最新一期生物化學(xué)期刊 (Journal of Biological Chemistry)的一份研究報告指出,，科學(xué)家找到了三個特殊的蛋白質(zhì)，可以使成熟的腦神經(jīng)細胞,，神奇的延伸細胞的長度,，比起平常的腦神經(jīng)細胞來說，足足大了四倍到八倍之多,。
據(jù)了解研究人員所發(fā)現(xiàn)的三個蛋白質(zhì) 分別稱為GPR3 ,、GPR6 和 GPR12，主導(dǎo)這個研究計劃的 Yoshinaga Saeki博士表示,，研究人員以大鼠 (Rat)的成熟腦細胞為實驗的材料,，在額外加入 GPR3、GPR6 和GPR12 這三個分子后,，原本已經(jīng)是屬于成熟的腦神經(jīng)細胞,，開始快速的延伸生長，相對于對照組而言,，就像是重復(fù)了三次的生長周期一般。
研究人員深入的分析,，發(fā)現(xiàn)這三個分子的加入,，都可以明顯的活化了神經(jīng)細胞里的 cAMP分子，而就過去的研究數(shù)據(jù)顯示,， cAMP分子在神經(jīng)細胞的生長過程之中,，扮演著關(guān)鍵性的角色，簡單的說,，已經(jīng)成熟的神經(jīng)細胞,，透過了 GPR3、 GPR6 和 GPR12的刺激,，再度啟動了生長的能力,，而延伸了原本的細胞長度。
科學(xué)家認(rèn)為這是一個相當(dāng)大的突破,，因為就那些因為中風(fēng),、外傷，因此造成腦部神經(jīng)組織受到傷害的患者來說,，可能透過這三個關(guān)鍵分子的發(fā)現(xiàn),，重建受傷的組織。
(資料來源 : Bio.com)
英文原文鏈接:
原始出處:
Originally published In Press as doi:10.1074/jbc.M700911200 on February 6, 2007
J. Biol. Chem., Vol. 282, Issue 14, 10506-10515, April 6, 2007
Neural Expression of G Protein-coupled Receptors GPR3, GPR6, and GPR12 Up-regulates Cyclic AMP Levels and Promotes Neurite Outgrowth*
Shigeru Tanaka, Ken Ishii, Kazue Kasai, Sung Ok Yoon¶, and Yoshinaga Saeki1
From the Dardinger Laboratory for Neuro-oncology and Neurosciences, Department of Neurological Surgery, ¶Department of Molecular and Cellular Biochemistry, and Center for Molecular Neurobiology, the Ohio State University, Columbus, Ohio 43210 and the Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan
Cyclic AMP regulates multiple neuronal functions, including neurite outgrowth and axonal regeneration. GPR3, GPR6, and GPR12 make up a family of constitutively active G protein-coupled receptors (GPCRs) that share greater than 50% identity and 65% similarity at the amino acid level. They are highly expressed in the central nervous system, and their expression in various cell lines results in constitutive stimulation of cAMP production. When the constitutively active GPCRs were overexpressed in rat cerebellar granule neurons in culture, the transfected neurons exhibited significantly enhanced neurite outgrowth and overcame growth inhibition caused by myelin-associated glycoprotein. GPR12-mediated neurite outgrowth was the most prominent and was shown to depend on Gs and cAMP-dependent protein kinase. Moreover, the GPR12-mediated rescue from myelin-associated glycoprotein inhibition was attributable to cAMP-dependent protein kinase-mediated inhibition of the small GTPase, RhoA. Among the three receptors, GPR3 was revealed to be enriched in the developing rat cerebellar granule neurons. When the endogenous GPR3 was knocked down, significant reduction of neurite growth was observed, which was reversed by expression of either GPR3 or GPR12. Taken together, our results indicate that expression of the constitutively active GPCRs up-regulates cAMP production in neurons, stimulates neurite outgrowth, and counteracts myelin inhibition. Further characterization of the GPCRs in developing and injured mammalian neurons should provide insights into how basal cAMP levels are regulated in neurons and could establish a firm scientific foundation for applying receptor biology to treatment of various neurological disorders.
