Lestanova Z, Puerta F, Alanazi M, Bacova Z, Kiss A, Castejon A M, Bakos Jan
Biomedical Research Center, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
College of Pharmacy, NOVA Southeastern University, Fort Lauderdale, FL, USA.
Neurochem Res. 2017 Apr;42(4):1006-1014. doi: 10.1007/s11064-016-2133-4. Epub 2016 Dec 19.
Oxytocin is a neuropeptide widely expressed in the brain. Oxytocin plays a role in both proliferation and differentiation of various cells. Previous studies have suggested that oxytocin could affect the morphology of neuronal cells, therefore the objective of the present study was to test whether (1) oxytocin receptor stimulation/inhibition by specific ligands may change cell morphology and gene expression of selected cytoskeletal proteins (2) oxytocin receptor silencing/knockdown may decrease the length of cell projections (3) oxytocin receptor knockdown may affect human glioblastoma U-87MG cell survival. We confirmed the stimulatory effect of retinoic acid (10 µM) and oxytocin (1 µM) on projection growth. The combination of retinoic acid (10 µM) and oxytocin receptor antagonist (L-371,257, 1 µM) decreased projections length. Contrary to our assumptions, oxytocin receptor silencing did not prevent stimulation of length of projection by retinoic acid. Retinoic acid's and oxytocin's stimulation of projections length was significantly blunted in U-87MG cells with oxytocin receptor knockdown. Cell viability was significantly decreased in U-87MG cells with oxytocin receptor knockdown. Significantly higher levels of mRNA for cytoskeletal proteins drebrin and vimentin were observed in response to oxytocin incubation for 48 h. The data obtained in the present study clearly show that oxytocin induces formation and elongation of cell projections in astrocyte-like U-87MG cells. The effect is mediated by oxytocin receptors and it is accompanied by an increase in gene expression of drebrin and vimentin. Thus, oxytocin receptor signaling, particularly in the glial cells, may play an important role in native cell life, differentiation processes, and tumor progression, as well.
催产素是一种在大脑中广泛表达的神经肽。催产素在各种细胞的增殖和分化中都发挥着作用。先前的研究表明,催产素可能会影响神经元细胞的形态,因此本研究的目的是测试:(1)特定配体对催产素受体的刺激/抑制是否会改变所选细胞骨架蛋白的细胞形态和基因表达;(2)催产素受体的沉默/敲低是否会缩短细胞突起的长度;(3)催产素受体的敲低是否会影响人胶质母细胞瘤U - 87MG细胞的存活。我们证实了视黄酸(10 μM)和催产素(1 μM)对突起生长的刺激作用。视黄酸(10 μM)和催产素受体拮抗剂(L - 371,257,1 μM)的组合会缩短突起长度。与我们的假设相反,催产素受体的沉默并未阻止视黄酸对突起长度的刺激。在催产素受体敲低的U - 87MG细胞中,视黄酸和催产素对突起长度的刺激作用明显减弱。催产素受体敲低的U - 87MG细胞的细胞活力显著降低。在催产素孵育48小时后,观察到细胞骨架蛋白脑桥蛋白和波形蛋白的mRNA水平显著升高。本研究获得的数据清楚地表明,催产素可诱导星形胶质细胞样U - 87MG细胞形成并延长细胞突起。该效应由催产素受体介导,并伴随着脑桥蛋白和波形蛋白基因表达的增加。因此,催产素受体信号传导,特别是在胶质细胞中,可能在天然细胞生命、分化过程以及肿瘤进展中也发挥着重要作用。