Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1148020 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30230824_1.fastq.gz | Fastqsanger.gz | |||
| SRR30230824_2.fastq.gz | Fastqsanger.gz | |||
| SRR30230825_1.fastq.gz | Fastqsanger.gz | |||
| SRR30230825_2.fastq.gz | Fastqsanger.gz | |||
| SRR30230826_1.fastq.gz | Fastqsanger.gz |
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Project description:This study investigated the role of mitochondrial function and the downstream long noncoding RNAs (lncRNAs) in regulating inflammation-induced changes to the cementoblastic differentiation of PDLSCs. We found that inflammatory cytokine-caused impairment to cementoblastic differentiation of PDLSCs was closely correlated to their mitochondrial function, and in terms of lncRNA microarray analysis and gain/loss-of-function studies, gastric cancer associated transcript 2 (GACAT2) was identified as a regulator across the cellular events of both inflammation-mediated mitochondrial function and cementoblastic differentiation. Next, comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and parallel reaction monitoring (PRM) assay revealed that GACAT2 was directly binded to protein pyruvate kinase M1/2 (PKM1/2). Further functional studies demonstrated that GACAT2 overexpression increased cellular protein expressions of PKM1/2, PKM2 tetramer and phosphorylated PKM2, led to an enhanced pyruvate kinase (PK) activity along with increased translocation of PKM2 into mitochondria. Finally, we found that GACAT2 overexpression could reverse inflammation-compromised mitochondrial function and cementoblastic differentiation of PDLSCs, and this function could be abolished by PKM1/2 knockdown. Our data suggest that lncRNA GACAT2 plays a critical role in inflammation-compromised mitochondrial function and cementoblastic differentiation by binding protein PKM1/2.
2022-03-23 | GSE176312 | GEO
Project description:Alternative splicing of the Pkm gene product generates the PKM1 and PKM2 isoforms of pyruvate kinase, and PKM2 expression is closely linked to embryogenesis, tissue regeneration, and cancer. To interrogate the functional requirement for PKM2 during development and tissue homeostasis, we generated germline PKM2 null mice (Pkm2-/-). Unexpectedly, despite being the primary isoform expressed in most wild-type adult tissues, we found that Pkm2-/- mice are viable and fertile. Thus, PKM2 is not required for embryonic or postnatal development. Loss of PKM2 leads to compensatory expression of PKM1 in the tissues that normally express PKM2. Strikingly, PKM2 loss leads to spontaneous development of hepatocellular carcinoma (HCC) with high penetrance that is accompanied by progressive changes in systemic metabolism characterized by altered systemic glucose homeostasis, inflammation, and hepatic steatosis. Therefore, in addition to its role in cancer metabolism, PKM2 plays a role in controlling systemic metabolic homeostasis and inflammation, thereby preventing HCC by a non-cell-autonomous mechanism. RNA was isolated from flash frozen ground whole liver tissue of 35 week old PKM2 KO and WT mice. Three independent mice from each condition were used as biological replicates.
2016-03-25 | E-GEOD-79535 | biostudies-arrayexpress
Project description:Compared with plasma sEV (Con-sEV) from control rats, plasma sEV (DM-sEV) from 8-week diabetic rats significantly induced cardiomyocyte apoptosis as evidenced by increased percentage of apoptotic cells and activity of pro-apoptotic protein caspase 3. The proapoptotic effect of DM-sEV was blunted by RNase but not proteinase K, suggesting that DM-sEV exerted the cardiotoxic effects mainly through their contained RNAs. Increasing evidence suggests that miRNAs are the most important molecules by which sEV regulate recipient cell function. To identify the sEV-containing specific miRNAs responsible for the effects, Con-sEV and DM-sEV were subjected to miRNA sequencing.
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Project description:Purpose: In this study, we compared transcriptome profiling (RNA-seq) between normal mouse embryonic stem cell (E14) and Hexokinase2 (Hk2)/ Pyruvate Kinase M2 (Pkm2) overexpressed E14 cell. Result: Using an optimized data analysis workflow, we mapped over 4 billion sequence reads per sample to the mouse genome (build mm9) and identified 28698 transcripts in 5 samples. Conclusion: Our study represents the first detailed analysis of Hk2/ Pkm2 overexpressed E14 cell transcriptomes, generated by RNA-seq technology We compared transcriptome profiling (RNA-Seq) between normal mouse embryonic stem cell (E14) and E14 cells over-expressing Hexokinase2 (Hk2)/Pyruvate Kinase M2 (Pkm2)
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Project description:Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. However, a comprehensive understanding of immune cells in HHcy-accelerated atherosclerotic aortas (HHcy-AA) and the underlying mechanisms are still lacking. In this study, single-cell RNA sequencing (scRNA-seq) analysis of aortas from three atherosclerotic models on ApoE-/- mice revealed 15 distinct immune cell clusters. Among them, B cells showed the most significant increase in the vessels of HHcy ApoE-/- mice compared with those in ApoE-/- mice fed a chow diet or western diet (WD). Further cell-cell contact reanalyses revealed that B cells, but not dendritic cells or macrophages, played a dominant role in the class II major histocompatibility complex (MHCII) signaling in HHcy-AA. Mechanistically, Hcy induced the nuclear translocation of pyruvate kinase M2 (PKM2) in B cells. Nuclear PKM2 interacted with and phosphorylated cyclic AMP-responsive element-binding protein 1 (CREB1), and then PKM2-CREB1 complex bound to promoter III of Ciita, a master transactivator of MHCII, and further induced MHCII expression. Adoptive transfer experiments demonstrated that nuclear PKM2-regulated B cell antigen presentation is essential for B cell-mediated T cell activation and atherogenesis. In summary, our study provides a comprehensive immune cell atlas of HHcy-AA, which is distinct with those in WD-fed ApoE-/- mice. MHCII-related antigen presentation may be the main function of aortic B cells. We also provide a novel perspective for the intervention in early development of atherosclerosis via the PKM2-CREB1-CIITA-MHCII axis in B cells, especially for HHcy-accelerated vascular inflammation.
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