Morita Mitsuhiro, Nakane Akira, Fujii Yuki, Maekawa Shohei, Kudo Yoshihisa
Department of Biology, Kobe University Graduate School of Science, Kobe, Japan.
Laboratory of Cellular Neurobiology, School of Life Science, Tokyo University of Pharmacy and Life Science, Tokyo, Japan.
PLoS One. 2015 Sep 23;10(9):e0137610. doi: 10.1371/journal.pone.0137610. eCollection 2015.
Calcium releases of non-excitable cells are generally a combination of oscillatory and non-oscillatory patterns, and factors affecting the calcium dynamics are still to be determined. Here we report the influence of cell density on calcium increase patterns of clonal cell lines. The majority of HeLa cells seeded at 1.5 x 104/cm2 showed calcium oscillations in response to histamine and ATP, whereas cells seeded at 0.5 x 104/cm2 largely showed transient and sustained calcium increases. Cell density also affected the response of HEK293 cells to ATP in a similar manner. High cell density increased the basal activity of the mitogen-activated protein (MAP) kinase and calcium store content, and both calcium oscillation and calcium store content were down-regulated by a MAP kinase inhibitor, U0126. Thus, MAP kinase-mediated regulation of calcium store likely underlie the effect of cell density on calcium oscillation. Calcium increase patterns of HeLa cells were conserved at any histamine concentrations tested, whereas the overexpression of histamine H1 receptor, which robustly increased histamine-induced inositol phospholipid hydrolysis, converted calcium oscillations to sustained calcium increases only at high histamine concentrations. Thus, the consequence of modulating inositol phospholipid metabolism was distinct from that of changing cell density, suggesting the effect of cell density is not attributed to inositol phospholipid metabolism. Collectively, our results propose that calcium increase patterns of non-excitable cells reflect calcium store, which is regulated by the basal MAP kinase activity under the influence of cell density.
非兴奋性细胞的钙释放通常是振荡模式和非振荡模式的组合,影响钙动力学的因素仍有待确定。在此,我们报告细胞密度对克隆细胞系钙增加模式的影响。以1.5×104/cm2接种的大多数HeLa细胞对组胺和ATP有钙振荡反应,而以0.5×104/cm2接种的细胞大多表现出瞬时和持续的钙增加。细胞密度也以类似方式影响HEK293细胞对ATP的反应。高细胞密度增加了丝裂原活化蛋白(MAP)激酶的基础活性和钙储存含量,并且钙振荡和钙储存含量均被MAP激酶抑制剂U0126下调。因此,MAP激酶介导的钙储存调节可能是细胞密度对钙振荡影响的基础。在任何测试的组胺浓度下,HeLa细胞的钙增加模式都是保守的,而组胺H1受体的过表达,其强烈增加组胺诱导的肌醇磷脂水解,仅在高组胺浓度下将钙振荡转变为持续的钙增加。因此,调节肌醇磷脂代谢的结果与改变细胞密度的结果不同,这表明细胞密度的影响并非归因于肌醇磷脂代谢。总体而言,我们的结果表明,非兴奋性细胞的钙增加模式反映了钙储存,其在细胞密度的影响下由基础MAP激酶活性调节。