The Effect of a Unique Region of Parvovirus B19 Capsid Protein VP1 on Endothelial Cells
Autor: | Rinkūnaitė, Ieva, Šimoliūnas, Egidijus, Bironaitė, Daiva, Rutkienė, Rasa, Bukelskienė, Virginija, Meškys, Rolandas, Bogomolovas, Julijus |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
endothelial stress Cell Survival MAP Kinase Signaling System media_common.quotation_subject viruses Pulmonary Artery Biochemistry Microbiology Article Umbilical vein 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Human Umbilical Vein Endothelial Cells Parvovirus B19 Human parvovirus B19 endothelial cells VP1u Animals Humans Cytotoxic T cell Rats Wistar Internalization Molecular Biology Cells Cultured Tropism Erythroid Precursor Cells media_common biology Parvovirus biology.organism_classification Recombinant Proteins QR1-502 Rats 3. Good health Cell biology 030104 developmental biology 030220 oncology & carcinogenesis Tissue tropism Viral Fusion Proteins |
Zdroj: | Biomolecules, Vol 11, Iss 606, p 606 (2021) Biomolecules Volume 11 Issue 4 Biomolecules, Basel : MDPI, 2021, vol. 11, iss. 4, art. no. 606, p. [1-14] |
ISSN: | 2218-273X |
Popis: | Parvovirus B19 (B19V) is a widespread human pathogen possessing a high tropism for erythroid precursor cells. However, the persistence or active replication of B19V in endothelial cells (EC) has been detected in diverse human pathologies. The VP1 unique region (VP1u) of the viral capsid has been reported to act as a major determinant of viral tropism for erythroid precursor cells. Nevertheless, the interaction of VP1u with EC has not been studied. We demonstrate that recombinant VP1u is efficiently internalized by rats’ pulmonary trunk blood vessel-derived EC in vitro compared to the human umbilical vein EC line. The exposure to VP1u was not acutely cytotoxic to either human- or rat-derived ECs, but led to the upregulation of cellular stress signaling-related pathways. Our data suggest that high levels of circulating B19V during acute infection can cause endothelial damage, even without active replication or direct internalization into the cells. |
Databáze: | OpenAIRE |
Externí odkaz: |