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. 2021 Feb;18(2):492-494.
doi: 10.1038/s41423-020-0371-5. Epub 2020 Feb 13.

Transplantation of murine neonatal cardiac macrophage improves adult cardiac repair

Affiliations

Transplantation of murine neonatal cardiac macrophage improves adult cardiac repair

Yandong Li et al. Cell Mol Immunol. 2021 Feb.
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Implication of neonatal cardiac macrophage ameliorates cardiac repair in myocardial infarction injured adult mice. a Experimental strategy for deleting macrophages using DT in CD11bDTR mice, followed by apical resection at day 1. DT is administrated from day 0 to 2 for consecutive three days. Mice are sacrificed at 21 days after the operation. b IF shows that macrophages infiltration after heart injury is suspended after DT administration in CD11bDTR mice. c Representative images for Masson’s trichrome staining show that heart cannot regenerate but with fibrosis formation in the macrophage-deleted group and DT administration leads to lower quantities of regenerative mice (n=16 for each group). d Representative images of echocardiography in macrophage-deleted mice after apical resection operation. Statistical analysis shows the lower EF% and FS% in macrophage-deleted mice. Data are mean ± SEM. ****P<0.0001. e IF shows that macrophages deletion suspends cardiomyocytes proliferation identified by decreased pH3 positive α-actinin. f Scheme of deletion of macrophages in adult mice, transplantation of neonatal cardiac macrophages into adult injured heart as a treatment therapy. Strategy of injecting GFP positive macrophages isolated from Cx3cr1GFP/+mice to CD11bDTR adult mice following myocardial infarction operation. g Kaplan-Meier survival curve in adult mice following myocardial injection induction shows that macrophages transplantation has the highest survival rate. Data are mean ± SEM. *P<0.05, **P<0.01. h Representative images for Masson’s trichrome staining shows macrophages injection has the smallest infarcted area in adult CD11bDTR mice (PBS+DMEM, n=12; DT+DMEM, n=14; DT+Macrophage n=14). i Neonatal cardiac macrophages (GFP positive) can be detected in adult mouse heart after injection. j Representative images of echocardiography in macrophage-injected mice after myocardial infarction operation. Statistical analysis shows the highest EF% and FS% in macrophage-injected adult mice. Data are mean±SEM. *P<0.05. k If shows that macrophages transplantation can induced adult cardiomyocytes proliferation (n=6 for each group). Data are mean±SEM. *P<0.05, **P<0.01

References

    1. Yue Z, et al. PDGFR-beta signaling regulates cardiomyocyte proliferation and myocardial regeneration. Cell Rep. 2019;28:966–978.e964. doi: 10.1016/j.celrep.2019.06.065. - DOI - PubMed
    1. Wang J, et al. A long noncoding RNA NR_045363 controls cardiomyocyte proliferation and cardiac repair. J. Mol. Cell. Cardiol. 2019;127:105–114. doi: 10.1016/j.yjmcc.2018.12.005. - DOI - PubMed
    1. He L, et al. Reassessment of c-Kit(+) cells for cardiomyocyte contribution in adult heart. Circulation. 2019;140:164–166. doi: 10.1161/CIRCULATIONAHA.119.039909. - DOI - PubMed
    1. Han C, et al. Acute inflammation stimulates a regenerative response in the neonatal mouse heart. Cell Res. 2015;25:1137–1151. doi: 10.1038/cr.2015.110. - DOI - PMC - PubMed
    1. Chen S, Yang J, Wei Y, Wei X. Epigenetic regulation of macrophages: from homeostasis maintenance to host defense. Cell. Mol. Immunol. 2020;17:36–49. doi: 10.1038/s41423-019-0315-0. - DOI - PMC - PubMed

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