Abstract:Long noncoding RNA SOX2OT is associated with myocardial fibrosis (MF) in heart failure (HF). This article aims to investigate the role of SOX2OT in MF. We constructed HF mouse models by subcutaneous injection of isoprenaline (ISO). Cardiac fibroblasts (CFs) were treated with ISO to induce MF. Hematoxylin-eosin, Masson, and Sirius-red staining were used to identify myocardial injury and collagen deposition in heart tissues. The relationship among SOX2OT, miR-138-5p, TGF-β1, and Smad3 were evaluated by chromatin… Show more
“…In recent years, significant progress has been made in the study of lncRNAs regulating cardiac fibrosis (Table 2, Ref. [47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62]). Zhang et al [47] demonstrated that the lncRNA H19 level was significantly downregulated in mice with MI.…”
Section: Lncrnas In Cardiac Fibrosismentioning
confidence: 99%
“…In recent years, significant progress has been made in the study of lncRNAs regulating cardiac fibrosis (Table 2 , Ref. [ 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 ]). Zhang et al .…”
Myocardial fibrosis is a common pathological feature of various terminal cardiovascular diseases. Progressive fibrosis is the pathological basis for the development and progression of many cardiac arrhythmias and heart failure. There are no effective reversal drugs for myocardial fibrosis due to the lack of understanding of the molecular mechanisms. Noncoding RNAs, a class of RNAs that do not function in coding proteins, have been found to be intimately involved in the life cycle of cardiomyocyte differentiation, transcription and apoptosis and are important regulators of cardiovascular disease. An increasing number of studies have shown that noncoding RNAs regulate the proliferation and transformation of cardiac fibroblasts through related signaling pathways and can be used as potential biomarkers and novel therapeutic targets for cardiac fibrosis. This article reviews the relationship between noncoding RNAs and cardiac fibrosis.
“…In recent years, significant progress has been made in the study of lncRNAs regulating cardiac fibrosis (Table 2, Ref. [47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62]). Zhang et al [47] demonstrated that the lncRNA H19 level was significantly downregulated in mice with MI.…”
Section: Lncrnas In Cardiac Fibrosismentioning
confidence: 99%
“…In recent years, significant progress has been made in the study of lncRNAs regulating cardiac fibrosis (Table 2 , Ref. [ 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 ]). Zhang et al .…”
Myocardial fibrosis is a common pathological feature of various terminal cardiovascular diseases. Progressive fibrosis is the pathological basis for the development and progression of many cardiac arrhythmias and heart failure. There are no effective reversal drugs for myocardial fibrosis due to the lack of understanding of the molecular mechanisms. Noncoding RNAs, a class of RNAs that do not function in coding proteins, have been found to be intimately involved in the life cycle of cardiomyocyte differentiation, transcription and apoptosis and are important regulators of cardiovascular disease. An increasing number of studies have shown that noncoding RNAs regulate the proliferation and transformation of cardiac fibroblasts through related signaling pathways and can be used as potential biomarkers and novel therapeutic targets for cardiac fibrosis. This article reviews the relationship between noncoding RNAs and cardiac fibrosis.
“…SMAD3 is also regulated by serotonin (55) which has been implicated in SUID (56). Variants in this gene have been described in patients that died of sudden cardiac death, heart failure and aortic aneurysm (57)(58)(59)(60)(61).…”
Section: Ros Pathway Variantsmentioning
confidence: 99%
“…SMAD3 is also regulated by serotonin (Chen, 2014) which has been implicated in SUID (Cummings, 2019). Variants in this gene have been described in patients that died of sudden cardiac death, heart failure and aortic aneurysm (Loeys, 2018; Engström, 2020; Ou, 2020; Hanna, 2021; Humeres, 2022).…”
PurposeIn this study we performed WGS of children that succumbed to SUID during their first year of life to gain insights into potential genetic risk factors that could contribute to an infant’s vulnerability to this tragic outcome.MethodsWhole genome sequencing was performed on 145 SUID cases, and 576 healthy adult controls. Variants were filtered by gnomAD allele frequencies and predictions of functional consequences using computational tools.ResultsIn 63.4% of our cohort, we identified 156 variants of interest in 86 genes, including 128 rare/ultra-rare variants in 71 genes that were previously associated with SIDS/SUID/SUDP. Eighty-eight variants were found in 43 genes that can be characterized as cardiac genes, and have previously been associated with cardiomyopathies, Brugada and Long QT syndromes, among others. Twenty-nine variants were also found in 22 genes previously reported in SIDS/SUID/SUDP that are related to neurologic function. Nineteen variants were found in 13 genes that are reported to be pathogenic for various systemic disorders, 11 of which occurred in six genes that have been previously described in SIDS/SUID/SUDP and eight that have not. We also identified 20 variants in eight genes implicated in the response to hypoxia and the regulation of reactive oxygen species (ROS) not previously described in SIDS/SUID/SUDP.ConclusionOur study confirms and further expands the list of genetic variants associated with SUID. The abundance of genes associated with heart disease and the discovery of variants associated with the redox metabolism has important mechanistic implications for the pathophysiology of SUID.
“…In an analysis by Poulet C et al on the potentially abnormal expression of lncRNAs in IPF, lncRNA SOX2OT (SOX2OT) has caught our attention (10). SOX2OT has been confirmed to play a vital part in mesangial cell and cardiomyocyte proliferation and fibrosis in diabetic nephropathy (11,12), suggesting the potentially important effect of SOX2OT on the fibrosis process of IPF. However, no studies have confirmed our view.…”
Materials and Methods
Cell dataHuman embryonic lung FBs MRC5, ordered from the American Type Culture Collection (ATCC), were cultured in the supporting culture medium. Trypsin was added for digestion when the cells were 80-90% confluent, followed by supernatant removal via centrifugation and the addition of 10% FBS-supplemented MEM medium for passage at a 1:2 ratio and further culture.
Polymerase chain reaction (PCR) testingTotal cell RNA was extracted by Trizol, and reverse transcribed into cDNA after its purity determination by ultraviolet spectrophotometer. Reverse transcription of 20 μg total RNA was then performed at 50℃ for 2 min, 95℃ for 10 min, 95℃ for 15s, and 60℃ for 60s, for 60 cycles. SOX2OT expression was calculated by 2 -ΔΔCt with GAPDH as an internal reference. Primer sequences, are
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