Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profiling and function analysis identified new microRNAs regulating cumulus expansion and apoptosis in cumulus cells

ABSTRACT: RNA- and miRNA-sequencing and bioinformatics using CCs from these cultured COCs/OOXs identified candidate apoptosis- and/or CE-regulating miRNAs. Transfection of COCs/OOXs with miRNA mimic or inhibitor validated that miR-212-5p and 149-5p promoted CE by facilitating Has2 expression; miR-31-5p and 27a-3p promoted CE by increasing both Has2 and Ptx3 expression; and miR-351-5p and 503-5p inhibited CE by suppressing Ptx3 expression. Furthermore, miR-212-5p, 149-5p and Nov798 inhibited CC apoptosis, involving both Bcl2/Bax and Fas signaling. Analysis using in vivo matured COCs further verified the above apoptosis- and/or CE-regulating miRNAs except for miR-149-5p. In conclusion, this study identified and validated new CE- and apoptosis-regulating miRNAs in CCs, which can be used as biomarkers to select competent oocytes/embryos and for elucidating how the oocyte-derived factors regulate CE and CC apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE189959 | GEO | 2023/11/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Mechanism of circADD2 as ceRNA in Childhood Acute lymphoblastic leukemia

Project description:In the present study, we found that circADD2 was down-regulated in ALL tissues and cell lines. Overexpression of circADD2 inhibited cell proliferation and promoted apoptosis both in vitro and in vivo. Additionally, we found that miR-149-5p may increase the expression of the target gene AKT2 through the mechanism of RNAa, and the level of AKT2 can be reversed by circADD2. Briefly, circADD2 could directly sponge miR-149-5p to downregulate AKT2 expression.

2021-03-16 | GSE166579 | GEO

miRNA profiling of Macaca mulatta colonic epithelium samples from chronic SIV infected rhesus macaques

Project description:The study describes miRNA expression in colonic epithelium of chronic SIV-infected rhesus macaques. We profiled and characterized miRNA/mRNA expression exclusively in colonic epithelium (CE) of 12 chronically SIV-infected and 8 control rhesus macaques (RMs). About 46 miRNAs were differentially expressed (DE) (20-up and 26-down) in CE during chronic SIV infection. Using TargetScan, we bioinformatically crossed the predicted targets of DE miRNAs to genome-wide transcriptomic data and identified several critical miRNA-mRNA pairings that suggested miRNA-mediated regulation of aberrant epithelial gene expression in CE. Immunofluorescence, luciferase reporter and miRNA overexpression studies confirmed the ability of miR-130a and miR-212 to bind the 3’ UTR and downregulate protein expression of occludin (OCLN) and peroxisome proliferator activator receptor gamma (PPAR), respectively, two proteins with pivotal roles in epithelial barrier function. MiR-130a and miR-212 overexpression in Caco-2 cells significantly reduced transepithelial electrical resistance (TEER). Interestingly, delta-9-tetrahydrocannabinol (9-THC) treatment restored TEER to levels observed with control miRNA mimic. Finally, ex-vivo 9-THC treatment of colon tissue from chronically SIV-infected RMs significantly increased PPAR gene expression. Our findings suggest that dysregulated miR-130a and miR-212 expression in CE during chronic HIV/SIV infection can facilitate epithelial barrier disruption by downregulating OCLN and PPAR protein expression. Most importantly, our results highlight the beneficial effects of cannabinoids on epithelial barrier function in not just HIV/SIV but potentially other chronic intestinal inflammatory diseases.

2018-02-01 | GSE104767 | GEO

RNA Sequencing of three pairs of gastric cancer tissues

Project description:Circular (circ) RNAs have been widely reported to be involved in gastric cancer (GC) pathogenesis and coiled coil domain containing 6 (CCDC6) is recognized as fused partner of multiple oncogenes; however, the underlying mechanisms of how circRNAs regulate CCDC6 expression in the progression and prognosis of GC remain unclear. Here, we discovered a novel circRNA derived from the DNA2 gene locus (circDNA2) through joint analysis of circRNA microarrays. By performing qRT-PCR and FISH assays with a human tissue microarray, circDNA2 was identified to be highly expressed in GC tissues and associated with lymphatic invasion of GC patients. Knockdown of circDNA2 suppressed the proliferation of GC cells by reducing CCDC6 expression in vitro. Mechanically, circDNA2 acted as a sponge for microRNA (miR)-149-5p, which was validated to target CCDC6 by dual luciferase reporter assays and rescue experiments. Both miR-149-5p low expression and CCDC6 high expression were related to unfavorable prognosis of GC patients. Moreover, GC patients with low miR-149-5p expression had shorter overall survival and higher risk of chemotherapy resistance compared with these with high miR-149-5p expression. In summary, our findings reveal that circDNA2 contributes to the growth and lymphatic metastasis of GC through upregulating CCDC6 expression via sponging miR-149-5p. The circDNA2/miR-149-5p/CCDC6 axis might be developed as a therapeutic target and prognostic indicator for GC patients.

2024-02-25 | GSE167512 | GEO

Patel2023 - miRNA-199a/b-5p regionation of chondrogenesis - enchanced

Project description:From a previous microarray study we developed a small chondrogenesis model. We performed qPCR and measured how knockdown of miR-199a-5p or miR-199b-5p could modulate chondrogenesis. Several experiments were used to determine the parameters of this model. We utilised parameter scan and manual sliding to refine the model. Within are two models - an initial model which only comprises of genes which we have data for, and an enhanced model which expands of the initial model to make more predictions - e.g. how miR-140-5p is indirectly regulated by miR-199a-5p and miR-199b-5p.

2023-06-06 | MODEL2305010001 | BioModels

Diffrential expression of urinary bladder cells microRNAs ( miRs) in cyclophosphamide induced cystitis

Project description:During cyclophosphamide (CYP) induced ctstitis progression differential expression of microRNAs (miRs) play a role in urinary bladder inflammation and detrusor function. We identified eight UBs miRs that are known to be involved in various other bladder pathologies which exhibited altered expression in CYP mice and e predicted to have a role in inflammation and smooth muscle function (miR-34c-5p, -34b-3p, -212-3p, -449a-5p, -21a-3p, -376b-3p, -376b-5p and -409-5p).

2023-09-18 | GSE243239 | GEO

U2OS osteosarcoma cells LC-MSMS

Project description:In order to identify the targets of miR-193a-5p in osteosarcoma U2OS cell line, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins. order to identify the targets of miR-193a-5p, we used a lentivirus-mediated expression system to overexpressing miR-193a precusor, miR-193a-5p target sequence and non-target sequence, respectively, in osteosarcoma cell line U2OS. A tandem mass tag (TMT)-based quantitative proteomic strategy was employed to identify the global profile of miR-193a-5p-regulated proteins.

2021-09-08 | PXD013987 | Pride

Expression data from different stages and types of oocytes and cumulus cells (CCs)

Project description:The bidirectional communication between bovine oocytes and CCs is vital for functioning and development of both cell types. We used microarray to identify genes which are differentially expressed between germinal vesicle (GV)- and metaphase II (MII)-stage oocytes and CCs and those differentially expressed when oocytes mature with or without the other. We also identified genes differentially expressed between CCs at GV and MII stages. Slaughterhouse ovaries were collected and GV-stage cumulus oocyte complexes (COCs) were aspirated. Different stages and types of oocytes and CCs were used for total RNA isolation and hybridisation on Affymetrix microarray.

2010-03-23 | E-GEOD-21005 | biostudies-arrayexpress

The microRNA-212/132 cluster regulates B cell development and apoptosis by targeting SOX4

Project description:MicroRNAs have emerged as key regulators of B cell fate decisions and immune function. Deregulation of several microRNAs in B cells leads to the development of autoimmune disease and cancer in mice. We demonstrate that the microRNA-212/132 cluster (miR-212/132) is induced in B cells in response to B cell receptor signaling. Enforced expression of miR-132 results in a block in early B cell development at the pre-pro-B cell to pro-B cell transition and induces apoptosis in primary bone marrow B cells. Importantly, loss of miR-212/132 results in increased B cell output under non-homeostatic conditions. We find that miR-212/132 regulates B lymphopoiesis by targeting the transcription factor SOX4. Co-expression of SOX4 with miR-132 rescues the defect in B cell development from over-expression of miR-132 alone. In addition, we show that the expression of miR-132 in cells that are prone to spontaneous B cell cancers can have a protective effect on cancer development. We have thus uncovered a novel regulator of B cell lineage specification that may potential applications in B cell cancer therapy RNA-seq of wild-type and microRNA-212/132 knock-out B-cells after IgM stimulation

2015-09-01 | E-GEOD-66882 | biostudies-arrayexpress

Transcriptome analysis of Wild Type and Mir-212/132ILN/ILN mouse mammary gland

Project description:Mice deficient for miR-212/132 have been reported to show impaired mammary gland development. However, another miR-212/132-deficient line does not demonstrate any obvious defects in mammary gland organogenesis. The transcriptome analysis in the mammary gland of the previously reported miR-212/132-deficient line by deep RNA-seq revealed significantly deregulated expression of genes flanking Mir-212/132 locus, such as HIC1, implying that the mammary gland phenotype might not be only due to loss of miR-212/132

2014-07-29 | GSE37952 | GEO

Proteomic analysis upon miR195/497 replacement reveals potential chemo sensitizing candidates for colorectal cancer

Project description:Patients with advanced colorectal cancer (CRC) are commonly treated with systemic combination therapy but suffer eventually from drug resistance. MicroRNAs (miRNAs) are suggested to play a role in treatment resistance of CRC. We studied whether restoring downregulated miR-195-5p and 497-5p sensitize CRC cells to currently used chemotherapeutics 5-fluorouracil, oxaliplatin and irinotecan. Sensitivity to 5-FU, oxaliplatin and irinotecan before and after transfection with miR-195-5p and miR-497-5p mimics was analyzed in CRC cell lines HCT116, RKO, DLD-1 and SW480. Mass spectrometry based proteomic analysis of transfected and wild-type cells was used to identify targets involved in sensitivity to chemotherapy. Proteomic analysis revealed 181 proteins with significantly altered expression after transfection with miR-195-5p mimic in HCT116 and RKO, including 118 downregulated and 63 upregulated proteins. After transfection with miR-497-5p mimic, 130 proteins were significantly downregulated and 102 were upregulated in HCT116 and RKO (P<0.05 and FC<-3 or FC>3). CHUK and LUZP1 were coinciding downregulated proteins in sensitized CRC cells after transfection with either mimic. Resistance mechanisms of these two proteins may be related to nuclear factor kappa-B signaling and G1 cell cycle arrest, respectively. Restoring miR-195-5p and miR-497-5p expression enhanced sensitivity to chemotherapy, mainly oxaliplatin, in CRC cells and could be a promising treatment strategy for patients with mCRC. Proteomics revealed potential targets of these miRNAs involved in sensitivity to chemotherapy.

2019-09-27 | PXD015369 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data