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Open AccessArticle

Angiotensin II Infusion Leads to Aortic Dissection in LRP8 Deficient Mice

1
Center for Thrombosis and Hemostasis, University Medical Center Mainz, 55131 Mainz, Germany
2
INSERM U1116, DCAC (Acute and Chronic Cardiovascular Deficiency), Université de Lorraine, 54500 Nancy, France
3
Center for Cardiology–Cardiology I, University Medical Center Mainz, 55131 Mainz, Germany
4
The Heart Research Institute, 7 Eliza Street, 2042 Newtown, Australia
5
DZHK (German Center for Cardiovascular Research), Partner Site Rhine Main, University Medical Center Mainz, 55131 Mainz, Germany
6
Department of Immunology and Microbial Science, Scripps Research, La Jolla, CA 92037, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(14), 4916; https://doi.org/10.3390/ijms21144916
Received: 27 May 2020 / Revised: 8 July 2020 / Accepted: 9 July 2020 / Published: 12 July 2020
(This article belongs to the Special Issue Molecular Research on Arteriosclerosis and Thrombosis)
Myeloid cells are crucial for the development of vascular inflammation. Low-density lipoprotein receptor-related protein 8 (LRP8) or Apolipoprotein E receptor 2 (ApoER2), is expressed by macrophages, endothelial cells and platelets and has been implicated in the development of cardiovascular diseases. Our aim was to evaluate the role of LRP8, in particular from immune cells, in the development of vascular inflammation. Methods. LRP8+/+ and LRP8−/− mice (on B6;129S background) were infused with angiotensin II (AngII, 1 mg/kg/day for 7 to 28 day) using osmotic minipumps. Blood pressure was recorded using tail cuff measurements. Vascular reactivity was assessed in isolated aortic segments. Leukocyte activation and infiltration were assessed by flow cytometry of aortic tissue and intravital videomicroscopy imaging. Histological analysis of aortic sections was conducted using sirius red staining. Results. AngII infusion worsened endothelial-dependent vascular relaxation and immune cells rolling and adherence to the carotid artery in both LRP8+/+ as well as LRP8−/− mice. However, only LRP8−/− mice demonstrated a drastically increased mortality rate in response to AngII due to aortic dissection. Bone marrow transplantation revealed that chimeras with LRP8 deficient myeloid cells phenocopied LRP8−/− mice. Conclusion. AngII-infused LRP8 deficient mice could be a useful animal model to study aortic dissection reflecting the lethality of this disease in humans. View Full-Text
Keywords: low-density lipoprotein receptor-related protein 8; angiotensin II; aortic dissection low-density lipoprotein receptor-related protein 8; angiotensin II; aortic dissection
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MDPI and ACS Style

Lagrange, J.; Finger, S.; Kossmann, S.; Garlapati, V.; Ruf, W.; Wenzel, P. Angiotensin II Infusion Leads to Aortic Dissection in LRP8 Deficient Mice. Int. J. Mol. Sci. 2020, 21, 4916. https://doi.org/10.3390/ijms21144916

AMA Style

Lagrange J, Finger S, Kossmann S, Garlapati V, Ruf W, Wenzel P. Angiotensin II Infusion Leads to Aortic Dissection in LRP8 Deficient Mice. International Journal of Molecular Sciences. 2020; 21(14):4916. https://doi.org/10.3390/ijms21144916

Chicago/Turabian Style

Lagrange, Jeremy; Finger, Stefanie; Kossmann, Sabine; Garlapati, Venkata; Ruf, Wolfram; Wenzel, Philip. 2020. "Angiotensin II Infusion Leads to Aortic Dissection in LRP8 Deficient Mice" Int. J. Mol. Sci. 21, no. 14: 4916. https://doi.org/10.3390/ijms21144916

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