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首页> 外文期刊>Cellular Physiology and Biochemistry >Cell Swelling-induced Peptide Hormone Secretion
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Cell Swelling-induced Peptide Hormone Secretion

机译：细胞膨胀诱导的肽激素分泌

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Cell swelling induces peptide exocytosis using unique signaling pathway. Hyposmotic-induced secretion in normal cells is not mediated by specific receptors, is independent from extra and intracellular Casup2+/sup, sodium and potassium channels activity, prostaglandins, leukotriens, does not involve cytoskeleton, cAMP generation, phospholipase Asub2/sub, G proteins, protein kinase C. It is promoted by swelling of the secretory vesicles. Resistance to endogenous inhibitors is frequent attribute of this type of secretion. Swelling-induced secretion involves also secretory vesicles not involved in conventional stimulation. Hyposmosis-induced insulin secretion is more sensitive to high cellular cholesterol than conventional one suggesting substantial difference between mechanisms. Participation of sequential exocytosis as dominating mechanism in swelling-induced exocytosis is hypothesized. Signaling and response in tumor cells often differs from native cells and varies markedly between cell lines. Pathogenetic implications cell swelling could be involved in alcohol induced hypoglycemia in diabetic patients and release of peptides from pituitary and neurons. Swelling-induced products could be mediators of ischemic preconditioning involved also in protection of diabetic heart. Swelling-induced exocytosis is an ancient mechanism generally present in cells; in cells engaged in water and salt regulation is covered by specific response mediated by specific signaling. Disturbance of specific response leads to swelling-induced - inappropriate secretion of antidiuretic hormone - SIADH.
机译：细胞膨胀使用独特的信号传导途径诱导肽胞吐作用。低渗诱导的正常细胞分泌不受特定受体介导，独立于细胞外和细胞内Ca 2 + ，钠和钾通道活性，前列腺素，白三烯，不涉及细胞骨架，cAMP生成，磷脂酶A 2 ，G蛋白，蛋白激酶C。它通过分泌小泡的溶胀而促进。对内源性抑制剂的抗性是这种分泌物的常见特征。肿胀诱导的分泌还涉及常规刺激中不涉及的分泌性囊泡。与传统的相比，低渗诱导的胰岛素分泌对高细胞胆固醇更敏感，表明机制之间存在实质性差异。假设顺序性胞吐作用是肿胀诱导的胞吐作用的主要机制。肿瘤细胞中的信号传导和反应通常不同于天然细胞，并且在细胞系之间明显不同。病因学暗示细胞肿胀可能与糖尿病患者酒精引起的低血糖以及垂体和神经元释放肽有关。肿胀诱导的产物可能是缺血预处理的介质，也参与了糖尿病心脏的保护。肿胀诱导的胞吐作用是细胞中普遍存在的古老机制。参与水和盐调节的细胞中的特异性被特定信号传导介导的特定反应所覆盖。特异性反应紊乱会导致肿胀诱导的抗利尿激素-SIADH分泌不当。

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