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10.3389/fcimb.2021.701278 http://scihub22266oqcxt.onion/10.3389/fcimb.2021.701278 34307198!8292147!34307198     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Cell+Infect+Microbiol 2021 ; 11 (ä): 701278 Nephropedia Template TP {{tp|p=34307198|t=2021. SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro |pdf=|usr=}}{{34307198}} gab.com Text SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro JO: Front Cell Infect Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=34307198 #FOAvip 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. Twit Text FOAVip SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro ????Front Cell Infect Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=34307198 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34307198 #FOAvip English Wikipedia <ref>{{Cite pmid|34307198}}</ref> SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro #MMPMID34307198 Liu F; Han K; Blair R; Kenst K; Qin Z; Upcin B; Worsdorfer P; Midkiff CC; Mudd J; Belyaeva E; Milligan NS; Rorison TD; Wagner N; Bodem J; Dolken L; Aktas BH; Vander Heide RS; Yin XM; Kolls JK; Roy CJ; Rappaport J; Ergun S; Qin X Front Cell Infect Microbiol 2021[]; 11 (ä): 701278 PMID34307198show ga 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. |*COVID-19[MESH] |*SARS-CoV-2[MESH] |Animals[MESH] |Disease Models, Animal[MESH] |Endothelial Cells[MESH] |Humans[MESH] |Lung[MESH] |Mice[MESH]SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro (epmc).pdf DeepDyve Pubget Overpricing