Gillardon F, Hata R, Hossmann K A
Max-Planck-Institut für Neurologische Forschung, Gleueler Str. 50, 50931, Köln, Germany.
Brain Res Mol Brain Res. 1998 Oct 30;61(1-2):207-10. doi: 10.1016/s0169-328x(98)00202-2.
The Zac1 gene encodes a zinc finger protein that regulates both apoptosis and cell cycle arrest in vitro. Furthermore, Zac1 protein seems to trans-activate the gene encoding the type I receptor for pituitary adenylate cyclase activating polypeptide (PACAP). Northern blot analysis revealed high levels of Zac1 mRNA in the rodent brain. In the present study, we demonstrate by in situ hybridization histochemistry a progressive increase in Zac1 transcripts in the mouse brain from day 1 to day 3 following transient focal cerebral ischemia. Moreover, we observed an up-regulation of PACAP type I receptor mRNA expression showing a similar temporospatial distribution. Late induction of cell death promoting Zac1 in the post-ischemic brain may be attributed to delayed or secondary cell death. Co-induction of the type I receptor for neurotrophic PACAP however, points to a role in restorative processes.
Zac1基因编码一种锌指蛋白，该蛋白在体外可调节细胞凋亡和细胞周期停滞。此外，Zac1蛋白似乎能反式激活垂体腺苷酸环化酶激活多肽（PACAP）I型受体的编码基因。Northern印迹分析显示，啮齿动物大脑中Zac1 mRNA水平较高。在本研究中，我们通过原位杂交组织化学证明，短暂局灶性脑缺血后第1天至第3天，小鼠大脑中Zac1转录本逐渐增加。此外，我们观察到PACAP I型受体mRNA表达上调，呈现出相似的时空分布。缺血后大脑中促进细胞死亡的Zac1的晚期诱导可能归因于延迟性或继发性细胞死亡。然而，神经营养性PACAP I型受体的共同诱导表明其在恢复过程中发挥作用。
