کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2200872 | 1099982 | 2012 | 7 صفحه PDF | دانلود رایگان |

We reported previously that CCR9 was neuroprotective in the mouse hippocampal neurons. This study was aimed to investigate if thymus-expressed chemokine (TECK)/CCL25 could promote survival of PC12 cells though its receptor CCR9. pEGFP-N1/CCR9 recombinant was constructed and transfected into PC12 cells. Along with this, 50 nM NGF was used to induce PC12 cells to differentiate into sympathetic-like neurons. We show here that under serum-free conditions and within a concentration range (50–200 nM), TECK rescued pEGFP-N1/CCR9 transfected PC12 cells from undergoing apoptosis in serum-free medium; however, it did not exert a similar effect on the cells in the control. On the other hand, the PC12 cells succumbed to a higher concentration of TECK (⩾300 nM). Bim expression was up-regulated in PC12 cells cultured in serum-free medium in the absence of factors or with anti-TECK + TECK; however, it was not up-regulated in TECK-treated PC12 cells. p-Akt was detected at 15 min which lasted for at least 60 min when PC12 cells were cultured in serum-free medium with TECK. Additionally, it was shown that such an effect was effectively blocked by PI3K inhibitor, Wortmannin. These data suggest that TECK promotes survival of serum-deprived PC12 cells through its receptor, CCR9, most likely via the PI3K/Akt signaling pathway.
► TECK promotes pEGFP-N1-CCR9 transfected PC12 cells survival in serum-free medium.
► However, the PC12 cells succumbed to a higher concentration of TECK (⩾300 nM).
► TECK promotes PC12 cells survival most likely via PI3K signaling pathway.
Journal: Neurochemistry International - Volume 60, Issue 2, January 2012, Pages 163–169