Fucoidan-Mediated Inhibition of Fibrotic Properties in Oral Submucous Fibrosis via the MEG3/miR-181a/Egr1 Axis DOI Creative Commons
Chih-Yuan Fang, Szu-Han Chen, Chun-Chung Huang

et al.

Pharmaceuticals, Journal Year: 2022, Volume and Issue: 15(7), P. 833 - 833

Published: July 5, 2022

Oral submucous fibrosis (OSF) is a chronic fibrotic remodeling disease that can progress to oral cancer. However, efficient clinical diagnosis and treatment methods for OSF are still lacking. This study investigated the anti-fibrotic effect of fucoidan on fibrosis. To evaluate ability (myofibroblast activities), we performed wound-healing, Transwell migration, collagen contraction assays by using patient-derived normal buccal fibroblasts (BMFs fBMFs, respectively). RNA-sequencing dual-luciferase reporter RNA immunoprecipitation chip were identify significance molecular mechanism non-coding RNAs. Fucoidan suppressed myofibroblast activities inhibited MEG3 in fBMFs. was overexpressed tissue positively associated with markers. Knockdown markedly activities, which restored inhibiting miR-181a overexpressing Egr1. The results from luciferase RIP confirmed functioned as competing endogenous (ceRNA) could directly target miR-181a, thereby preventing miR-181a-mediated translational repression demonstrated exerts profibrotic targeting miR-181a/Egr1. Therefore, administration may serve potential therapeutic strategy overexpression MEG3.

Language: Английский

MEG3: an Oncogenic Long Non-coding RNA in Different Cancers DOI

Arwa Al-Rugeebah,

Mohammed Alanazi,

Narasimha Reddy Parine

et al.

Pathology & Oncology Research, Journal Year: 2019, Volume and Issue: 25(3), P. 859 - 874

Published: Feb. 21, 2019

Language: Английский

Citations

177
TGF-β/Smad and Renal Fibrosis DOI

Taotao Ma,

Xiao‐Ming Meng

Advances in experimental medicine and biology, Journal Year: 2019, Volume and Issue: unknown, P. 347 - 364

Published: Jan. 1, 2019

Language: Английский

Citations

156
DNMT1-mediated lncRNA MEG3 methylation accelerates endothelial-mesenchymal transition in diabetic retinopathy through the PI3K/Akt/mTOR signaling pathway DOI
Yue He,

Yujiao Dan,

Xiaorong Gao

et al.

AJP Endocrinology and Metabolism, Journal Year: 2020, Volume and Issue: 320(3), P. E598 - E608

Published: Dec. 7, 2020

Diabetic retinopathy (DR) is one of the serious complications that occurs in diabetic patients frequently causes blindness. Long noncoding RNAs (lncRNAs) have been associated with DR pathology. This study aimed to determine underlying mechanism lncRNA maternally expressed gene 3 (MEG3) association DNA methyltransferase 1 (DNMT1) endothelial-mesenchymal transition (endMT) DR. A rat model was induced by streptozotocin (STZ) injection, and a high-glucose (HG)-induced cell established exposing microvascular endothelial cells obtained from retina rats HG. Subsequently, MEG3 overexpressed models characterize its impact on endMT involvement phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target rapamycin (mTOR) signaling pathway. Furthermore, methylation level promoter region determined application methylation-specific polymerase chain reaction, followed chromatin immunoprecipitation assay for enrichment. Finally, we examined regulation DNMT1 HG-induced model. The results revealed downregulated expression models. Overexpressed shown suppress through inhibition PI3K/Akt/mTOR Notably, could promote inhibit recruiting methyltransferase, which activated pathway accelerate These findings further highlighted inhibitory effect DR, thus presenting novel therapeutic candidate treatment.

Language: Английский

Citations

113
Non-coding RNAs in kidney injury and repair DOI Open Access
Zhiwen Liu, Ying Wang,

Shaoqun Shu

et al.

AJP Cell Physiology, Journal Year: 2019, Volume and Issue: 317(2), P. C177 - C188

Published: April 10, 2019

Acute kidney injury (AKI) is a major disease featured by rapid decline of renal function. Pathologically, AKI characterized tubular epithelial cell and death. Besides its acute consequence, contributes critically to the development progression chronic (CKD). After AKI, surviving cells regenerate repair. Normal repair restores integrity, while maladaptive or incomplete results in fibrosis eventually CKD. Non-coding RNAs (ncRNAs) are functional RNA molecules that transcribed from DNA but not translated into proteins, which mainly include microRNAs (miRNAs), long non-coding (lncRNAs), circular (circRNAs), small nucleolar (snoRNAs), tRNAs. Accumulating evidence suggests ncRNAs play important roles In this review, we summarize recent advances understanding ncRNAs, especially miRNAs lncRNAs repair, discuss potential application as biomarkers well therapeutic targets for treating impeding AKI-CKD transition, highlight future research directions

Language: Английский

Citations

102
m6A-induced lncRNA MALAT1 aggravates renal fibrogenesis in obstructive nephropathy through the miR-145/FAK pathway DOI Creative Commons
Peihua Liu, Bo Zhang, Zhi Chen

et al.

Aging, Journal Year: 2020, Volume and Issue: 12(6), P. 5280 - 5299

Published: March 23, 2020

Renal fibrosis is a key factor in chronic kidney disease (CKD).Long non-coding RNAs (lncRNAs) play important roles the physiological and pathological progression of human diseases.However, underlying mechanisms lncRNAs renal still need to be discovered.In this study, we first displayed increased lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression patients with obstructive nephropathy (ON).Then found that transforming growth beta (TGF-β1) induced epithelial-mesenchymal transition (EMT) extracellular matrix (ECM) protein deposition, which promoted viability, proliferation migration proximal tubular epithelial (HK2) cells.Next, MALAT1/miR-145/focal adhesion kinase (FAK) pathway was confirmed an importment role TGF-β1induced fibrosis.In addition, MALAT1/miR-145/FAK involved effect dihydroartemisinin (DHA) on TGF-β1-induced vitro vivo.Furthermore, m 6 A methyltransferase methyltransferase-like 3 (METTL3) shown main modification MALAT1.

Language: Английский

Citations

101
A systematic review of epigenetic interplay in kidney diseases: Crosstalk between long noncoding RNAs and methylation, acetylation of chromatin and histone DOI Open Access

Ruizhi Tan,

Jian Jia,

Tong Li

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 176, P. 116922 - 116922

Published: June 13, 2024

The intricate crosstalk between long noncoding RNAs (lncRNAs) and epigenetic modifications such as chromatin/histone methylation acetylation offer new perspectives on the pathogenesis treatment of kidney diseases. lncRNAs, a class transcripts longer than 200 nucleotides with no protein-coding potential, are now recognized key regulatory molecules influencing gene expression through diverse mechanisms. They modulate by recruiting or blocking enzymes responsible for adding removing methyl acetyl groups, DNA, N6-methyladenosine (m6A) histone acetylation, subsequently altering chromatin structure accessibility. In diseases acute injury (AKI), chronic disease (CKD), diabetic nephropathy (DN), glomerulonephritis (GN), renal cell carcinoma (RCC), aberrant patterns DNA/RNA/histone have been associated onset progression, revealing complex interplay lncRNA dynamics. Recent studies highlighted how lncRNAs can impact pathology affecting function genes involved in cycle control, fibrosis, inflammatory responses. This review will separately address roles diseases, particular emphasis elucidating bidirectional effects underlying mechanisms conjunction addition to potential exacerbating renoprotective pathologies. Understanding reciprocal relationships not only shed light molecular underpinnings pathologies but also present avenues therapeutic interventions biomarker development, advancing precision medicine nephrology.

Language: Английский

Citations

9
Emerging role of miRNAs in renal fibrosis DOI Open Access

Youling Fan,

Hongtao Chen, Zhenxing Huang

et al.

RNA Biology, Journal Year: 2019, Volume and Issue: 17(1), P. 1 - 12

Published: Sept. 24, 2019

As one type of the most common endogenous short noncoding RNAs (ncRNAs), microRNAs (miRNAs) act as posttranscriptional regulators gene expression and have great potential biological functions in physiological pathological processes various diseases. The role miRNAs renal fibrosis has also attracted attention previous 20 years, new therapeutic strategies targeting appear to be promising. Some researchers previously reviewed roles miRNA disease, but numerous studies emerged over recent 5 years. It is necessary update summarize research progress fibrosis. Thus, this review, we miRNA-mediated last years evaluate some different stages Furthermore, expound clinical applications these provide insights into treatment disease.

Language: Английский

Citations

59
IL-6 accelerates renal fibrosis after acute kidney injury via DNMT1-dependent FOXO3a methylation and activation of Wnt/β-catenin pathway DOI
Xiaoli Guo, Yan Zhu,

Yongmin Sun

et al.

International Immunopharmacology, Journal Year: 2022, Volume and Issue: 109, P. 108746 - 108746

Published: May 12, 2022

Language: Английский

Citations

33
Epigenetics as a versatile regulator of fibrosis DOI Creative Commons
Yang Liu, Dongsheng Wen, Chiakang Ho

et al.

Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)

Published: March 2, 2023

Abstract Fibrosis, a process caused by excessive deposition of extracellular matrix (ECM), is common cause and outcome organ failure even death. Researchers have made many efforts to understand the mechanism fibrogenesis develop therapeutic strategies; yet, remains unsatisfactory. In recent years, advances in epigenetics, including chromatin remodeling, histone modification, DNA methylation, noncoding RNA (ncRNA), provided more insights into fibrotic suggested possibility novel therapy for fibrosis. this review, we summarize current research on epigenetic mechanisms involved fibrosis their possible clinical applications. Graphical

Language: Английский

Citations

22
LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process DOI

Haibing Zhan,

Xuhong Chang, Xiaoxia Wang

et al.

Environmental Toxicology, Journal Year: 2021, Volume and Issue: 36(6), P. 1099 - 1110

Published: Feb. 6, 2021

Abstract Nickel oxide nanoparticles (NiO NPs) causes pulmonary fibrosis via activating transforming growth factor‐β1 (TGF‐β1) in rats, but its upstream regulatory mechanisms are unknown. This study aimed to explore the role of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) NiO NPs‐induced collagen deposition. Male Wistar rats were intratracheally instilled with NPs (0.015, 0.06, and 0.24 mg/kg b.w.) twice a week for 9 weeks. Human lung adenocarcinoma epithelial cells (A549 cells) cultured (25, 50, 100 μg/ml) establish deposition model. We discovered that rat was accompanied by epithelial‐mesenchymal transition (EMT) occurrence MEG3 down‐regulation tissues. In cell model, also evoked EMT decreased expression dose‐dependent manner A549 cells. By overexpressing cells, we found inhibited level TGF‐β1, process formation. Moreover, our data showed SB431542 (TGF‐β1 inhibitor) had an inhibitory effect on Our results indicated regulating TGF‐β1‐mediated process, which may provide some clues insighting into fibrosis.

Language: Английский

Citations

32