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10.1093/cvr/cvab082 http://scihub22266oqcxt.onion/10.1093/cvr/cvab082 33705542!7989620!33705542     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33705542&cmd=llinks): Failed to open stream: HTTP request failed! 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Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression |pdf=|usr=}}{{33705542}} gab.com Text Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression JO: Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=33705542 #FOAvip AIMS: Patients with severe respiratory syndrome caused by SARS-CoV-2 undergo cardiac complications due to hyper-inflammatory conditions. Although the presence of the virus has been detected in the myocardium of infected patients, and infection of induced pluripotent cell-derived cardiomyocytes has been demonstrated, the reported expression of Angiotensin-Converting Enzyme-2 (ACE2) in cardiac stromal cells suggests that SARS-CoV-2 may determine cardiac injury by sustaining productive infection and increasing inflammation. METHODS AND RESULTS: We analysed expression of ACE2 receptor in primary human cardiac stromal cells derived from cardiospheres, using proteomics and transcriptomics before exposing them to SARS-CoV-2 in vitro. Using conventional and high sensitivity PCR methods, we measured virus release in the cellular supernatants and monitored the intracellular viral bioprocessing. We performed high-resolution imaging to show the sites of intracellular viral production and demonstrated the presence of viral particles in the cells with electron microscopy. We finally used RT-qPCR assays to detect genes linked to innate immunity and fibrotic pathways coherently regulated in cells after exposure to the virus. CONCLUSIONS: Our findings indicate that cardiac stromal cells are susceptible to SARS-CoV-2 infection and produce variable viral yields depending on the extent of cellular ACE2 receptor expression. Interestingly, these cells also evolved towards hyper-inflammatory/pro-fibrotic phenotypes independently of ACE2 levels. Thus, SARS-CoV-2 infection of myocardial stromal cells could be involved in cardiac injury and explain the high number of complications observed in severe cases of COVID-19. Twit Text FOAVip Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression ????Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=33705542 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33705542 #FOAvip English Wikipedia <ref>{{Cite pmid|33705542}}</ref> Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression #MMPMID33705542 Amendola A; Garoffolo G; Songia P; Nardacci R; Ferrari S; Bernava G; Canzano P; Myasoedova V; Colavita F; Castilletti C; Sberna G; Capobianchi MR; Piacentini M; Agrifoglio M; Colombo GI; Poggio P; Pesce M Cardiovasc Res 2021[May]; 117 (6): 1557-1566 PMID33705542show ga AIMS: Patients with severe respiratory syndrome caused by SARS-CoV-2 undergo cardiac complications due to hyper-inflammatory conditions. Although the presence of the virus has been detected in the myocardium of infected patients, and infection of induced pluripotent cell-derived cardiomyocytes has been demonstrated, the reported expression of Angiotensin-Converting Enzyme-2 (ACE2) in cardiac stromal cells suggests that SARS-CoV-2 may determine cardiac injury by sustaining productive infection and increasing inflammation. METHODS AND RESULTS: We analysed expression of ACE2 receptor in primary human cardiac stromal cells derived from cardiospheres, using proteomics and transcriptomics before exposing them to SARS-CoV-2 in vitro. Using conventional and high sensitivity PCR methods, we measured virus release in the cellular supernatants and monitored the intracellular viral bioprocessing. We performed high-resolution imaging to show the sites of intracellular viral production and demonstrated the presence of viral particles in the cells with electron microscopy. We finally used RT-qPCR assays to detect genes linked to innate immunity and fibrotic pathways coherently regulated in cells after exposure to the virus. CONCLUSIONS: Our findings indicate that cardiac stromal cells are susceptible to SARS-CoV-2 infection and produce variable viral yields depending on the extent of cellular ACE2 receptor expression. Interestingly, these cells also evolved towards hyper-inflammatory/pro-fibrotic phenotypes independently of ACE2 levels. Thus, SARS-CoV-2 infection of myocardial stromal cells could be involved in cardiac injury and explain the high number of complications observed in severe cases of COVID-19. |Aged[MESH] |Aged, 80 and over[MESH] |Angiotensin-Converting Enzyme 2/genetics/*metabolism[MESH] |Animals[MESH] |COVID-19/complications/*virology[MESH] |Chlorocebus aethiops[MESH] |Female[MESH] |Fibrosis[MESH] |Heart Diseases/enzymology/pathology/*virology[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Inflammation Mediators/metabolism[MESH] |Male[MESH] |Middle Aged[MESH] |Myocardium/*enzymology/ultrastructure[MESH] |Phenotype[MESH] |Receptors, Virus/genetics/*metabolism[MESH] |SARS-CoV-2/*pathogenicity/ultrastructure[MESH] |Spheroids, Cellular[MESH] |Stromal Cells/enzymology/ultrastructure/*virology[MESH] |Vero Cells[MESH]Human cardiosphere-derived stromal cells exposed to SARS-CoV-2 evolve (epmc).pdf DeepDyve Pubget Overpricing