AbstractBackgroundStanford type B-acute aortic dissection (type B-AAD) is often life-threatening without invasive surgery. Multilineage-differentiating stress enduring cell (Muse cells), which comprise several percent of mesenchymal stem cells (MSCs), are endogenous pluripotent-like stem cells that selectively home to damaged tissue and replace damaged/apoptotic cells by in-vivo differentiation.MethodsMortality, aortic diameter expansion, cell localization, cell differentiation, and inflammation of the dissected aorta were evaluated in type B-AAD model mice intravenously injected with human-Muse cells, -elastin-knockdown (KD)-Muse cells, -human leukocyte antigen-G (HLA-G)-KD-Muse cells, or MSCs, all without immunosuppressant.ResultsHere, we show the Muse (50,000 cells) group has a lower incidence of aortic rupture and mortality of AAD compared with the MSC-50K (50,000 human-MSCs) and vehicle groups.

摘要背景斯坦福B型急性主动脉夹层（B-AAD型）通常在没有侵入性手术的情况下危及生命。多谱系分化应激耐受细胞（Muse细胞）包含间充质干细胞（MSCs）的百分之几，是内源性多能干细胞，可选择性地归巢于受损组织并通过体内分化替代受损/凋亡细胞。方法在静脉注射人Muse细胞，-弹性蛋白敲低（KD）-Muse细胞，-人白细胞抗原-G（HLA-G）-KD-Muse细胞或MSCs的B-AAD模型小鼠中评估解剖主动脉的死亡率，主动脉直径扩张，细胞定位，细胞分化和炎症，均无免疫抑制剂。结果在这里，我们显示Muse（50000个细胞）组与MSC-50K（50000个人类MSCs）和载体组相比，主动脉破裂和AAD死亡率较低。

Spectrum computed tomography in-vivo dynamics and 3-dimensional histologic analyses demonstrate that Muse cells more effectively home to the AAD tissue and survive for 8 weeks in the Muse group than in the MSC-750K (750,000 human-MSCs containing 50,000 Muse cells) group. Homing of Muse cells is impeded in the HLA-G-KD-Muse (50,000 cells) group.

光谱计算机断层扫描体内动力学和三维组织学分析表明，Muse组中的Muse细胞比MSC-750K（含有50000个Muse细胞的750000个人类MSC）组更有效地归巢于AAD组织并存活8周。在HLA-G-KD-Muse（50000个细胞）组中，Muse细胞的归巢受到阻碍。

Differentiation of homed Muse cells into CD31(+) and alpha-smooth muscle actin (+) cells, production and reorganization of elastic fibers in the AAD tissue, and suppression of diameter expansion are greater in the Muse group than in the MSC-750K and elastin-KD-Muse (50,000 cells) groups.ConclusionsIntravenously administered Muse cells reconstruct the dissected aorta and improve mortality and diameter enlargement rates.

Muse组中归巢的Muse细胞分化为CD31（+）和α平滑肌肌动蛋白（+）细胞，AAD组织中弹性纤维的产生和重组以及直径扩张的抑制作用大于MSC-750K和弹性蛋白KD Muse（50000个细胞）组。结论连续给药的Muse细胞重建了解剖的主动脉，提高了死亡率和直径扩大率。

Moreover, small doses of purified Muse cells are more effective than large doses of MSCs. HLA-G is suggested to contr.

此外，小剂量纯化的Muse细胞比大剂量的MSC更有效。建议控制HLA-G。

Acute aortic dissection (AAD) is a serious disease in which the largest artery in the body, called the aorta, enlarges and ruptures. Surgery is often required to prevent death. Cells called Muse cells have been injected into people during clinical trials to treat other diseases. In this study, we injected Muse cells into mice with dissected aorta.

急性主动脉夹层（AAD）是一种严重的疾病，体内最大的动脉（称为主动脉）会扩大并破裂。通常需要手术来预防死亡。在临床试验期间，被称为Muse细胞的细胞被注射到人体内以治疗其他疾病。在这项研究中，我们将Muse细胞注射到主动脉夹层的小鼠中。

The cells accumulated in damaged parts of the aorta and strengthened the structure of the aorta, reducing the number of mice that died. If further research shows this treatment works in humans, this could enable AAD to be treated without surgery and potentially improve the treatment and survival of people with AAD..

这些细胞聚集在主动脉受损部位，增强了主动脉的结构，减少了死亡小鼠的数量。如果进一步的研究表明这种治疗方法对人类有效，这可能使AAD不需要手术治疗，并有可能改善AAD患者的治疗和生存。。

IntroductionAcute aortic dissection (AAD) is a common, life-threatening disease that occurs with chest pain and/or back pain, mainly related to high blood pressure. AAD begins with a tear (entry) in the intima of the aortic wall and progresses into the media, forming the original aortic lumen (true lumen) and a newly created wall lumen (false lumen), and is associated with inflammation of the aortic tissue1,2,3,4.

引言急性主动脉夹层（AAD）是一种常见的危及生命的疾病，伴有胸痛和/或背痛，主要与高血压有关。AAD始于主动脉壁内膜的撕裂（进入），并进入介质，形成原始主动脉腔（真腔）和新产生的壁腔（假腔），并与主动脉组织的炎症有关1,2,3,4。

AAD is classified into two types5; Stanford type A-AAD (Stanford A-AAD), which involves the ascending aorta, requires emergent surgery to place a prosthetic vascular graft because the prognosis is generally poor; Stanford type B-AAD (Stanford B-AAD) that does not involve the ascending aorta but extends distal to the aortic arch is usually treated conservatively for avoiding surgical risks if there are no complications6,7.

AAD分为两种类型5；涉及升主动脉的斯坦福A-AAD（Stanford A-AAD）需要紧急手术来放置人工血管移植物，因为预后通常很差；如果没有并发症，通常保守治疗不涉及升主动脉但延伸至主动脉弓远端的斯坦福型B-AAD（斯坦福B-AAD）以避免手术风险6,7。

However, in Stanford B-AAD, the vulnerable dissected aorta often dilates over time and develops an aneurysmal transformation, increasing the risk of rupture8, which ultimately leads to significant mortality. This requires highly invasive surgery with the risk of serious complications such as spinal cord infarction9.

然而，在斯坦福B-AAD中，脆弱的解剖主动脉通常会随着时间的推移而扩张，并发生动脉瘤转化，增加破裂的风险8，最终导致严重的死亡率。这需要高度侵入性的手术，并有严重并发症的风险，如脊髓梗塞9。

Thoracic endovascular aortic repair (TEVAR), a surgical treatment intended to close the entry that connects the true lumen and false lumen, in the acute phase may improve mortality and aneurysmal changes during the chronic phase10, while this treatment includes risk of complications. In other words, there is no debate that emergency surgery is necessary for Stanford A-AAD, while surgery for the acute phase of Stanford B-AAD remains controversial.

胸主动脉腔内修复术（TEVAR）是一种手术治疗，旨在关闭连接真腔和假腔的入口，在急性期可能会提高慢性期的死亡率和动脉瘤变化10，而这种治疗包括并发症的风险。换句话说，斯坦福A-AAD需要紧急手术是没有争议的，而斯坦福B-AAD急性期的手术仍然存在争议。

We focused on Stanford type B-AAD, expecting to avoid surgery in the chronic phase through structural strengthening of the dissected aorta in the acute phase by cell-based therapy.Multili.

我们专注于斯坦福B-AAD型，期望通过基于细胞的治疗在急性期通过解剖主动脉的结构强化来避免慢性期的手术。多利。

Data availability

数据可用性

The source data for Figs. 1c, f, 2b, d, f, 3a, b, d, e, 5b, c, e, f, 6a, b, c, e and Supplementary Figs. 2d, 5 and 6 are in the Supplementary Data file. The CT images obtained during this study are deposited in the Science Data Bank32 URL: https://www.scidb.cn/en/detail?dataSetId=f1b7da634c334aaca05609c88740d65b.

图1c，f，2b，d，f，3a，b，d，e，5b，c，e，f，6a，b，c，e和补充图2d，5和6的源数据在补充数据文件中。本研究期间获得的CT图像保存在科学数据库32 URL中：https://www.scidb.cn/en/detail?dataSetId=f1b7da634c334aaca05609c88740d65b.

Further datasets obtained whilst undertaking this study are available from the corresponding author on reasonable request..

在进行这项研究时获得的进一步数据集可根据合理的要求从通讯作者处获得。。

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Download referencesAcknowledgementsThis study was supported by a Grant-in-Aid for Scientific Research (C) (K18K087230), a Grant-in-Aid for Scientific Research B (20H04510), and a Grant-in-Aid for Exploratory Research (19H22648), Japan Society for the Promotion of Science.Author informationAuthors and AffiliationsDivision of Cardiovascular Surgery and Tohoku University Graduate School of Medicine1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, JapanMakoto Takahashi & Yoshikatsu SaikiDepartment of Stem Cell Biology and Histology, Tohoku University Graduate School of Medicine, Sendai, JapanMakoto Takahashi, Yoshihiro Kushida, Yasumasa Kuroda, Shohei Wakao & Mari DezawaDepartment of Biochemistry, Dokkyo Medical University School of Medicine, Mibu, Tochigi, JapanYasuhiro Horibata & Hiroyuki SugimotoAuthorsMakoto TakahashiView author publicationsYou can also search for this author in.

下载参考文献致谢本研究得到了日本科学促进会科学研究资助（C）（K18K087230），科学研究资助B（20H04510）和探索性研究资助（19H22648）的支持。作者信息作者和附属机构心血管外科和东北大学医学研究生院1-1 Seiryo machi，Aoba ku，Sendai，Miyagi，JapanMakoto Takahashi＆Yoshikatsu SaikidDepartment of Stem Cell Biology and Histology，东北大学医学研究生院，Sendai，JapanMakoto Takahashi，Yoshihiro Kushida，Yasumasa Kuroda，Shohei Wakao＆Mari Dezawa Dokkyo Medical University School of Medicine，Mibu，Tochigi，JapanYasuhiro Horibata＆Hiroyuki Sugimotoauth Orsmakoto TakahashiView作者出版物您也可以在中搜索此作者。

PubMed Google ScholarYoshihiro KushidaView author publicationsYou can also search for this author in

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PubMed Google ScholarContributionsM.T., Yo.K., Ya.K., S.W., Y.H., and H.S. collected the data. M.T., Yo.K., Ya.K., S.W., and Y.S. analyzed the data. M.D., M.T., and Y.S. wrote the manuscript.Corresponding authorsCorrespondence to

PubMed谷歌学术贡献。T、 ，哟。K、 ，是的。K、 ，S.W.，Y.H。和H.S.收集了数据。M、 T.，哟。K、 ，是的。K、 ，S.W。和Y.S.分析了数据。M、 D.，M.T。和Y.S.撰写了手稿。通讯作者通讯

Makoto Takahashi, Mari Dezawa or Yoshikatsu Saiki.Ethics declarations

Makoto Takahashi、Mari Dezawa或Yoshikatsu Saiki。道德宣言

Competing interest

竞争利益

The authors declare the following competing interests: Yoshihiro Kushida, Shohei Wakao, Yasumasa Kuroda, and Mari Dezawa have a patent for Muse cells (WO2011007900). All other authors have no competing interests to declare.

作者声明了以下相互竞争的利益：Kushida Yoshihiro，Shohei Wakao，Yasumasa Kuroda和Mari Dezawa拥有Muse cells的专利（WO2011007900）。所有其他作者都没有相互竞争的利益。

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Reprints and permissionsAbout this articleCite this articleTakahashi, M., Kushida, Y., Kuroda, Y. et al. Structural reconstruction of mouse acute aortic dissection by intravenously administered human Muse cells without immunosuppression.

转载和许可本文引用本文Takahashi，M.，Kushida，Y.，Kuroda，Y。等人。通过静脉注射人Muse细胞在不受免疫抑制的情况下对小鼠急性主动脉夹层进行结构重建。

Commun Med 4, 174 (2024). https://doi.org/10.1038/s43856-024-00597-6Download citationReceived: 10 July 2023Accepted: 28 August 2024Published: 09 September 2024DOI: https://doi.org/10.1038/s43856-024-00597-6Share 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.

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