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The P2Y Receptor Antagonist Ticagrelor Reduces Lysosomal pH and Autofluorescence in Retinal Pigmented Epithelial Cells From the ABCA4 Mouse Model of Retinal Degeneration.P2Y受体拮抗剂替格瑞洛降低视网膜色素上皮细胞的溶酶体pH值并减少来自视网膜变性ABCA4小鼠模型的视网膜色素上皮细胞的自发荧光。
Front Pharmacol. 2018 Apr 19;9:242. doi: 10.3389/fphar.2018.00242. eCollection 2018.
2
CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes.CALHM3 对于 G 蛋白偶联受体味觉介导的快速离子通道介导的嘌呤能神经传递是必需的。
Neuron. 2018 May 2;98(3):547-561.e10. doi: 10.1016/j.neuron.2018.03.043. Epub 2018 Apr 19.
3
Stimulation of TLR3 triggers release of lysosomal ATP in astrocytes and epithelial cells that requires TRPML1 channels.TLR3 的刺激会触发星形胶质细胞和上皮细胞溶酶体 ATP 的释放,这需要 TRPML1 通道。
Sci Rep. 2018 Apr 10;8(1):5726. doi: 10.1038/s41598-018-23877-3.
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P2Y but not P2Y Purinergic Receptor Controls Postnatal Rat Retinogenesis In Vivo.P2Y 而非 P2Y 嘌呤能受体调控体内出生后大鼠视网膜发生。
Mol Neurobiol. 2018 Nov;55(11):8612-8624. doi: 10.1007/s12035-018-1012-1. Epub 2018 Mar 25.
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Stimulation of the adenosine A3 receptor, not the A1 or A2 receptors, promote neurite outgrowth of retinal ganglion cells.刺激腺苷 A3 受体而非 A1 或 A2 受体可促进视网膜神经节细胞的轴突生长。
Exp Eye Res. 2018 May;170:160-168. doi: 10.1016/j.exer.2018.02.019. Epub 2018 Feb 24.
6
Treatment with A receptor antagonist KW6002 and caffeine intake regulate microglia reactivity and protect retina against transient ischemic damage.A 受体拮抗剂 KW6002 和咖啡因摄入的治疗可调节小胶质细胞的反应性,并保护视网膜免受短暂性缺血损伤。
Cell Death Dis. 2017 Oct 5;8(10):e3065. doi: 10.1038/cddis.2017.451.
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The P2X7 Receptor Primes IL-1β and the NLRP3 Inflammasome in Astrocytes Exposed to Mechanical Strain.P2X7受体在受到机械牵张的星形胶质细胞中启动白细胞介素-1β和NLRP3炎性小体。
Front Cell Neurosci. 2017 Aug 8;11:227. doi: 10.3389/fncel.2017.00227. eCollection 2017.
8
Injury-induced purinergic signalling molecules upregulate pluripotency gene expression and mitotic activity of progenitor cells in the zebrafish retina.损伤诱导的嘌呤能信号分子上调斑马鱼视网膜祖细胞的多能性基因表达和有丝分裂活性。
Purinergic Signal. 2017 Dec;13(4):443-465. doi: 10.1007/s11302-017-9572-5. Epub 2017 Jul 14.
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Novel channel-mediated choline transport in cholinergic neurons of the mouse retina.小鼠视网膜胆碱能神经元中新型通道介导的胆碱转运
J Neurophysiol. 2017 Oct 1;118(4):1952-1961. doi: 10.1152/jn.00506.2016. Epub 2017 Jul 12.
10
Vesicular nucleotide transporter (VNUT): appearance of an actress on the stage of purinergic signaling.囊泡核苷酸转运蛋白(VNUT):嘌呤能信号转导舞台上的一位女演员。
Purinergic Signal. 2017 Sep;13(3):387-404. doi: 10.1007/s11302-017-9568-1. Epub 2017 Jun 14.

嘌呤能信号在视网膜中的作用:从发育到疾病。

Purinergic signaling in the retina: From development to disease.

机构信息

Department of Neurobiology, Neuroscience Program, Fluminense Federal University, Niterói, RJ, Brazil.

Department of Anatomy and Cell Biology, Ophthalmology, and Physiology, University of Pennsylvania, Philadelphia, PA 19104, United States.

出版信息

Brain Res Bull. 2019 Sep;151:92-108. doi: 10.1016/j.brainresbull.2018.10.016. Epub 2018 Nov 17.

DOI:10.1016/j.brainresbull.2018.10.016
PMID:30458250
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6525091/
Abstract

Retinal injuries and diseases are major causes of human disability involving vision impairment by the progressive and permanent loss of retinal neurons. During development, assembly of this tissue entails a successive and overlapping, signal-regulated engagement of complex events that include proliferation of progenitors, neurogenesis, cell death, neurochemical differentiation and synaptogenesis. During retinal damage, several of these events are re-activated with both protective and detrimental consequences. Purines and pyrimidines, along with their metabolites are emerging as important molecules regulating both retinal development and the tissue's responses to damage. The present review provides an overview of the purinergic signaling in the developing and injured retina. Recent findings on the presence of vesicular and channel-mediated ATP release by retinal and retinal pigment epithelial cells, adenosine synthesis and release, expression of receptors and intracellular signaling pathways activated by purinergic signaling in retinal cells are reported. The pathways by which purinergic receptors modulate retinal cell proliferation, migration and death of retinal cells during development and injury are summarized. The contribution of nucleotides to the self-repair of the injured zebrafish retina is also discussed.

摘要

视网膜损伤和疾病是导致人类视力障碍的主要原因,其原因是视网膜神经元的进行性和永久性丧失。在发育过程中,组织的组装需要一系列连续且重叠的信号调节事件的参与,包括祖细胞的增殖、神经发生、细胞死亡、神经化学分化和突触形成。在视网膜损伤时,其中一些事件会被重新激活,产生保护和有害的后果。嘌呤和嘧啶及其代谢物正在成为调节视网膜发育和组织对损伤反应的重要分子。本综述概述了发育中和损伤的视网膜中的嘌呤能信号转导。本文报道了视网膜和视网膜色素上皮细胞中存在囊泡和通道介导的 ATP 释放、腺苷的合成和释放、嘌呤能信号转导在视网膜细胞中激活的受体和细胞内信号通路的表达。总结了嘌呤能受体在发育和损伤过程中调节视网膜细胞增殖、迁移和死亡的途径。还讨论了核苷酸对斑马鱼受损视网膜自我修复的贡献。