CD47在调节细胞可塑性和代谢可塑性中的细胞自主功能-动脉网

Cell autonomous functions of CD47 in regulating cellular plasticity and metabolic plasticity

Nature 等信源发布 2024-07-23 10:40

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AbstractCD47 is a ubiquitously expressed cell surface receptor, which is widely known for preventing macrophage-mediated phagocytosis by interacting with signal regulatory protein α (SIRPα) on the surface of macrophages. In addition to its role in phagocytosis, emerging studies have reported numerous noncanonical functions of CD47 that include regulation of various cellular processes such as proliferation, migration, apoptosis, differentiation, stress responses, and metabolism.

摘要CD47是一种普遍表达的细胞表面受体，通过与巨噬细胞表面的信号调节蛋白α（SIRPα）相互作用来预防巨噬细胞介导的吞噬作用。除了其在吞噬作用中的作用外，新兴研究报道了CD47的许多非经典功能，包括调节各种细胞过程，如增殖，迁移，凋亡，分化，应激反应和代谢。

Despite lacking an extensive cytoplasmic signaling domain, CD47 binds to several cytoplasmic proteins, particularly upon engaging with its secreted matricellular ligand, thrombospondin 1. Indeed, the regulatory functions of CD47 are greatly influenced by its interacting partners. These interactions are often cell- and context-specific, adding a further level of complexity.

尽管缺乏广泛的细胞质信号传导结构域，但CD47与几种细胞质蛋白结合，特别是在与其分泌的基质细胞配体血小板反应蛋白1结合时。事实上，CD47的调节功能受到其相互作用伙伴的极大影响。这些交互通常是特定于细胞和上下文的，增加了进一步的复杂性。

This review addresses the downstream cell-intrinsic signaling pathways regulated by CD47 in various cell types and environments. Some of the key pathways modulated by this receptor include the PI3K/AKT, MAPK/ERK, and nitric oxide signaling pathways, as well as those implicated in glucose, lipid, and mitochondrial metabolism.

本综述讨论了CD47在各种细胞类型和环境中调节的下游细胞内在信号传导途径。该受体调节的一些关键途径包括PI3K/AKT，MAPK/ERK和一氧化氮信号传导途径，以及与葡萄糖，脂质和线粒体代谢有关的途径。

These pathways play vital roles in maintaining tissue homeostasis, highlighting the importance of understanding the phagocytosis-independent functions of CD47. Given that CD47 expression is dysregulated in a variety of cancers, improving our understanding of the cell-intrinsic signals regulated by this molecule will help advance the development of CD47-targeted therapies..

这些途径在维持组织稳态中起着至关重要的作用，突出了理解CD47吞噬作用独立功能的重要性。鉴于CD47表达在多种癌症中失调，提高我们对该分子调节的细胞内在信号的理解将有助于促进CD47靶向治疗的发展。。

Facts

CD47 is a ubiquitously expressed cell surface receptor, widely known for its role in preventing phagocytosis through its interaction with SIRPα.

CD47是一种普遍表达的细胞表面受体，因其通过与SIRPα的相互作用在预防吞噬作用中的作用而广为人知。

CD47 also influences cellular behaviors beyond its “don’t eat me” signal function, including cellular and metabolic plasticity.

CD47还影响其“不吃我”信号功能以外的细胞行为，包括细胞和代谢可塑性。

Through its cytoplasmic tail, CD47 regulates cell-intrinsic functions.

。

Depending on the cellular context and the ligand it binds to, CD47 modulates cellular responses to stress, cell-motility, migration, cell death and cell proliferation.

根据细胞环境及其结合的配体，CD47调节细胞对压力，细胞运动，迁移，细胞死亡和细胞增殖的反应。

Furthermore, it regulates cellular metabolism, including glycolysis, mitochondrial, fatty acid and nucleotide metabolism.

此外，它调节细胞代谢，包括糖酵解，线粒体，脂肪酸和核苷酸代谢。

Outstanding Questions

悬而未决的问题

What factors determine cell-type-specific function of CD47?

什么因素决定CD47的细胞类型特异性功能？

How does CD47 regulate the cell-autonomous functions upon binding to a ligand?

CD47如何在与配体结合后调节细胞自主功能？

Is there crosstalk between CD47’s canonical and noncanonical functions?

CD47的规范函数和非规范函数之间是否存在串扰？

How does targeting CD47 affect its cell-autonomous functions?

靶向CD47如何影响其细胞自主功能？

Can CD47 serve as a target for other autoinflammatory diseases?

CD47能否作为其他自身炎症性疾病的靶标？

IntroductionCluster of differentiation 47 (CD47) structure and isoformsCD47 (also known as IAP, MER6, or OA3) is a cell surface, integrin-associated glycoprotein belonging to the immunoglobulin (Ig) superfamily [1]. Structurally, it is composed of a single, glycosylated, extracellular variable Ig domain, a presenilin domain comprising five transmembrane-spanning segments, and a short variably spliced C-terminal cytoplasmic tail that gives rise to four isoforms [2, 3].

引言分化簇47（CD47）结构和同种型CD47（也称为IAP，MER6或OA3）是属于免疫球蛋白（Ig）超家族的细胞表面整合素相关糖蛋白。在结构上，它由单个糖基化的细胞外可变Ig结构域，包含五个跨膜片段的早老素结构域和产生四种同种型的短可变剪接的C末端细胞质尾部组成[2，3]。

Isoform 2 is the most abundant isoform of CD47, which is expressed primarily by hematopoietic, endothelial, and epithelial cells [4]. Isoforms 3 and 4 are expressed predominantly in neural tissue, while isoform 1 is mainly present in keratinocytes [4]. Besides the proposed roles of isoforms 3 and 4 in memory retention and isoform 2 in transducing signals between the extracellular matrix (ECM) and cytoskeleton of astrocytes, the functional significance of alternate CD47 RNA splicing is poorly understood [5].CD47 ligands and binding partInitially recognized for associating with the Rhesus (Rh) antigen complex on red blood cells (RBCs), subsequent early studies revealed that CD47 engages with ανβ3 integrin in human placenta and granulocytes and functions as an overexpressed tumor antigen in ovarian cancer [6,7,8,9,10].

同种型2是CD47最丰富的同种型，主要由造血细胞，内皮细胞和上皮细胞表达（4）。同种型3和4主要在神经组织中表达，而同种型1主要存在于角质形成细胞中。除了提出的同工型3和4在记忆保留中的作用以及同工型2在星形胶质细胞的细胞外基质（ECM）和细胞骨架之间转导信号的作用外，人们对替代CD47 RNA剪接的功能意义知之甚少。CD47配体和结合最初被认为与红细胞（RBC）上的恒河猴（Rh）抗原复合物相关，随后的早期研究表明CD47与人胎盘和粒细胞中的ανβ3整联蛋白结合，并在卵巢癌中作为过表达的肿瘤抗原起作用[6,7,8,9,10]。

Affinity labeling and CD47-deficient mouse model studies further demonstrated that thrombospondin 1 (TSP1), a secreted ECM glycoprotein, acts as a trans-spanning ligand for CD47, while signal regulatory protein α (SIRPα) serves as its cognate receptor [11, 12]. Subsequently, CD47 has been shown to interact with integrins, including αIIbβ3, α2β1, ανβ3, α4β1, α6β1, and αмβ2, as well as with caveolin-1, VEGFR2 and NOX1 in a cis configuration across different cell types [13,14,15,16,17,18,19,20,21,.

亲和标记和CD47缺陷小鼠模型研究进一步表明，血小板反应蛋白1（TSP1）是一种分泌的ECM糖蛋白，可作为CD47的跨反式配体，而信号调节蛋白α（SIRPα）可作为其同源受体[11，12]。随后，CD47已被证明与整合素相互作用，包括αIIbβ3，α2β1，ανβ3，α4β1，α6β1和αмβ2，以及在不同细胞类型中以顺式构型与caveolin-1，VEGFR2和NOX1相互作用[13,14,15,16,17,18,19,20,21]，。

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Download referencesAcknowledgementsRP is supported by the University of South Australia Research Training Program (RTP) Scholarship. NR and SP are funded by the National Health and Medical Research Council, Australia; NeuroSurgical Research Foundation (NRF); Tour de Cure and University of South Australia; Fay Fuller Foundation.

下载参考文献致谢SRP得到了南澳大利亚大学研究培训计划（RTP）奖学金的支持。NR和SP由澳大利亚国家卫生与医学研究委员会资助；神经外科研究基金会（NRF）；Tour de Cure和南澳大利亚大学；费·富勒基金会。

The authors would also like to thank Jessica Tamanini of Insight Editing London for their assistance in preparing this manuscript.FundingOpen Access funding enabled and organized by CAUL and its Member Institutions.Author informationAuthor notesRaja GanesanPresent address: Institute for Molecular Immunology, CECAD Research Center, University Hospital Cologne, Cologne, GermanyAuthors and AffiliationsCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, AustraliaRuhi Polara, Raja Ganesan, Stuart M.

作者还要感谢Insight Editing London的杰西卡·塔马尼尼（JessicaTamanini）为编写这份手稿提供的帮助。基金开放获取基金由CAUL及其成员机构启用和组织。作者信息作者注释Raja Ganesan目前的地址：分子免疫学研究所，CECAD研究中心，科隆大学医院，科隆，德国作者和附属机构癌症生物学，南澳大学和SA病理学，阿德莱德，SA，澳大利亚Aruhi Polara，Raja Ganesan，Stuart M。

Pitson & Nirmal RobinsonAdelaide Medical School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, AustraliaStuart M. Pitson & Nirmal RobinsonSchool of Biological Sciences, The University of Adelaide, Adelaide, SA, AustraliaStuart M. PitsonAuthorsRuhi PolaraView author publicationsYou can also search for this author in.

Pitson＆Nirmal RobinsonAdelaide医学院，健康与医学院，阿德莱德大学，阿德莱德，SA，AustraliaStuart M.Pitson＆Nirmal RobinsonSchool of Biological Sciences，阿德莱德大学，阿德莱德，SA，AustraliaStuart M.PitsonAuthorsRuhi PolaraView作者出版物您也可以在中搜索这位作者。

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PubMed Google ScholarContributionsRP wrote, revised the manuscript, and designed the figures. RG wrote the manuscript. SMP wrote the manuscript. NR conceptualized, wrote, and revised the manuscript.Corresponding authorCorrespondence to

PubMed Google ScholarContributionsRP撰写、修改了手稿并设计了数字。RG写了手稿。SMP撰写了手稿。NR对稿件进行了概念化，撰写和修订。对应作者对应

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Reprints and permissionsAbout this articleCite this articlePolara, R., Ganesan, R., Pitson, S.M. et al. Cell autonomous functions of CD47 in regulating cellular plasticity and metabolic plasticity.

转载和许可本文引用本文Polara，R.，Ganesan，R.，Pitson，S.M.等人CD47在调节细胞可塑性和代谢可塑性中的细胞自主功能。

Cell Death Differ (2024). https://doi.org/10.1038/s41418-024-01347-wDownload citationReceived: 07 March 2024Revised: 09 July 2024Accepted: 11 July 2024Published: 23 July 2024DOI: https://doi.org/10.1038/s41418-024-01347-wShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

细胞死亡不同（2024）。https://doi.org/10.1038/s41418-024-01347-wDownload引文收到日期：2024年3月7日修订日期：2024年7月9日接受日期：2024年7月11日发布日期：2024年7月23日OI：https://doi.org/10.1038/s41418-024-01347-wShare本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。复制到剪贴板。

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