Satoh T, Furuta K, Suzuki M, Watanabe Y
Department of Neuroscience, Osaka Bioscience Institute, 6-2-4 Furuedai, Suita-shi, Osaka, 565-0874, Japan.
Biochem Biophys Res Commun. 1999 Apr 29;258(1):50-3. doi: 10.1006/bbrc.1999.0587.
Although A- and J-type prostaglandins (PG's) arrest the cell cycle at the G1 phase in vitro and suppress tumor growth in vivo, their effects on neuronal cells have not so far been clarified. Here, we found promotion of neurite outgrowth as a novel biological function of PGJ's. In PC12h cells, PGJ's (PGJ2, Delta12-PGJ2 and 15-deoxy-Delta12,14-PGJ2) promoted neurite outgrowth in the presence of nerve growth factor (NGF), whereas they themselves did not show such a promotion. The potency of promoting neurite outgrowth was PGJ2 < Delta12-PGJ2 < 15-deoxy-Delta12,14-PGJ2. However, troglitazone, an activator of peroxisome proliferator-activated receptorgamma (PPARgamma), and other PG's including PGA1, PGA2 and PGD2 did not promote neurite outgrowth. These results suggest that PGJ's promote neurite outgrowth independently of PPARgamma activation.
虽然A类和J类前列腺素(PGs)在体外可使细胞周期停滞于G1期,并在体内抑制肿瘤生长,但它们对神经元细胞的作用迄今尚未阐明。在此,我们发现PGJ类具有促进神经突生长这一新的生物学功能。在PC12h细胞中,PGJ类(PGJ2、Δ12 - PGJ2和15 - 脱氧 - Δ12,14 - PGJ2)在存在神经生长因子(NGF)的情况下可促进神经突生长,而它们自身并无此促进作用。促进神经突生长的效力为PGJ2 < Δ12 - PGJ2 < 15 - 脱氧 - Δ12,14 - PGJ2。然而,过氧化物酶体增殖物激活受体γ(PPARγ)的激活剂曲格列酮以及包括PGA1、PGA2和PGD2在内的其他PGs并未促进神经突生长。这些结果表明,PGJ类促进神经突生长独立于PPARγ激活。