Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA663975 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:SARS-CoV-2 is considered to affect the central nervous system (CNS) by interacting with the blood–brain barrier (BBB), which is defined by tight junctions that seal paracellular gaps between brain microvascular endothelial like cells (BMECs). Although SARS-CoV-2 infection of BMECs has been reported, the mechanism has not been fully elucidated. Here, we investigated the mechanism using iPSC derived brain microvascular endothelial like cells (iPSC-BMELCs). We observed that iPSC-BMELCs were infected with SARS-CoV-2, which resulted in inflammatory responses. RNA-seq analysis revealed that SARS-CoV-2 modulated the expression of signal molecules in iPSC-BMELCs. These findings suggest that SARS-CoV-2 infection causes BBB dysfunction in humans.
2024-02-01 | GSE254309 | GEO
Project description:The purpose is to obtain samples for microRNA analysis in primary human microvascular endothelial cells infected with wild type Mers-CoV (icMERS). Human microvascular endothelial cells were infected with a multiplicity of infection of 5 PFU per cell. Infected samples were collected in quintuplet; time-matched mocks were collected in quintuplet in parallel with infected samples. Time points: 12 and 24 h post-infection. MERSCOV002.0P references the write up of the experimental procedure.
2016-04-06 | E-GEOD-79216 | biostudies-arrayexpress
Project description:The purpose is to obtain samples for mRNA analysis in primary human microvascular endothelial cells infected with wild type Mers-CoV (icMERS). Human microvascular endothelial cells were infected with a multiplicity of infection of 5 PFU per cell. Infected samples were collected in quintuplet; time-matched mocks were collected in quintuplet in parallel with infected samples. Time points: 0, 12, 24, 36, and 48 h post-infection. MERSCOV002.0P references the write up of the experimental procedure.
2016-03-25 | E-GEOD-79218 | biostudies-arrayexpress
Project description:SARS-CoV-2 seriously injures human alveoli and causes severe respiratory illness. Histopathologic evidences suggested alveolar-capillary barrier integrity is compromised in COVID-19 deaths, however, little is known about how it is disrupted. In this study, we investigated the effects of SARS-CoV-2 infection on alveolar epithelium and pulmonary microvascular endothelium, and tried to elucidate the cross-talk between them during viral infection. Under monoculture system, SARS-CoV-2 infection caused massive virus replication and dramatic organelles re-modeling in alveolar epithelial cells. While, as for pulmonary microvascular endothelial cells, direct viral exposure had little effect on them, but treatment with culture supernatant from infected epithelial cells significantly damaged them, which suggested SARS-CoV-2 affected endothelium indirectly, possibly by substances released from infected alveolar epithelium. Then, we tested SARS-CoV-2 infection in an alveolar epithelium/endothelium co-culture system, and found viral infection caused global proteomic modulations and ultrastructural changes in both cell types. Especially for alveolar epithelial cells, viral infection elicited significant protein changes and structural reorganizations across many sub-cellular compartments. Among the affected organelles, mitochondrion seems to be a primary target organelle. In addition, based on proteomic analysis and EM clues, we tested several autophagy inhibitors, and discovered one of them, Daurisoline, could inhibit virus replication effectively in cells. Collectively, our study revealed the distinctive responses of alveolar epithelium and microvascular endothelium to SARS-CoV-2 infection, which will expand our understanding of COVID-19 and helpful for targeted drug development.
2021-11-11 | PXD029653 | Pride
Project description:SARS-CoV-2 seriously injures human alveoli and causes severe respiratory illness. Histopathologic evidences suggested alveolar-capillary barrier integrity is compromised in COVID-19 deaths, however, little is known about how it is disrupted. In this study, we investigated the effects of SARS-CoV-2 infection on alveolar epithelium and pulmonary microvascular endothelium, and tried to elucidate the cross-talk between them during viral infection. Under monoculture system, SARS-CoV-2 infection caused massive virus replication and dramatic organelles re-modeling in alveolar epithelial cells. While, as for pulmonary microvascular endothelial cells, direct viral exposure had little effect on them, but treatment with culture supernatant from infected epithelial cellls significantly damaged them, which suggested SARS-CoV-2 affected endothelium indirectly, possibly by substances released from infected alveolar epithelium. Then, we tested SARS-CoV-2 infection in an alveolar epithelium/endothelium co-culture system, and found viral infection caused global proteomic modulations and ultrastructual changes in both cell types. Especially for alveolar epithelial cells, viral infection elicited significant protein changes and structural reorganizations across many sub-cellular compartments. Among the affected organelles, mitochondrion seems to be a primary target organelle. In addition, based on proteomic analysis and EM clues, we tested several autophagy inhibitors, and discovered one of them, Daurisoline, could inhibit virus replication effectively in cells. Collectively, our study revealed the distinctive responses of alveolar epithelium and microvascular endothelium to SARS-CoV-2 infection, which will expand our understanding of COVID-19 and helpful for targeted drug development.
2020-12-04 | PXD020470 | Pride
Project description:The SARS-CoV-2 virus has already caused over a million COVID-19 cases and over fifty-thousand deaths globally. There is an urgent need to create novel models to study SARS-CoV-2 virus using human disease-relevant cells and tissues to understand key features of virus biology. We present a platform comprised of nine different cell and organoid derivatives from human pluripotent stem cells (hPSCs) representing all three primary germ layers, including lung progenitors and alveolar type II (AT2) cells, pancreatic endocrine cells, liver organoids, endothelial cells, cardiomyocytes, macrophages, microglia, and both cortical and dopaminergic neurons. We systematically probed which cell types are permissive to SARS-CoV-2 infection. Human pancreatic beta cells and hepatocytes were strikingly permissive to SARS-CoV-2 infection, further validated using adult primary human islets and liver organoids. Both in vitro and in a humanized mouse model, human lung progenitors and AT2 cells express the ACE2 viral receptor and were highly permissive to SARS-CoV-2 infection. Transcriptomic analysis following SARS-CoV-2 infection of hPSC-derived pancreatic and lung organoids revealed upregulation of chemokines but not type I/III interferon signaling, similar to what was seen in primary human COVID-19 pulmonary infection. Therefore, hPSC-derived cells phenocopy human COVID-19 disease and provide a valuable resource to understand SARS-CoV-2 biology and search for novel therapeutics.
2020-06-11 | GSE147903 | GEO
Project description:We report the transcriptional changes of an hipsc-derived model of the blood-brain barrier to infection with SARS-CoV-2. Furthermore, the neurovascular niche was isolated from human brain biopsies to compare the transcriptional signatures of hipsc-derived endothelial cells and human neurovascular niche.
2021-07-14 | GSE179923 | GEO
Project description:We also used Affymetrix array technology to investigate the global alteration in the gene expression of human brain microvascular endothelial cells (hBMECs) and rat brain microvascular endothelial cells (rBMVECs) in response to N. caninum infection at 24 hours post infection.
2020-08-10 | E-MTAB-9411 | biostudies-arrayexpress
Project description:Neurological complications are common in patients with COVID-19. While SARS-CoV-2, the causal pathogen of COVID-19, has been detected in some patient brains, its ability to infect brain cells and impact their function are not well understood, and experimental models using human brain cells are urgently needed. Here we investigated the susceptibility of human induced pluripotent stem cell (hiPSC)-derived monolayer brain cells and region-specific brain organoids to SARS-CoV-2 infection. We found modest numbers of infected neurons and astrocytes, but greater infection of choroid plexus epithelial cells. We optimized a protocol to generate choroid plexus organoids from hiPSCs, which revealed productive SARS-CoV-2 infection that leads to increased cell death and transcriptional dysregulation indicative of an inflammatory response and cellular function deficits. Together, our results provide evidence for SARS-CoV-2 neurotropism and support use of hiPSC-derived brain organoids as a platform to investigate the cellular susceptibility, disease mechanisms, and treatment strategies for SARS-CoV-2 infection.
2020-09-23 | GSE157852 | GEO
Project description:The purpose is to obtain samples for mRNA analysis in primary human microvascular endothelial cells infected with wild type MERS-CoV (icMERS).
2016-03-25 | GSE79218 | GEO