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Endothelins in Inflammation
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Giles A. Rae, Maria G. M. O. Henriques
The proliferation and migration of endothelial cells play a crucial role in the vascular remodeling which takes place during the healing of injured tissue. In this regard, ETs have been found to stimulate proliferation of many cells types, including endothelial cells, as recently reviewed elsewhere (203). ETs can act as true mitogens in some instances, but in most cases they are potent primers or co-mitogens. In the later case, they synergize with various growth factors by stimulating, via Ras protein activation, the serine-threonine and tyrosine kinase cascades which control the expression of immediate early genes such as c-myc and c-fos (204). ET-1 and ET-3 are equipotent in stimulating proliferation and DNA synthesis in either bovine or human cultured endothelial cells, with efficacies similar to that of 10% fetal bovine serum, but lower than that of fibroblast growth factor (205). In addition and like fibroblast growth factor, ET-1 and ET-3 also induced migration of both kinds of endothelial cells in microchemotaxis chambers. The proliferative and migratory effects of the ETs were unaffected by an ETA receptor antagonist, but virtually abolished by an ETB receptor antagonist. This contrasts with findings in vascular smooth muscle cells, in which the proliferative effects of ET-1 involve activation of ETA receptors (206).
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
Not all the activators of the angiogenic switch are well understood. The best understood is the hypoxia-inducible factor (HIF) pathway, which is one of the angiogenic “master regulator” transcription factors. Endothelial cells carry oxygen sensors, which have prolyl hydroxylase activity that hydroxylates HIF1a and targets it for ubiquitin-mediated degradation. In the hypoxic state, intact HIF1a combines with constitutively produced HIF1b and activates genes with hypoxia response elements. The angiogenic cascade goes through sequential phases, with initiation happening through a tissue- and context-dependent angiogenic switch, for example, suppression of quiescence mediators and upregulation of activation mediators, which likely happens through a cooperation or convergence of ETS transcription factors like ETS1 (originally named “erythroblast transformation specific”) and Erg (ETS-related gene), and HIF1 and 2. The initial angiogenic signal is magnified through transcriptional, intracrine, autocrine, and paracrine short- and long-feedback amplification loops, which can be diverse and tissue context dependent.
Pharmacology of Endothelins in the Gastrointestinal Tract
Published in T. S. Gaginella, Regulatory Mechanisms — in — Gastrointestinal Function, 2017
Considering that ET-1 is relatively abundant in the small and large intestines, particularly in the latter, and that it can affect mucosal secretory mechanisms, ETs may well be important regulators of processes of ion secretion and absorption. Furthermore, as intestinal ET-1-like immunoreactivity is elevated in patients with Crohn’s disease or with ulcerative colitis,110these peptides may be significant determinants of the diarrhea associated with inflammatory bowel disease.
Heterogeneity of T cells and macrophages in chlorine-induced acute lung injury in mice using single-cell RNA sequencing
Published in Inhalation Toxicology, 2022
Chen-qian Zhao, Jiang-zheng Liu, Meng-meng Liu, Xiao-ting Ren, De-qin Kong, Jie Peng, Meng Cao, Rui Liu, Chun-xu Hai, Xiao-di Zhang
T-helper lymphocytes (Th) can reflect the balance between pro-inflammatory and anti-inflammatory (Zedler et al. 1999). The conversion of the Th1 phenotype to T-helper 2 (Th2) at the onset of ALI suggests that the anti-inflammatory response tends to be enhanced at the onset of ALI, and the enhancement of the anti-inflammatory response induces a depressed cellular immune function in the body. In this study, we identified many genes and signaling pathways associated with activation of T cell immune response by top10 marker gene. Ets1, Elf1 and Elk3 expression were upregulated. Ets1 has an important role as a key transcriptional repressor in blocking the differentiation of Th2 and Th17 cells, thus inhibiting the onset and progression of inflammation (Lee et al. 2019). Elf1 not only regulates CD25, which is involved in T cell activation, but also CD247, which couples antigen recognition of T cell receptors to several intracellular signaling pathways (Goudy et al. 2013; Ben Khalaf et al. 2019). Intercellular adhesion molecule-1 (ICAM-1) is a major factor in the damage of inflammatory organs (Zhang et al. 2010). Interestingly, over-expression of Elk3 suppresses the protein levels of (Radbel et al. 2020; Cao et al. 2021). Therefore, these genes are expected to be a target gene for the treatment of ALI caused by Cl2. The mechanism of Ets1, Elf1 and Elk3 in Cl2 injury needs further study.
LncRNA LINC00963 promotes osteogenic differentiation of hBMSCs and alleviates osteoporosis progression by targeting miRNA-760/ETS1 axis
Published in Autoimmunity, 2021
Lirong Ren, Limin Guo, Nannan Kou, Jia Lv, Zhihua Wang, Kaishun Yang
ETS1 is a transcriptional factor that regulates critical functions in normal cell homeostasis and can contribute to tumour progression by regulating downstream target genes [40]. It is also identified as a key regulator of MSCs (marrow-derived mesenchymal stem cells) osteogenesis [41]. One study reported that the RING finger protein RNF11 is expressed in bone cells during osteogenesis and is regulated by ETS1 [42]. Another study also demonstrated that PEBP2alphaA and ETS1 cooperate in vivo to regulate the expression of opn gene in skeletal tissues [43]. Cbfa1 (core binding factor alpha 1) and Ets-1 are transcription factors that play important roles in the differentiation of MSCs to osteoblasts [44]. All these studies suggested that ETS1 is crucial in osteogenesis differentiation of hBMSCs. In this study, ETS1 was predicted to be a direct target of miR-760. In addition, previous studies demonstrated that miRNAs interact with target mRNAs at specific sites to downregulate gene expression either by degradation of mRNA or by inhibition of protein translation [15,45,46]. We demonstrated that miR-760 could directly bind to the 3′-UTR of ETS1 and then may guide the cleavage of ETS1 transcripts, leading to decreased expression levels of ETS1 at both mRNA and protein levels.
Potential value of circulating microRNA-126 and microRNA-210 as biomarkers for type 2 diabetes with coronary artery disease
Published in British Journal of Biomedical Science, 2018
KS Amr, H Abdelmawgoud, ZY Ali, S Shehata, HM Raslan
The downregulation of miR-126 in diabetes patients might be caused by hyperglycaemia that reduces the miR-126 content of endothelial apoptotic bodies, or prolonged hyperglycaemia may lead to further decrease of endothelial miR-126. These findings might relate to impaired peripheral angiogenic signalling in patients with diabetes due to the loss of endothelial protective role of miR-126 [13]. The epigenetic effect of miR-126 is encoded within an intron of Egfl7 and it is enriched in endothelial cell. Its expression has been shown to be partly driven by vascular-associated Ets transcription factors. These transcription factors play important roles in vasculogenesis, angiogenesis, inflammation, and remodelling [18]. For example, miR-126 promotes vascular endothelial growth factor (VEGF) signalling by suppressing two negative regulators of the VEGF pathway [19]. The lower plasma miR-126 in diabetes patients with CAD may be explained by its depletion from endothelial cells during hyperglycaemia resulting in its decrease in plasma [13] as well as circulating miR-126 was consumed during transcoronary passage [20].