Cited by 106RNA Interference and Gene DeliveryNanoparticle-Based Drug DeliveryCardiac Fibrosis and Remodeling

Gold nanoparticle-based miR155 antagonist macrophage delivery restores the cardiac function in ovariectomized diabetic mouse model

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Jia, Chengming, Chen, Hui, Wei, Mengying, Chen, Xiangjie, Zhang, Yajun, Cao, Liang, Yuan, Ping, Wang, Fangyuan +2 more·2017·International Journal of Nanomedicine

Abstract

Diabetic cardiomyopathy is a common disease in postmenopausal women, in whom the estrogen deficiency aggravates the pathology. In this study, we have found that estrogen deficiency due to ovariectomy aggravates the inflammation in the hearts of diabetic mice, as depicted by excessive proinflammatory type 1 macrophages (M1) over anti-inflammatory type 2 macrophages (M2). Accordingly, an additional increase of reactive oxygen species, cell apoptosis, cardiac hypertrophy, and fibrosis was observed in the hearts of ovariectomized diabetic mice, in comparison with the diabetes-only group. Significantly, miR155, a potent promoter of M1 polarization, was found to be additionally enhanced in the macrophages and hearts by ovariectomy. Tail vein injection of miR155-AuNP, in which thiol-modified antago-miR155 was covalently conjugated with gold nanoparticle (AuNP), preferentially delivered the nucleic acids into the macrophages via phagocytosis. Together with the increased M2 ratio and reduced inflammation, in vivo delivery of antago-miR155 reduced cell apoptosis and restored the cardiac function. The restoration efficacy of miR155-AuNP was much better than general macrophage depletion by clodrosome. In summary, we revealed that M1/M2 imbalance contributes to the aggravated cardiomyopathy in ovariectomized diabetic mice, and therapeutically reducing miR155 in macrophages by AuNP serves as a promising strategy in improving cardiac function.

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  • Overexpression of miR-155 enhances ROS production and miR-155 is a potent promoter of M1 polarization.

    “ROS production was also enhanced via overexpression by miR-155 [156], which was identified as a potent promoter of M1 polarization.”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [156]

    The Results section (page unavailable) calls miR155 a potent M1 promoter and reports that miR155 transfection increased IL-1β while reducing IL-10 in macrophages. The cited paper does not report that miR-155 overexpression enhances ROS production; searches for ROS and reactive oxygen species found no supporting passage. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Jia, C., Chen, H., Wei, M., Chen, X., Zhang, Y., Cao, L., Yuan, P., Wang, F., Yang, G., & Ma, J.
Affiliations
  • Xijing Hospital (CN)
  • Tang Du Hospital (CN)
  • Air Force Medical University (CN)
  • Southeast University (CN)
Corresponding author
  • Yang, Guodong
  • Ma, Jing
Venue
International Journal of Nanomedicine
Published
2017-07
Volume
Volume 12
Pages
4963-4979
ISSN
  • 1176-9114 (ISSN-L)
  • 1178-2013
OpenAlex
W2735256643
Cited by
106
References
1
Citations by year
2026: 10 · 2025: 13 · 2024: 15 · 2023: 11 · 2022: 19 · 2021: 15 · 2020: 7 · 2019: 9 · 2018: 6
FWCI
2.46
Type
journal article
Language
en
Open access
Locations
  • International Journal of Nanomedicine (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
  • Physical Sciences › Materials Science › Biomaterials › Nanoparticle-Based Drug Delivery
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
diabetic cardiomyopathy, miR-155, gold nanoparticles, macrophage polarization, estrogen deficiency, ovariectomy, cardiac inflammation, myocardial fibrosis, cardiac hypertrophy, apoptosis, reactive oxygen species, postmenopausal women, nanoparticle drug delivery
MeSH terms
Animals, Diabetes Mellitus, Experimental, Female, Fibrosis, Gold, Macrophages, Mice, Inbred C57BL, Myocarditis, Myocardium, Ovariectomy, Drug Delivery Systems, Apoptosis, MicroRNAs, Nanoparticles, Diabetic Cardiomyopathies

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