Silva Thayane Martins, França Guilherme Rapozeiro, Ornelas Isis Moraes, Loiola Erick Correia, Ulrich Henning, Ventura Ana Lucia Marques
Programa de Neurociências, Departamento de Neurobiologia, Instituto de Biologia, Universidade Federal Fluminense, Outeiro de São João Batista s/n, Niterói, RJ, 24020-141, Brazil.
Purinergic Signal. 2015 Jun;11(2):183-201. doi: 10.1007/s11302-015-9444-9. Epub 2015 Feb 10.
When retinal cell cultures were mechanically scratched, cell growth over the empty area was observed. Only dividing and migrating, 2 M6-positive glial cells were detected. Incubation of cultures with apyrase (APY), suramin, or Reactive Blue 2 (RB-2), but not MRS 2179, significantly attenuated the growth of glial cells, suggesting that nucleotide receptors other than P2Y1 are involved in the growth of glial cells. UTPγS but not ADPβS antagonized apyrase-induced growth inhibition in scratched cultures, suggesting the participation of UTP-sensitive receptors. No decrease in proliferating cell nuclear antigen (PCNA(+)) cells was observed at the border of the scratch in apyrase-treated cultures, suggesting that glial proliferation was not affected. In apyrase-treated cultures, glial cytoplasm protrusions were smaller and unstable. Actin filaments were less organized and alfa-tubulin-labeled microtubules were mainly parallel to scratch. In contrast to control cultures, very few vinculin-labeled adhesion sites could be noticed in these cultures. Increased Akt and ERK phosphorylation was observed in UTP-treated cultures, effect that was inhibited by SRC inhibitor 1 and PI3K blocker LY294002. These inhibitors and the FAK inhibitor PF573228 also decreased glial growth over the scratch, suggesting participation of SRC, PI3K, and FAK in UTP-induced growth of glial cells in scratched cultures. RB-2 decreased dissociated glial cell attachment to fibronectin-coated dishes and migration through transwell membranes, suggesting that nucleotides regulated adhesion and migration of glial cells. In conclusion, mechanical scratch of retinal cell cultures induces growth of glial cells over the empty area through a mechanism that is dependent on activation of UTP-sensitive receptors, SRC, PI3K, and FAK.
当对视网膜细胞培养物进行机械刮擦时,可观察到空区域上的细胞生长。仅检测到正在分裂和迁移的、2 M6 阳性神经胶质细胞。用腺苷三磷酸双磷酸酶(APY)、苏拉明或活性蓝 2(RB - 2)而非 MRS 2179 孵育培养物,可显著减弱神经胶质细胞的生长,这表明除 P2Y1 之外的核苷酸受体参与了神经胶质细胞的生长。UTPγS 而非 ADPβS 可拮抗腺苷三磷酸双磷酸酶诱导的刮擦培养物中的生长抑制,提示 UTP 敏感受体的参与。在腺苷三磷酸双磷酸酶处理的培养物中,刮擦边界处未观察到增殖细胞核抗原(PCNA(+))细胞减少,这表明神经胶质细胞增殖未受影响。在腺苷三磷酸双磷酸酶处理的培养物中,神经胶质细胞质突起更小且不稳定。肌动蛋白丝组织性较差,α - 微管蛋白标记的微管主要与刮痕平行。与对照培养物相比,在这些培养物中几乎未观察到纽蛋白标记的黏附位点。在 UTP 处理的培养物中观察到 Akt 和 ERK 磷酸化增加,该效应被 SRC 抑制剂 1 和 PI3K 阻滞剂 LY294002 抑制。这些抑制剂以及 FAK 抑制剂 PF573228 也减少了刮痕上神经胶质细胞的生长,提示 SRC、PI3K 和 FAK 参与了 UTP 诱导的刮擦培养物中神经胶质细胞的生长。RB - 2 减少了解离的神经胶质细胞与纤连蛋白包被培养皿的附着以及通过 Transwell 膜的迁移,这表明核苷酸调节神经胶质细胞的黏附和迁移。总之,视网膜细胞培养物的机械刮擦通过依赖于 UTP 敏感受体、SRC、PI3K 和 FAK 激活的机制诱导神经胶质细胞在空区域上生长。