Refine
Has Fulltext
- yes (59) (remove)
Is part of the Bibliography
- yes (59)
Year of publication
Document Type
- Journal article (58)
- Conference Proceeding (1)
Language
- English (59)
Keywords
- blood vessel (3)
- cancer (3)
- inflammation (3)
- organoid (3)
- 18F-FDG (2)
- Myokarditis (2)
- PET (2)
- TGFβ signaling (2)
- angiogenesis (2)
- diabetic retinopathy (2)
Institute
- Institut für Anatomie und Zellbiologie (59)
- Institut für diagnostische und interventionelle Radiologie (Institut für Röntgendiagnostik) (11)
- Klinik und Poliklinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie (Chirurgische Klinik I) (5)
- Klinik und Poliklinik für Unfall-, Hand-, Plastische und Wiederherstellungschirurgie (Chirurgische Klinik II) (4)
- Medizinische Klinik und Poliklinik I (4)
- Deutsches Zentrum für Herzinsuffizienz (DZHI) (3)
- Institut für Pharmakologie und Toxikologie (3)
- Klinik und Poliklinik für Nuklearmedizin (3)
- Abteilung für Funktionswerkstoffe der Medizin und der Zahnheilkunde (2)
- Graduate School of Life Sciences (2)
Sonstige beteiligte Institutionen
EU-Project number / Contract (GA) number
- 701983 (2)
SARS-CoV-2 infection can cause fatal inflammatory lung pathology, including thrombosis and increased pulmonary vascular permeability leading to edema and hemorrhage. In addition to the lung, cytokine storm-induced inflammatory cascade also affects other organs. SARS-CoV-2 infection-related vascular inflammation is characterized by endotheliopathy in the lung and other organs. Whether SARS-CoV-2 causes endotheliopathy by directly infecting endothelial cells is not known and is the focus of the present study. We observed 1) the co-localization of SARS-CoV-2 with the endothelial cell marker CD31 in the lungs of SARS-CoV-2-infected mice expressing hACE2 in the lung by intranasal delivery of adenovirus 5-hACE2 (Ad5-hACE2 mice) and non-human primates at both the protein and RNA levels, and 2) SARS-CoV-2 proteins in endothelial cells by immunogold labeling and electron microscopic analysis. We also detected the co-localization of SARS-CoV-2 with CD31 in autopsied lung tissue obtained from patients who died from severe COVID-19. Comparative analysis of RNA sequencing data of the lungs of infected Ad5-hACE2 and Ad5-empty (control) mice revealed upregulated KRAS signaling pathway, a well-known pathway for cellular activation and dysfunction. Further, we showed that SARS-CoV-2 directly infects mature mouse aortic endothelial cells (AoECs) that were activated by performing an aortic sprouting assay prior to exposure to SARS-CoV-2. This was demonstrated by co-localization of SARS-CoV-2 and CD34 by immunostaining and detection of viral particles in electron microscopic studies. Moreover, the activated AoECs became positive for ACE-2 but not quiescent AoECs. Together, our results indicate that in addition to pneumocytes, SARS-CoV-2 also directly infects mature vascular endothelial cells in vivo and ex vivo, which may contribute to cardiovascular complications in SARS-CoV-2 infection, including multipleorgan failure.