The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Exosomes derived from mature dendritic cells increase endothelial inflammation and atherosclerosis via membrane TNF‐α mediated NF‐κB pathway
Open accessAbstract
Whether dendritic cell (DC) derived exosomes play a role in the progression of endothelial inflammation and atherosclerosis remains unclear. Using a transwell system and exosome release inhibitor GW 4869, we demonstrated that mature DC s contributed to endothelial inflammation and exosomes were involved in the process. To further confirm this finding, we isolated exosomes from bone marrow dendritic cell (BMDC) culture medium (named DC‐exos) and stimulated human umbilical vein endothelial cell (HUVEC) with these DC‐exos. We observed that mature DC‐exos increased HUVEC inflammation through NF‐κB pathway in a manner similar to that of lipopolysaccharide. After a protein array analysis of exosomes, we identified and confirmed tumour necrosis factor (TNF)‐α on exosome membrane being the trigger of NF‐κB pathway in HUVEC s. We then performed an in vivo study and found that the aorta endothelial of mice could uptake intravenously injected exosomes and was activated by these exosomes. After a period of 12 weeks of mature DC‐exos injection into ApoE−/− mice, the atherosclerotic lesions significantly increased. Our study demonstrates that mature DC s derived exosomes increase endothelial inflammation and atherosclerosis via membrane TNF‐α mediated NF‐κB pathway. This finding extends our knowledge on how DC s affect inflammation and provides a potential method to prevent endothelial inflammation and atherosclerosis.
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Cites
Biological properties of extracellular vesicles and their physiological functions
Yáñez‐Mó, M., Siljander, P. R. ‐., Andreu, Z., Bedina Zavec, A., Borràs, F. E., Buzas, E. I., Buzas, K., Casal, E., Cappello, F., Carvalho, J., et al. (2015) · Journal of Extracellular Vesicles · doi:10.3402/jev.v4.27066 · Cited by 5,926
The immune system in atherosclerosis
Hansson, G. K., & Hermansson, A. (2011) · Nature Immunology · doi:10.1038/ni.2001 · Cited by 2,317
MicroRNAs bind to Toll-like receptors to induce prometastatic inflammatory response
Fabbri, M., Paone, A., Calore, F., Galli, R., Gaudio, E., Santhanam, R., Lovat, F., Fadda, P., Mao, C., Nuovo, G. J., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1209414109 · Cited by 1,434
Mechanism of transfer of functional microRNAs between mouse dendritic cells via exosomes.
Montecalvo, A., Larregina, A. T., Shufesky, W. J., Beer Stolz, D., Sullivan, M. L. G., Karlsson, J. M., Baty, C. J., Gibson, G. A., Erdos, G., Wang, Z., et al. (2012) · Blood · doi:10.1182/blood-2011-02-338004 · Cited by 1,429
Bang, C., Batkai, S., Dangwal, S., Gupta, S. K., Foinquinos, A., Holzmann, A., Just, A., Remke, J., Zimmer, K., Zeug, A., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci70577 · Cited by 979
Schneider, P., Holler, N., Bodmer, J.-L., Hahne, M., Frei, K., Fontana, A., & Tschopp, J. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.187.8.1205 · Cited by 812
Exosome-delivered microRNAs modulate the inflammatory response to endotoxin
Alexander, M., Hu, R., Runtsch, M. C., Kagele, D. A., Mosbruger, T. L., Tolmachova, T., Seabra, M. C., Round, J. L., Ward, D. M., & O’Connell, R. M. (2015) · Nature Communications · doi:10.1038/ncomms8321 · Cited by 769
Downregulation of Fas ligand by shedding
Tanaka, M., Itai, T., Adachi, M., & Nagata, S. (1998) · Nature Medicine · doi:10.1038/nm0198-031 · Cited by 669
LAULAGNIER, K., MOTTA, C., HAMDI, S., ROY, S., FAUVELLE, F., PAGEAUX, J.-F., KOBAYASHI, T., SALLES, J.-P., PERRET, B., BONNEROT, C., et al. (2004) · Biochemical Journal · doi:10.1042/bj20031594 · Cited by 647
Plasma Exosomes Protect the Myocardium From Ischemia-Reperfusion Injury
Vicencio, J. M., Yellon, D. M., Sivaraman, V., Das, D., Boi-Doku, C., Arjun, S., Zheng, Y., Riquelme, J. A., Kearney, J., Sharma, V., et al. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.02.026 · Cited by 544
Cited by
Medina-Leyte, D. J., Zepeda-García, O., Domínguez-Pérez, M., González-Garrido, A., Villarreal-Molina, T., & Jacobo-Albavera, L. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22083850 · Cited by 623
Mesenchymal Stem Cell-Derived Exosomes: Applications in Regenerative Medicine
Hade, M. D., Suire, C. N., & Suo, Z. (2021) · Cells · doi:10.3390/cells10081959 · Cited by 607
Hybrid exosomes, exosome-like nanovesicles and engineered exosomes for therapeutic applications
Mondal, J., Pillarisetti, S., Junnuthula, V., Saha, M., Hwang, S. R., Park, I.-K., & Lee, Y.-K. (2023) · Journal of Controlled Release · doi:10.1016/j.jconrel.2022.12.027 · Cited by 416
Lim, Y. J., Sidor, N. A., Tonial, N. C., Che, A., & Urquhart, B. L. (2021) · Toxins · doi:10.3390/toxins13020142 · Cited by 373
Chen, H.-X., Liang, F.-C., Gu, P., Xu, B.-L., Xu, H.-J., Wang, W.-T., Hou, J.-Y., Xie, D.-X., Chai, X.-Q., & An, S.-J. (2020) · Cell Death & Disease · doi:10.1038/s41419-020-2473-5 · Cited by 319
Metadata
- Authors
- Gao, W., Liu, H., Yuan, J., Wu, C., Huang, D., Ma, Y., Zhu, J., Ma, L., Guo, J., Shi, H., Zou, Y., & Ge, J.
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2016-08-12
- Volume
- 20
- Issue
- 12
- Pages
- 2318-2327
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- OpenAlex
- W2513725953
- Cited by
- 264
- References
- 31
- FWCI
- 6.62
- Type
- journal article
- Language
- en
- Open access
- gold
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- Gao, W., Liu, H., Yuan, J., Wu, C., Huang, D., Ma, Y., Zhu, J., Ma, L., Guo, J., Shi, H., Zou, Y., & Ge, J. (2016). Exosomes derived from mature dendritic cells increase endothelial inflammation and atherosclerosis via membrane TNF‐α mediated NF‐κB pathway. Journal of Cellular and Molecular Medicine. https://doi.org/10.1111/jcmm.12923
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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