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MicroRNA expression profiling of urine exosomes in children with congenital cytomegalovirus infection

ABSTRACT: MicroRNA expression profiling of urine exosomes in children with congenital cytomegalovirus infection

PROVIDER: PRJNA1062752 | ENA |

REPOSITORIES: ENA

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MicroRNA expression profiling of urine exosomes in children with congenital cytomegalovirus infection

Project description:To investigate the extent of neuronal damage in patients with cCMV, exosomal miRNA expression in the urine obtained in early infancy was investigated in cCMV-infected infants and controls.

2024-01-15 | GSE252811 | GEO

MicroRNA expression profiling of urine exosomes in children with congenital cytomegalovirus infection.

Project description:Congenital cytomegalovirus (cCMV) infection can damage the central nervous system in infants; however, its prognosis cannot be predicted from clinical evaluations at the time of birth. Urinary exosomes can be used to analyze neuronal damage in neuronal diseases. To investigate the extent of neuronal damage in patients with cCMV, exosomal miRNA expression in the urine was investigated in cCMV-infected infants and controls. Microarray analysis of miRNA was performed in a cohort of 30 infants, including 11 symptomatic cCMV (ScCMV), 7 asymptomatic cCMV (AScCMV), and one late-onset ScCMV cases, and 11 healthy controls (HC). Hierarchical clustering analysis revealed the distinct expression profile of ScCMV. The patient with late-onset ScCMV was grouped into the ScCMV cluster. Pathway enrichment analysis of the target mRNAs differed significantly between the ScCMV and HC groups; this analysis also revealed that pathways related to brain development were linked to upregulated pathways. Six miRNAs that significantly different between groups (ScCMV vs. HC and ScCMV vs. AScCMV) were selected for digital PCR in another cohort for further validation. Although these six miRNAs seemed insufficient for predicting ScCMV, expression profiles of urine exosomal miRNAs can reveal neurological damage in patients with ScCMV compared to those with AcCMV or healthy infants.

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Array-CGH in Chinese children with congenital heart disease

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Conditioning of porcine kidneys during dynamic preservation with exosomes derived from Urine Progenitor Cells

Project description:Backgroud: among strategies to limit ischemia/reperfusion (IR) injuries in transplantation, cell therapy using stem cells to condition/repair transplanted organ appears promising. We hypothesized that using a cell therapy based on exosomes derived from Urine Progenitor Cells (UPCs) during hypothermic and normothermic machine perfusion can prevent IR-related kidney damages. Methods: we isolated and characterized porcine UPCs and their exosomes (Exo). Then these were used in an ex vivo preclinical porcine kidney preservation model. Kidneys were subjected to warm ischemia (32min) then preserved by Hypothermic Machine Perfusion (HMP) for 24h before 5h of Normothermic Machine Perfusion (NMP). Three groups were performed (n=5-6): Group 1 (G1): HMP/vehicle + NMP/vehicle, Group 2 (G2): HMP/Exo + NMP/vehicle, Group 3 (G3): HMP/Exo + NMP/Exo. Results: porcine UPCs were successfully isolated from urine and fully characterized as well as their exosomes which were found of expected size/phenotype. RNA-seq performed on kidney biopsies showed different profiles between G1 and G3 with regulation of potential IR targets of Exo therapy. Conclusions: we showed the feasibility/efficacy of UPC-exosomes for hypothermic/normothermic kidney conditioning prior to transplantation, paving the way of combining machine perfusion with exosome-based cell therapy for organ conditioning.

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Human Otic progenitor cell models of congenital hearing loss applied to to Zika virus and cytomegalovirus infections

Project description:Congenital hearing loss is a common chronic condition affecting children in both developed and developing nations. In many cases, congenital hearing loss is ultimately attributed to viral infection, most often by cytomegalovirus (CMV), but also in Congenital Zika Syndrome (CZS). The mechanisms by which CMV and ZIKV virus cause these cranial developmental defects have not been elucidated. Inner ear development has been particularly difficult to study, given the inaccessibility and scarcity of the tissue in animal models or on human autopsy; however, it is now possible to culture stem-cell derived otic progenitor cells (OPCs). Here we describe successful in-vitro infection of OPCs with either CMV or ZIKV. We find that ZIKV infection rapidly and strongly induces the expression of type I IFN and inflammatory genes, while simultaneously decreasing otic cell viability in culture that is at least in part attributable to apoptosis. In contrast, CMV infection did not appear to elicit either of these effects and instead demonstrated a clear dysregulation of the expression of many key genes and pathways associated with inner ear development and function, including Cochlin, NGFR, SOX11 and TGF-β signaling. These findings suggest that ZIKV and CMV infections cause congenital hearing loss through very different pathways; that is, by killing progenitor cells in the case of ZIKV infection, and via disruption of critical developmental pathways in the case of CMV infection. In addition to demonstrating differential hCMV and ZIKV pathogenesis mechanisms in OPCs, this study highlights the advantages of otic progenitor cell models for the study of congenital hearing loss induced by viral infection.

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Transcriptomics integrated with metabolomics reveals partial molecular mechanisms of nutritional risk and neurodevelopment in children with congenital heart disease

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