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深痛觉与一种截断的肽有关,该肽是由 DRG CA8-204 的组织特异性选择性剪接产生的,受外显子水平顺式 eQTL 调控。

Profound analgesia is associated with a truncated peptide resulting from tissue specific alternative splicing of DRG CA8-204 regulated by an exon-level cis-eQTL.

机构信息

Department of Anesthesiology, Perioperative Medicine and Pain Management, University of Miami Miller School of Medicine, Miami, Florida, United States of America.

Alan Edwards Centre for Research on Pain, McGill University Department of Anesthesiology, Montreal, Quebec, Canada.

出版信息

PLoS Genet. 2019 Jun 14;15(6):e1008226. doi: 10.1371/journal.pgen.1008226. eCollection 2019 Jun.

Abstract

Carbonic anhydrase-8 (CA8) is an intracellular protein that functions as an allosteric inhibitor of inositol trisphosphate receptor-1 (ITPR1) critical to intracellular Ca++ release, synaptic functions and neuronal excitability. We showed previously that murine nociception and analgesic responses are regulated by the expression of this gene in dorsal root ganglion (DRG) associated with a cis-eQTL. In this report, we identify an exon-level cis-eQTL (rs6471859) that regulates human DRG CA8 alternative splicing, producing a truncated 1,697bp transcript (e.g., CA8-204). Our functional genomic studies show the "G" allele at rs6471859 produces a cryptic 3'UTR splice site regulating expression of CA8-204. We developed constructs to study the expression and function of the naturally occurring CA8-204G transcript (G allele at rs6471859), CA8-204C (C allele at rs6471859 reversion mutation) and CA8-201 (full length transcript). CA8-204G transcript expression occurred predominantly in non-neuronal cells (HEK293), while CA8-204C expression was restricted to neuronal derived cells (NBL) in vitro. CA8-204G produced a stable truncated transcript in HEK293 cells that was barely detectable in NBL cells. We also show CA8-204 produces a stable peptide that inhibits pITPR1 and Ca++ release in HEK293 cells. These results imply homozygous G/G individuals at rs6471859, which are common in the general population, produce exclusively CA8-204G that is barely detectable in neuronal cells. CA8 null mutations that greatly impact neuronal functions are associated with severe forms of spinal cerebellar ataxia, and our data suggest G/G homozygotes should display a similar phenotype. To address this question, we show in vivo using AAV8-FLAG-CA8-204G and AAV8-V5-CA8-201 gene transfer delivered via intra-neural sciatic nerve injection (SN), that these viral constructs are able to transduce DRG cells and produce similar analgesic and anti-hyperalgesic responses to inflammatory pain. Immunohistochemistry (IHC) examinations of DRG tissues further show CA8-204G peptide is expressed in advillin expressing neuronal cells, but to a lesser extent compared to glial cells. These findings explain why G/G homozygotes that exclusively produce this truncated functional peptide in DRG evade a severe phenotype. These genomic studies significantly advance the literature regarding structure-function studies on CA8-ITPR1 critical to calcium signaling pathways, synaptic functioning, neuronal excitability and analgesic responses.

摘要

碳酸酐酶 8(CA8)是一种细胞内蛋白,作为肌醇三磷酸受体 1(ITPR1)的别构抑制剂发挥作用,对于细胞内 Ca++释放、突触功能和神经元兴奋性至关重要。我们之前的研究表明,小鼠的痛觉和镇痛反应受到与背根神经节(DRG)相关的顺式表达数量基因座(cis-eQTL)中该基因表达的调节。在本报告中,我们确定了一个外显子水平的 cis-eQTL(rs6471859),它调节人类 DRG CA8 的可变剪接,产生一个截断的 1697bp 转录本(例如,CA8-204)。我们的功能基因组研究表明,rs6471859 的“G”等位基因产生一个隐藏的 3'UTR 剪接位点,调节 CA8-204 的表达。我们开发了构建体来研究天然存在的 CA8-204G 转录本(rs6471859 处的“G”等位基因)、CA8-204C(rs6471859 处的 C 等位基因回复突变)和 CA8-201(全长转录本)的表达和功能。CA8-204G 转录本的表达主要发生在非神经元细胞(HEK293)中,而 CA8-204C 的表达仅限于体外神经元来源的细胞(NBL)。CA8-204G 在 HEK293 细胞中产生稳定的截断转录本,在 NBL 细胞中几乎检测不到。我们还表明,CA8-204 产生一种稳定的肽,可抑制 HEK293 细胞中的 pITPR1 和 Ca++释放。这些结果表明,rs6471859 处的纯合子 G/G 个体在普通人群中很常见,它们只产生几乎无法在神经元细胞中检测到的 CA8-204G。严重影响神经元功能的 CA8 缺失突变与严重的脊髓小脑共济失调有关,我们的数据表明 G/G 纯合子应该表现出类似的表型。为了解决这个问题,我们使用通过坐骨神经内神经注射(SN)递送至体内的 AAV8-FLAG-CA8-204G 和 AAV8-V5-CA8-201 基因转移,在体内表明,这些病毒构建体能够转导 DRG 细胞,并对炎症性疼痛产生类似的镇痛和抗痛觉过敏反应。DRG 组织的免疫组织化学(IHC)检查进一步表明,CA8-204G 肽在表达 advillin 的神经元细胞中表达,但程度低于神经胶质细胞。这些发现解释了为什么仅在 DRG 中产生这种截断功能性肽的 G/G 纯合子逃避严重表型。这些基因组研究极大地推进了关于 CA8-ITPR1 的结构功能研究的文献,CA8-ITPR1 对于钙信号通路、突触功能、神经元兴奋性和镇痛反应至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd34/6615631/39f614fe2412/pgen.1008226.g001.jpg

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