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人诱导多能干细胞来源的间充质干细胞衍生的外泌体通过激活 Akt/Nrf2/HO-1 轴改善重症急性胰腺炎引起的心肌损伤。

Exosomes from human induced pluripotent stem cells derived mesenchymal stem cells improved myocardial injury caused by severe acute pancreatitis through activating Akt/Nrf2/HO-1 axis.

机构信息

Department of Critical Care Medicine, Affiliated Hospital of Putian University, No. 999 Dongzhen Road, Putian, Fujian, China.

Department of Critical Care Medicine, Fujian Medical University Union Hospital, No. 29 Xinquan Road, Fuzhou, Fujian, China.

出版信息

Cell Cycle. 2022 Aug;21(15):1578-1589. doi: 10.1080/15384101.2022.2057762. Epub 2022 Apr 15.

DOI:10.1080/15384101.2022.2057762
PMID:35422193
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9291715/
Abstract

Human induced pluripotent stem cell-derived mesenchymal stem cells (iMSCs) have been believed to be a promising alternative for the stem cell transplantation therapy. The exosomes (Exo) from iMSCs play an important role in several kinds of life activities. The role of exosomes from iMSCs in severe acute pancreatitis (SAP) induced myocardial injury (MI) has not been investigated. The Exo were isolated from iMSCs through differential centrifugation method. The SAP rat model was established with 5% sodium taurocholate injection into the distal end of the bilepancreatic duct. RT-PCR and western blotting were used to measure related gene expression. Masson trichrome and Sirius Red stainings were used to evaluate MI injury. Cardiac function was detected through cardiac ultrasound.Exo promoted cell viability through activating Akt/nuclear factor E2 related factors 2 (Nrf2)/heme oxygenase 1 (HO-1) signaling pathway . Exo improved MI induced by SAP through activating Akt/Nrf2/HO-1 signaling pathway. Exo improved cardiac function, and suppressed oxidative status in the SAP model. Exo increased the expression of von Willebrand Factor (vWF) and vascular endothelial growth factor (VEGF) through activating Nrf2/HO-1 signaling pathway. Our data indicated that the Exo from iMSCs could improve MI caused by SAP through activating Nrf2/HO-1 axis. These findings firstly unfold the potential application of Exo from iMSCs in treating MI induced by SAP. LVEF: Left ventricular ejection fraction; LVFS: left ventricular fractional shorten; LVDd: left ventricular end-diastolic diameter; LVDs: left ventricular end-systolic diameter; MI: Myocardial infarction; MSCs: Mesenchymal stem cells; iPSCs: Human-induced pluripotent stem cells; SAP: Severe acute pancreatitis; iMSCs: iPSCs derived VEGF: MSCs; vascular endothelial growth factor; Nrf2: Nuclear factor erythroid 2-related factor; RT-PCR: Real-time polymerase chain reaction; HE: Hematoxylin-eosin; MODS: Multiple organ dysfunction syndrome; PI3K: Phosphatidylinositol 3-kinase; SOD: Superoxide dismutase; FBS: Fetal bovine serum; ECL: Enhanced chemiluminescence; IHC: Immunohistochemistry.

摘要

人诱导多能干细胞衍生的间充质干细胞（iMSCs）已被认为是干细胞移植治疗的一种有前途的替代方法。iMSCs 的外泌体（Exo）在多种生命活动中发挥重要作用。iMSCs 的外泌体在重症急性胰腺炎（SAP）诱导的心肌损伤（MI）中的作用尚未得到研究。通过差速离心法从 iMSCs 中分离 Exo。通过向胆胰胆管末端注射 5%牛磺胆酸钠建立 SAP 大鼠模型。通过实时聚合酶链反应和蛋白质印迹测量相关基因表达。Masson 三色和 Sirius Red 染色用于评估 MI 损伤。通过心脏超声检测心脏功能。Exo 通过激活 Akt/核因子 E2 相关因子 2（Nrf2）/血红素加氧酶 1（HO-1）信号通路促进细胞活力。Exo 通过激活 Akt/Nrf2/HO-1 信号通路改善 SAP 诱导的 MI。Exo 改善 SAP 模型中的心脏功能，并抑制氧化应激。Exo 通过激活 Nrf2/HO-1 信号通路增加血管性血友病因子（vWF）和血管内皮生长因子（VEGF）的表达。我们的数据表明，iMSCs 的 Exo 通过激活 Nrf2/HO-1 轴可以改善 SAP 引起的 MI。这些发现首次揭示了 iMSCs 的 Exo 在治疗 SAP 诱导的 MI 中的潜在应用。LVEF：左心室射血分数；LVFS：左心室短轴缩短率；LVDd：左心室舒张末期直径；LVDs：左心室收缩末期直径；MI：心肌梗死；MSCs：间充质干细胞；iPSCs：人诱导多能干细胞；SAP：重症急性胰腺炎；iMSCs：iPSCs 衍生的 VEGF：MSCs；血管内皮生长因子；Nrf2：核因子红细胞 2 相关因子；实时聚合酶链反应；HE：苏木精-伊红；MODS：多器官功能障碍综合征；PI3K：磷脂酰肌醇 3-激酶；SOD：超氧化物歧化酶；FBS：胎牛血清；ECL：增强化学发光；IHC：免疫组织化学。

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本文引用的文献

[1]
MicroRNAs and exosomes: Cardiac stem cells in heart diseases.

Pathol Res Pract. 2022-1

[2]
Restoring Cardiac Functions after Myocardial Infarction-Ischemia/Reperfusion via an Exosome Anchoring Conductive Hydrogel.

ACS Appl Mater Interfaces. 2021-12-8

[3]
Mesenchymal stem cells derived from human induced pluripotent stem cells improve the engraftment of myogenic cells by secreting urokinase-type plasminogen activator receptor (uPAR).

Stem Cell Res Ther. 2021-10-9

[4]
Exosomes secreted by FNDC5-BMMSCs protect myocardial infarction by anti-inflammation and macrophage polarization via NF-κB signaling pathway and Nrf2/HO-1 axis.

Stem Cell Res Ther. 2021-9-28

[5]
Astrocyte-derived exosomes protect hippocampal neurons after traumatic brain injury by suppressing mitochondrial oxidative stress and apoptosis.

Aging (Albany NY). 2021-9-13

[6]
Catalpol Weakens Depressive-like Behavior in Mice with Streptozotocin-induced Hyperglycemia via PI3K/AKT/Nrf2/HO-1 Signaling Pathway.

Neuroscience. 2021-10-1

[7]
Antidepressant mechanism of catalpol: Involvement of the PI3K/Akt/Nrf2/HO-1 signaling pathway in rat hippocampus.

Eur J Pharmacol. 2021-10-15

[8]
Triclosan regulates the Nrf2/HO-1 pathway through the PI3K/Akt/JNK signaling cascade to induce oxidative damage in neurons.

Environ Toxicol. 2021-9

[9]
Rosuvastatin and low-dose carvedilol combination protects against isoprenaline-induced myocardial infarction in rats: Role of PI3K/Akt/Nrf2/HO-1 signalling.

Clin Exp Pharmacol Physiol. 2021-10

[10]
Conditioned medium from induced pluripotent stem cell-derived mesenchymal stem cells accelerates cutaneous wound healing through enhanced angiogenesis.

Stem Cell Res Ther. 2021-5-20

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