Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA386505 | ENA |
REPOSITORIES: ENA
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Project description:POWV isolate from Long Island (POWV-LI-9) is released basolaterally from humban brain microvascular endothelial cells (hBMECs) and infects primary human brain vascular pericutes (hBVPs).
2021-06-08 | GSE176252 | GEO
Project description:POWV isolate from Long Island (POWV-LI-9) is released basolaterally from humban brain microvascular endothelial cells (hBMECs) and infects primary human brain vascular pericutes (hBVPs).
2021-06-08 | GSE176251 | GEO
Project description:The re-emergence of Zika virus (ZIKV) in the Western Hemisphere has resulted in global public health crisis since 2015. ZIKV preferentially infects and targets human neural progenitor cells (hNPCs) and causes fetal microcephaly upon maternal infection. hNPCs not only play critical roles during fetal brain development, but also persist in adult brain throughout life. Yet the mechanism of innate antiviral immunity in hNPCs remains largely unknown. Here, we show that ZIKV infection triggers the abundant production of virus-derived small interfering RNAs in hNPCs, but not in the more differentiated progenies or somatic cells. Ablation of key RNAi machinery components significantly enhances ZIKV replication in hNPCs. Furthermore, enoxacin, a broad-spectrum antibiotic that is known as an RNAi enhancer, exerts potent anti-ZIKV activity in hNPCs and other RNAi-competent cells. Strikingly, enoxacin treatment completely prevents ZIKV infection and circumvents ZIKV-induced microcephalic phenotypes in brain organoid models that recapitulate human fetal brain development. Our findings highlight the physiological importance of RNAi-mediated antiviral immunity during the early stage of human brain development, uncovering a novel strategy to combat human congenital viral infections through enhancing RNAi.
2019-04-15 | GSE125520 | GEO
Project description:Brain microvessels (BMVs) were isolated from frozen human and mouse cerebral cortices, as well as frozen mouse cerebrums. BMVs and cultured brain microvascular endothelial cells (BMECs), such as hCMEC/D3, HBMEC/ci, and primary BMECs, were analyzed via data-independent acquisition using liquid chromatography-mass spectrometry.
2025-07-23 | PXD060008 | JPOST Repository
Project description:The suspected link between infection by Zika virus (ZIKV), a re-emerging flavivirus, and microcephaly, is an urgent global health concern. The direct target cells of ZIKV in developing human fetuses are not clear. Here we show that ZIKV serially passaged in monkey and mosquito cell lines infects human induced pluripotent stem cells (hiPSCs)-derived cortical neural progenitor cells (hNPCs) with much higher efficiency compared to hiPSCs and hNPC-derived immature cortical neurons. Infected hNPCs produces infectious ZIKV particles. Importantly, ZIKV infection increases cell death and dysregulates cell cycle progression, resulted in attenuated hNPC growth. RNA-sequencing analysis of infected hNPCs further reveals transcriptional dysregulation, notably genes in cell cycle pathways. Our results identify human cortical neural precursors as a major and direct target of ZIKV infection and establish a tractable experimental model system to investigate the impact and mechanism of ZIKV on human brain development and a platform to screen therapeutic compounds.
2016-03-04 | GSE78711 | GEO
Project description:Zika virus (ZIKV) infects fetal and adult human brains, and is associated with serious neurological complications including microcephaly and Guillain-Barré Syndrome (GBS). To date, no prophylactic or therapeutic treatment is available to prevent or treat ZIKV infection. Here, we performed a high content chemical screen using a library containing FDA-approved drugs or drug candidates. Two compounds, hippeastrine hydrobromide (HH) and amodiaquine dihydrochloride dihydrate (AQ), were discovered to inhibit ZIKV infection in human cortical neuron progenitor cells (hNPCs). HH was further validated to inhibit ZIKV infection and to rescue ZIKV-induced growth and differentiation defects in hNPCs and human fetal-like forebrain organoids. Finally, HH and AQ suppressed ZIKV infection in adult mouse brain in vivo. Strikingly, HH and AQ fully rescued the severe limb paralysis syndrome developed in ZIKV infected adult mice. This study identifies drug candidates for treatment of ZIKV infection and ZIKV-related neurological complications in fetal and adult patients.
2017-07-06 | GSE89334 | GEO
Project description:Zika virus (ZIKV), a flavivirus transmitted primarily by Aedes mosquitoes, has spread to 59 countries and territories throughout the world. ZIKV-infected patients can have several symptoms and there is scientific consensus that ZIKV is a cause of microcephaly. Most studies are focusing on the central nervous system (CNS), and it is largely unknown whether ZIKV also affects the developing peripheral nervous system. Here, using a human pluripotent stem cell-based model, we demonstrated that Puerto Rican ZIKV strain, PRVABC59, efficiently infects human neural crest cells (hNCCs). In contrast to little infection of CNS neurons, ZIKV readily infects human peripheral neurons (hPNs), leading to cell death. Global gene expression analyses of infected hNCCs and hPNs reveal transcriptional dysregulation, notably of cell-death- and cell-cycle-related pathways. Our results identify hNCCs and hPNs as a direct ZIKV target and provide a framework to investigate the ZIKV pathology on the peripheral neurons.
2017-07-07 | GSE87750 | GEO
Project description:We compare the proteome of the brain endothelial cells obtained with the newly optimized protocol (iCE-BECs) to the primary human brain microvascular endothelial cells (HBMVECs) and the widely used immortalized brain endothelial cell line HCMECD3. The goal is to investigate the applicability of iCE-BECs for transport assays, measuring the expression of transporters and receptors with whole cell proteomics.
2025-08-08 | PXD062808 | Pride
Project description:primary human brain microvascular endothelial cells long non-coding RNAs transcriptome
| PRJNA347541 | ENA