Long noncoding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis

Tao, Hui; Cao, Wei; Yang, Jingjing; Shi, Kai-Hu; Zhou, Xiao; Liu, Liping; Li, Jun

doi:10.1016/j.carpath.2016.05.005

Cited by 80 publications

(43 citation statements)

References 27 publications

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“…In these studies, HULC expression was related to TNM stage, intrahepatic metastases, HCC recurrence, and postoperative survival [1,38,39]. Furthermore, HULC acts as a ceRNA to activate the EMT process through the HULC/miR-200a-3p/ZEB1 signaling pathway and stimulates HCC progression and metastasis [38,60]. Li et al [85] demonstrates that HULC specifically binds to Y-box protein-1 (YB-1) to promote its phosphorylation through ERK kinase and then regulates the interaction of YB-1 with certain oncogenic mRNAs, consequently accelerating the translation of these oncogenic mRNAs in hepatic carcinogenesis.…”

Section: Hulcmentioning

confidence: 99%

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

Kim

Park

Lee

2020

IJMS

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Long non-coding RNAs (lncRNAs) are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including hepatocellular carcinoma (HCC). However, the involvement of these molecules in chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and viral hepatitis, has only recently been considered in scientific research. While extensive studies on the pathogenesis of the development of HCC from hepatic fibrosis have been conducted, their regulatory molecular mechanisms are still only partially understood. The underlying mechanisms related to lncRNAs leading to HCC from chronic liver diseases and cirrhosis have not yet been entirely elucidated. Therefore, elucidating the functional roles of lncRNAs in chronic liver disease and HCC can contribute to a better understanding of the molecular mechanisms, and may help in developing novel diagnostic biomarkers and therapeutic targets for HCC, as well as in preventing the progression of chronic liver disease to HCC. Here, we comprehensively review and briefly summarize some lncRNAs that participate in both hepatic fibrosis and HCC.

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Section: Hulcmentioning

confidence: 99%

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

Kim

Park

Lee

2020

IJMS

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“…However, in cultured neonatal rat ventricular myocytes selective inhibitors for class I histone deacetylases (HDACs) led to decreased DUSP5 expression, and overexpression of DUSP5 promoted ERK1/2 inactivation and the reduction in agonist-induced hypertrophy [72]. DUSP5 was also shown to dephosphorylate ERK1/2 during cardiac fibroblast proliferation [73]. Finally, while Dusp5 KO mice are viable, the effect of gene deletion on cardiac growth and remodeling has yet to be investigated [74].…”

Section: Dusps In Cardiac Remodeling Through Mapk Regulationmentioning

confidence: 99%

Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs)

Liu

Molkentin

2016

Journal of Molecular and Cellular Cardiology

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Mitogen-activated protein kinases (MAPKs) play a critical role in regulating cardiac hypertrophy and remodeling in response to increased workload or pathological insults. The spatiotemporal activities and inactivation of MAPKs are tightly controlled by a family of dual-specificity MAPK phosphatases (DUSPs). Over the past 2 decades, we and others have determined the critical role for selected DUSP family members in controlling MAPK activity in the heart and the ensuing effects on ventricular growth and remodeling. More specifically, studies from mice deficient for individual Dusp genes as well as heart-specific inducible transgene-mediated overexpression have implicated select DUSPs as essential signaling effectors in the heart that function by dynamically regulating the level, subcellular and temporal activities of the extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinases (JNKs) and p38 MAPKs. This review summarizes recent literature on the physiological and pathological roles of MAPK-specific DUSPs in regulating MAPK signaling in the heart and the effect on cardiac growth and remodeling.

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“…In diabetic rats, the downregulation of lncRNAMALAT1 has been revealed to inhibit cardiac myocyte apoptosis and attenuate left ventricular function (9), as well as suppress the proliferation and migration of retinal endothelial cells, and attenuate retinal vascular injury inflammation and function (10). Tao et al (11) demonstrated that downregulation of lncRNAH19 inhibits the proliferation of cardiac fibroblasts. Pan (12) revealed that lncRNAH19 regulates the proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) and vascular smooth muscle cells (VSMCs) via modulation of the mitogen-activated protein kinase and nuclear factor-κB signaling pathways, which subsequently regulate atherosclerosis formation.…”

Section: Introductionmentioning

confidence: 99%

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

et al. 2018

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Angiogenesis refers to the formation of new blood vessels from existing blood vessels. The proliferation and migration of endothelial cells serves a key function in this process. Previous research has demonstrated that rapamycin suppresses endothelial cell proliferation and migration, as well as angiogenesis. However, the mechanism by which rapamycin inhibits the proliferation and migration of endothelial cells remains unclear. Long noncoding RNAs (lncRNAs) serve a key function in the regulation of endothelial cell function. The aim of the current study was to investigate whether lncRNA taurine upregulated 1 (lncRNATUG1) is involved in rapamycin-induced inhibition of proliferation and migration in human umbilical vein endothelial cells (HUVECs). Reverse transcription quantitative polymerase chain reaction results indicated that the expression of lncRNATUG1 was upregulated in HUVECs that had been cultured with rapamycin. Subsequently, HUVECs were transfected with siRNAs and CCK-8 assays were performed to detect cell proliferation; additionally, flow cytometry was employed to detect cell apoptosis, and wound healing assays were performed to investigate cell migration. The results demonstrated that rapamycin suppressed the proliferation and migration of HUVECs, and promoted the apoptosis of HUVECs. In addition, rapamycin downregulated the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2 and MMP-9 in HUVECs. However, silencing of lncRNATUG1 was revealed to attenuate rapamycin-induced inhibition of cellular proliferation and migration of HUVECs, as well as upregulating the expression of VEGF, MMP2 and MMP-9. These results suggested that lncRNATUG1 regulates rapamycin-induced inhibition of endothelial cell proliferation and migration. Therefore, lncRNATUG1 may serve a key function in rapamycin-induced inhibition of endothelial cell proliferation and migration.

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Long noncoding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis

Cited by 80 publications

References 27 publications

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs)

Effect of silencing lncRNATUG1 on rapamycin‑induced inhibition of endothelial cell proliferation and migration

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