The increase of miR-378a-3p in keratinocyte associated with pathogenesis of psoriasis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA674820 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the high-throughput profiling of human primary keratinocytes transfected with either miR-378 mimic or miR-378 inhibitor at 24 or 48 hours. Our study focused on the dysregulation of microRNAs that might partially be a fundamental mechanism leading to psoriasis development. We knock-in and knock-out a specific miR-378 and see the cellular responses. As expected, overexpression of miR-378a inhibited the proliferation, enhanced the apoptosis and disturbed the cell cycle. Regarding to the confirm experiment, our results suggested that the expression of miR-378a associated with the psoriasis pathogenesis enhancing the severity of psoriatic lesion, and might useful for further development of therapeutic strategy for psoriasis.
2020-11-06 | GSE160906 | GEO
Project description:In 2019, our group performed small RNA-sequencing on keratinocytes isolated from lesional and non-lesional psoriasis skin as well as from healthy skin, and identified miRNAs with altered levels in psoriasis keratinocytes (Srivastava et al., 2019). One of the miRNAs we identified to be overexpressed in psoriasis keratinocytes was miR-378a-3p. In this study, we aimed to explore the regulation and function of miR-378a in keratinocytes and its potential role in psoriasis. We used microarrays to identify differentially expressed genes upon miR-378a overexpression in primary human keratinocytes as part of the study and gain insights about the modulation of specific pathways.
2021-03-08 | GSE164400 | GEO
Project description:Wild-type (WT) miR-378a-3p or edited miR-378a-3p were expressed in SB2 KD-ADAR1 cells to identify the genes regulated by edited miR-378a-3p vs WT miR-378a-3p. PARVA was one of the genes identified to be regulated by edited miR-378a-3p. We demonstrate that this regulation of PARVA is lost in highly metastatic melanoma cells. Microarray analysis was used to evaluate the robustness and reproducibility of the method used to generate the ex vivo tumor tissue model and confirm its ability to recapitulate the essential features of the original tumor.
2018-02-22 | GSE107088 | GEO
Project description:miR-378a regulates keratinocyte responsiveness to IL-17A in psoriasis
| PRJNA690544 | ENA
Project description:To gain further knowledge on the role of microRNAs (miRNAs) in the pathogenesis of Burkitt lymphoma (BL), we performed small RNA sequencing in BL cell lines and normal germinal center B (GC-B) cells. This revealed 26 miRNAs with significantly different expression levels. Altered levels were validated by qRT-PCR for six of eight selected miRNAs. For five miRNAs, the differential expression pattern was confirmed in BL primary tissues compared to GC-B cells. Inhibition of miR-378a-3p reduced the growth of multiple BL cell lines. RNA immunoprecipitation of Argonaute 2 followed by microarray analysis (Ago2-RIP-Chip) upon inhibition and ectopic overexpression of miR-378a-3p revealed 63 and 20 putative miR-378a-3p targets, respectively. These included 28 genes with a putative miR-378a-3p binding site. Effective targeting by miR-378a-3p was confirmed by luciferase reporter assays for four out of eight selected genes: MNT, FOXP1, IRAK4, and lncRNA JPX, all of which have been implicated in proliferation and cancer. In summary, our study identified several differentially expressed miRNAs in BL. We identified miR-378a-3p as a miRNA with an oncogenic role in BL and revealed 4 novel miR-378a-3p target genes, i.e. MNT, FOXP1, IRAK4, and JPX.
2020-06-30 | GSE141691 | GEO
Project description:Edited miR-378a-3p target genes
| PRJNA418978 | ENA
Project description:The current study is aimed on determine the functional impact of microRNA-378a-3p and microRNA-146b on embryo development. For such purpose, we supplemented miR-378/miR-146b mimics or inhibitors to the culture medium containing presumed zygotes at 1 dpi and cultured them until day 8, thus allowing miR-378/miR-146b mimics or inhibitors to influence further embryo development and quality. Further on, to gain more in-depth molecular insights, we performed transcriptome profiling of blastocysts cultured in the presence of miR-378/miR-146b mimics or inhibitors.
2022-03-10 | GSE197876 | GEO
Project description:MiR-378a-3p is critical for Burkitt lymphoma cell growth
| PRJNA594376 | ENA
Project description:Psoriasis is a chronic inflammatory skin disease that is mediated by a complex crosstalk between immune cells and keratinocytes (KCs). Emerging studies showed a specific psoriatic microRNAs signature where miR-21 is one of the most upregulated miRNAs. In this study, we focused our investigations on the passenger miR-21-3p strand that is poorly studied in skin and in psoriasis pathogenesis. Here, we transfected the HaCaT cells with synthetic oligoncucleotides form of miR-21-3p and evaluated the impact of the over-expression of this miRNA in these call by RNA-seq analysis. We identified a network of differentially expressed genes involved in abnormal proliferation control and immune regulatory genes implicated in the molecular pathogenesis of psoriasis in response to miR-21-3p overexpression in KCs. These results were confirmed by functional assays that validate the proliferative potential of miR-21-3p. All these findings highlight the importance of miR-21-3p, an underestimated miRNA, in psoriasis and provide novel molecular targets for therapeutic purposes.
2021-04-02 | GSE154968 | GEO
Project description:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demostrated that a dominante mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrehic dermatitis. We defined ZNF750 as a nuclear effector that is atrongly activated in and essiential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differnetiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier Gene expression analysis: To determine the differentaition signature for HaCaT keratinocytes, with ZNF750 gene silencing, total RNA was isolated in biologic triplicates from cells induced to differentiate for twelve days and hybridized to Affymerix Human Gene 1.0 ST arrays.
2012-09-24 | E-GEOD-38039 | biostudies-arrayexpress