Ghrelin Relieves Obesity-Induced Myocardial Injury by Regulating the Epigenetic Suppression of &lt;b&gt;&lt;i&gt;miR-196b&lt;/i&gt;&lt;/b&gt; Mediated by lncRNA HOTAIR

Chai

et al. 2023

Genes

Animal fat deposition has a significant impact on meat flavor and texture. However, the molecular mechanisms of fat deposition are not well understood. LncPLAAT3-AS is a naturally occurring transcript that is abundant in porcine adipose tissue. Here, we focus on the regulatory role of lncPLAAT3-AS in promoting preadipocyte proliferation and adipocyte differentiation. By overexpressing or repressing lncPLAAT3 expression, we found that lncPLAAT3-AS promoted the transcription of its host gene PLAAT3, a regulator of adipocyte differentiation. In addition, we predicted the region of lncPLAAT3-AS that binds to miR-503-5p and showed by dual luciferase assay that lncPLAAT3-AS acts as a sponge to absorb miR-503-5p. Interestingly, miR-503-5p also targets and represses PLAAT3 expression and helps regulate porcine preadipocyte proliferation and differentiation. Taken together, these results show that lncPLAAT3-AS upregulates PLAAT3 expression by absorbing miR-503-5p, suggesting a potential regulatory mechanism based on competing endogenous RNAs. Finally, we explored lncPLAAT3-AS and PLAAT3 expression in adipose tissue and found that both molecules were expressed at significantly higher levels in fatty pig breeds compared to lean pig breeds. In summary, we identified the mechanism by which lncPLAAT3-AS regulates porcine preadipocyte proliferation and differentiation, contributing to our understanding of the molecular mechanisms of lipid deposition in pigs.

“…Adipocyte differentiation is essential for lipid deposition in mammals [28]. It has been shown that the normal expression of the PLAAT3 gene promotes lipid deposition in mice.…”

Section: Discussionmentioning

confidence: 99%

LncPLAAT3-AS Regulates PLAAT3-Mediated Adipocyte Differentiation and Lipogenesis in Pigs through miR-503-5p

Chai

et al. 2023

Genes

“…HOTAIR (HOX transcript antisense RNA) [46] and CCL11 [47] are master regulator that are activated in cardiovascular diseases. HOTAIR (HOX transcript antisense RNA) [48], SLC15A1 [49] and CRH (corticotropin releasing hormone) [50] genes might be related to the pathophysiology of obesity. HOTAIR (HOX transcript antisense RNA) [51], CCL11 [52] and CRH (corticotropin releasing hormone) [53] expression is related to the patients with diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Screening of the Key Genes and Signaling Pathways for Schizophrenia Using Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad,

Vastrad

2023

Preprint

Schizophrenia is thought to be the most prevalent chronic psychiatric disorder. Numerous proteins have been identified that are associated with the occurrence and development of schizophrenia. This study aimed to identify potential core genes and pathways involved in schizophrenia, through exhaustive bioinformatic and next generation sequencing (NGS) data analyses using GSE20966 NGS data of neural progenitor cells and neurons obtained from healthy controls and patients with schizophrenia. The NGS data were downloaded from the Gene Expression Omnibus database. NGS data was processed by the DESeq2 package in R software and the differentially expressed genes (DEGs) were identified. Gene Ontology (GO) enrichment analysis and REACTOME pathway enrichment analysis were carried out to identify potential biological functions and pathways of the DEGs. Protein-protein interaction (PPI) network, module, miRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were performed to identify the hub genes, miRNA and TFs. Potential hub genes were analyzed using receiver operating characteristic (ROC) curves in the R package (pROC). In this investigation, an overall 955 DEGs were identified: 478 genes were remarkably up regulated and 477 genes were distinctly down regulated. These genes were enriched for GO terms and pathways mainly involved in the multicellular organismal process, GPCR ligand binding, regulation of cellular process and amine ligand-binding receptors. MYC, FN1, CDKN2A, EEF1G, CAV1, ONECUT1, SYK, MAPK13, TFAP2A and BTK were considered the potential hub genes. miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed successfully. On the whole, the findings of this investigation enhance our understanding of the potential molecular mechanisms of schizophrenia and provide potential targets for further investigation.

“…Ghrelin, a polypeptide with cardioprotective properties, has been observed to target the lncRNA H19/miR-29a/insulin-like growth factor 1 (IGF-1) signaling pathway and the lncRNA HOTAIR/miR-196b/IGF-1 signaling pathway, thereby mitigating cardiomyocyte injury associated with obesity. 138,139 These studies not only enhance our comprehension of the mechanisms by which lncRNAs regulate obesity-associated CVDs, but also offer novel avenues and insights for future research and clinical interventions.…”

Section: Obesity-induced Lncrna Alterations On Cvdsmentioning

confidence: 99%

Epigenetic modifications in obesity‐associated diseases

Long,

Mao,

Liu

et al. 2024

MedComm

The global prevalence of obesity has reached epidemic levels, significantly elevating the susceptibility to various cardiometabolic conditions and certain types of cancer. In addition to causing metabolic abnormalities such as insulin resistance (IR), elevated blood glucose and lipids, and ectopic fat deposition, obesity can also damage pancreatic islet cells, endothelial cells, and cardiomyocytes through chronic inflammation, and even promote the development of a microenvironment conducive to cancer initiation. Improper dietary habits and lack of physical exercise are important behavioral factors that increase the risk of obesity, which can affect gene expression through epigenetic modifications. Epigenetic alterations can occur in early stage of obesity, some of which are reversible, while others persist over time and lead to obesity‐related complications. Therefore, the dynamic adjustability of epigenetic modifications can be leveraged to reverse the development of obesity‐associated diseases through behavioral interventions, drugs, and bariatric surgery. This review provides a comprehensive summary of the impact of epigenetic regulation on the initiation and development of obesity‐associated cancers, type 2 diabetes, and cardiovascular diseases, establishing a theoretical basis for prevention, diagnosis, and treatment of these conditions.