered. These results in the Par-C5 cell line indicate 1) [Ca(2+)](i) is regulated by muscarinic and P2Y-nucleotide receptors and partly by alpha(1)-adrenergic receptors; 2) IP(3)-sensitive and -insensitive Ca(2+) stores exist; 3) Ca(2+) influx activated by ACh, ATP or TG is mediated by the store-operated Ca(2+) entry pathway; and 4) muscarinic agonist-stimulated Ca(2+) mobilization is altered by the cytokine TNF-alpha. |
| Databáze: | OpenAIRE |
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