Macrophage-Derived Exosomal Mir-155 Regulating Cardiomyocyte Pyroptosis and Hypertrophy in Uremic Cardiomyopathy
[Display omitted] •miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart.•The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the...
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| Published in | JACC. Basic to translational science Vol. 5; no. 2; pp. 148 - 166 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.02.2020
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | [Display omitted]
•miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart.•The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class in cardiomyocytes.•Macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. Inhibiting secretion from macrophage-derived miR-155–containing exosomes represents a novel therapeutic strategy for the management of uremic cardiomyopathy.
miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. |
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| AbstractList | [Display omitted]
•miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart.•The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class in cardiomyocytes.•Macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. Inhibiting secretion from macrophage-derived miR-155–containing exosomes represents a novel therapeutic strategy for the management of uremic cardiomyopathy.
miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. Visual Abstract • miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. • The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class in cardiomyocytes. • Macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. Inhibiting secretion from macrophage-derived miR-155–containing exosomes represents a novel therapeutic strategy for the management of uremic cardiomyopathy. miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. Key Words: exosome, FoxO3a, miR-155, pyroptosis, uremic cardiomyopathy miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155-containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice.miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155-containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155-containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice. |
| Author | Liu, Bi-Cheng Zhang, Aiqing Shi, Hao-Jie Ji, Jia-Ling Du, Jie Wang, Xiaonan H. Wang, Ze-Mu Wang, Bin Lv, Linli Gan, Weihua Tang, Taotao Li, Zuolin Wang, Hao |
| AuthorAffiliation | a Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China e Department of Medicine, Renal Division, Emory University, Atlanta, Georgia d Beijing Anzhen Hospital, Capital Medical University, Beijing, China c Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China b Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China |
| AuthorAffiliation_xml | – name: b Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – name: c Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – name: e Department of Medicine, Renal Division, Emory University, Atlanta, Georgia – name: d Beijing Anzhen Hospital, Capital Medical University, Beijing, China – name: a Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China |
| Author_xml | – sequence: 1 givenname: Bin surname: Wang fullname: Wang, Bin organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China – sequence: 2 givenname: Ze-Mu surname: Wang fullname: Wang, Ze-Mu organization: Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 3 givenname: Jia-Ling surname: Ji fullname: Ji, Jia-Ling organization: Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 4 givenname: Weihua surname: Gan fullname: Gan, Weihua organization: Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 5 givenname: Aiqing surname: Zhang fullname: Zhang, Aiqing organization: Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 6 givenname: Hao-Jie surname: Shi fullname: Shi, Hao-Jie organization: Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 7 givenname: Hao surname: Wang fullname: Wang, Hao organization: Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China – sequence: 8 givenname: Linli surname: Lv fullname: Lv, Linli organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China – sequence: 9 givenname: Zuolin surname: Li fullname: Li, Zuolin organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China – sequence: 10 givenname: Taotao surname: Tang fullname: Tang, Taotao organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China – sequence: 11 givenname: Jie surname: Du fullname: Du, Jie organization: Beijing Anzhen Hospital, Capital Medical University, Beijing, China – sequence: 12 givenname: Xiaonan H. surname: Wang fullname: Wang, Xiaonan H. organization: Department of Medicine, Renal Division, Emory University, Atlanta, Georgia, USA – sequence: 13 givenname: Bi-Cheng surname: Liu fullname: Liu, Bi-Cheng email: liubc64@163.com organization: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, Jiangsu, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32140622$$D View this record in MEDLINE/PubMed |
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| Keywords | FoxO IL uremic cardiomyopathy FoxO3a LV miRs pyroptosis TUNEL miR-155 AAV 3’-UTRs exosome CKD UCM microRNAs chronic kidney disease 3’-untranslated regions left ventricle deoxyuridine triphosphate nick-end labeling adeno-associated virus forkhead transcription factors of the O class interleukin LV, left ventricle 3’-UTRs, 3’-untranslated regions AAV, adeno-associated virus TUNEL, deoxyuridine triphosphate nick-end labeling FoxO, forkhead transcription factors of the O class IL, interleukin miRs, microRNAs UCM, uremic cardiomyopathy CKD, chronic kidney disease |
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•miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart.•The released exosomal fusion... Visual Abstract miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma... miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma... • miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. • The released exosomal fusion with the plasma... |
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| Title | Macrophage-Derived Exosomal Mir-155 Regulating Cardiomyocyte Pyroptosis and Hypertrophy in Uremic Cardiomyopathy |
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