Cross Talk Between Heat Shock and Oxidative Stress Inducible Genes During Myocardial Adaptation to Ischemia
John J. Lemasters, Constance Oliver in Cell Biology of Trauma, 2020
Although the aforementioned adaptation techniques have been proven beneficial against ischemia reperfusion, the precise mechanism of adaptation remains unknown. Many questions remain unanswered. Are these adaptations interrelated? Most of the stress adaptations cause synthesis of heat shock proteins and/or oxidative stress-inducible proteins. Is there a common link? Stress adaptation also results in the induction of genes. How does the post-transcriptional regulation occur? To answer some of these questions, the heart was adapted to stress by three different methods, ischemic stress, oxidative stress, and heat shock. The results of myocardial adaptation to ischemia were compared by examining the induction of the gene expression and by studying the antioxidant status of the heart and myocardial performance during ischemia and reperfusion following adaptation.
Placental development and omics
Moshe Hod, Vincenzo Berghella, Mary E. D'Alton, Gian Carlo Di Renzo, Eduard Gratacós, Vassilios Fanos in New Technologies and Perinatal Medicine, 2019
MicroRNAs (miRNAs) are small, noncoding RNAs approximately 18–25 nucleotides long, which bind to the 3′-untranslated regions of their target mRNAs (38). They regulate gene expression by either cleaving specific mRNAs and repressing their translation or activating transcriptional regulation. Profiling studies have identified miRNA species that are specifically expressed in trophoblast cells and are termed trophomiRs. The most abundant trophomiRs are expressed from a gene cluster located on chromosome 19, the chromosome 19 miRNA cluster (C19MC), which spans 100 kb of genomic DNA and expresses 58 miRNA species (39). Placenta miRNAs are located intracellularly and can be secreted extracellularly via exosomes, apoptotic bodies, or microvesicles (40). Like exosomes, the placental-derived miRNAs released in the maternal bloodstream contribute to cell-cell communication at the maternal-fetal interface.
Role of Histone Methyltransferase in Breast Cancer
Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman in Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Regulation of gene expressions in eukaryotic organisms is regulated synergistically through different transcriptional factors, including chromatin remodelers, specific histone variants, transcriptional machinery, and histone modifications but not limited to these factors. Active domains of chromatin are usually characterized by apparent series associated with histone marks. H3K4me1 and H3K27ac are connected with specific active enhancers [10]. The H3K4me3 level is high at promoter sequences of active genes, and acetylation of H4 and H3 are within specific promoters of active genes [11–13]. Active gene bodies are mostly enriched in H4 and H3 acetylation [14], H2BK120u1 [15,16] and H3K79me3 acetylation [7], and H3K36me3 acetylation increasing toward the 30 end [17]. These different histone marks might regulate transcriptional regulation of genes by generating open chromatin structures along with effector recruitment that helps to mediate competent state transcriptionally. Although the varied function of various active modifications of histone proteins is not fully recognizable and understandable, there is still an abundance of data available in the literature that shows that deposition of these histone marks is necessary for the appropriate gene expression regulation mechanism. There are various distinct positive crosstalk mechanisms found between several distinct modifications of histone proteins, which play a crucial role in maintenance and recruitment at the site of active genes through histone modifications.
Protective effect of Qingluotongbi formula against Tripterygium wilfordii induced liver injury in mice by improving fatty acid β-oxidation and mitochondrial biosynthesis
Published in Pharmaceutical Biology, 2023
Jie Zhou, Ming Li, Zhichao Yu, Changqing Li, Lingling Zhou, Xueping Zhou
Transcriptional regulation is an important way to regulate metabolic processes (Desvergne et al. 2006). Peroxisome proliferator-activated receptor alpha (PPARα), a member of nuclear receptor superfamily, is the master regulator of energy metabolism and lipid catabolism in the liver (Kersten and Stienstra 2017). Previous studies showed that the suppression of PPARα is linked to the hepatotoxic mechanisms of Tripterygium glycosides tablets and Tripterygium wilfordii tablets, two preparations of TW (Dai et al. 2022). PPARα activation can alleviate triptolide-induced liver injury in mice (Hu et al. 2019). The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) controls multiple hepatic metabolic pathways (Duan et al. 2022), and acts as a coactivator of PPARα to coordinately regulate the transcription of genes related to fatty acid oxidation and mitochondrial biogenesis (Vega et al. 2000). PPARα/PGC-1α pathway plays a central role in the regulation of cellular metabolism (Cheng et al. 2018). The activation of PPARα/PGC-1α can improve mitochondrial function (Kelly and Scarpulla 2004) and reduce lipotoxicity by enhancing lipid metabolism (Kim et al. 2022). We therefore speculate that the hepatic protective effect of QLT is probably related to the PPARα/PGC-1α pathway.
Risk of vaso-occlusive episodes in patients with sickle cell disease exposed to systemic corticosteroids: a comprehensive review
Published in Expert Review of Hematology, 2022
Christophe Ferreira de Matos, Thibault Comont, Marie-Pierre Castex, Margaux Lafaurie, Ondine Walter, Guillaume Moulis, Jérémie Dion, Pierre Cougoul
More precisely, in terms of pharmacodynamics, 90% of cortisol is bound to corticosteroid-binding globulins in the blood stream. Free cortisol is the active form of the hormone. In cytoplasm, cortisol bounds with the glucocorticoid receptor (GCR). The GCR is a member of the nuclear receptor superfamily. It has three mechanisms. First, the cortisol–GCR complex activates specific DNA sequences (Glucocorticoid Response Element), allowing the synthesis of anti-inflammatory mediators (annexin-1 and interleukin [IL]-10). The second, the mechanism is an indirect transcription regulation. The complex inhibits the expression of the nuclear factor-κB (NF-κB) pro-inflammatory pathway by binding to NF-κB DNA sequences. In the third mechanism, called the non-genomic pathway, it interacts with membrane-associated pro-inflammatory receptors and second messengers.
T cell subtypes and its therapeutic potential in autoimmune diseases and cancer
Published in International Reviews of Immunology, 2019
Amit Awasthi, Himanshu Kumar
Post-transcriptional regulation is important for the fine-tuning of protein expression and its subsequent function. Non-coding RNA is the post-transcriptional regulator and broadly consist of three members: the long non-coding (lnc) RNA, the circular (cir) RNA, and the micro (mi) RNA. These regulatory RNAs are pivotal in the development and differentiation process of various biological process, including the development of specific T cell types. The last review by Roy et al describes the role of lncRNA and miRNA in T cell subset differentiation and sheds light on its dysregulation leading to the development of the autoimmune disease [4]. The authors also highlighted the potential of miRNA as a biomarker, which could be developed as a potential diagnostic and prognostic markers for various autoimmune diseases (Figure 1).
Related Knowledge Centers
- DNA
- Eukaryote
- Molecular Biology
- Rna
- Genetics
- Transcription
- Regulation of Gene Expression
- Gene
- Evolutionary Developmental Biology
- Transcription Factor