LncRNA FAF inhibits fibrosis induced by angiotensinogen II via the TGFβ1-P-Smad2/3 signalling by targeting FGF9 in cardiac fibroblasts

Sun, Junran; Wang, Zimu; Shi, Haojie; Gu, Lingfeng; Wang, Sibo; Wang, Hao; Li, Yafei; Wei, Tianwen; Wang, Qiming; Wang, Liansheng

doi:10.1016/j.bbrc.2019.10.175

Cited by 16 publications

(14 citation statements)

References 22 publications

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“…In prior studies, lncRNA FAF was demonstrated to be involved in MI and could regulate the apoptosis of cardiomyocytes and fibrosis in cardiac fibroblasts by altering the transcription of FGF9. 22 , 23 In the present study, we firstly demonstrated that overexpression of lncRNA FAF with adenovirus exhibited antipyrotpotic effects both in vivo and in vitro. Improved cardiac function and reduced infarct size were also observed in FAF‐overexpressed MI rats.…”

Section: Discussionmentioning

confidence: 59%

“…LncRNAs exert biological function through various mechanisms, including chromatin organization, epigenetic modification, transcriptional and translation regulation 19,43 . In our previous study, lncRNA FAF exerts its biological function by regulating gene transcription in nucleus 22,23 . It is worth noting that lncRNAFAF is characterized as a cytoplasmic lncRNA, which tends to modulate gene expression by acting as a miRNA sponge in cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

“… 19 , 43 In our previous study, lncRNA FAF exerts its biological function by regulating gene transcription in nucleus. 22 , 23 It is worth noting that lncRNAFAF is characterized as a cytoplasmic lncRNA, which tends to modulate gene expression by acting as a miRNA sponge in cytoplasm. In this study, we further investigated the potential molecular mechanism of lncRNA FAF acting as a miRNA sponge.…”

Section: Discussionmentioning

confidence: 99%

“…For assessment of the cardiac structure and function, rats were anaesthetized and examined by a transthoracic echocardiography detection system (Visuasonics, Canada) as previously described 23 . Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were automatically measured by a microcomputer of the echocardiography system.…”

Section: Methodsmentioning

confidence: 99%

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LncRNA FAF attenuates hypoxia/ischaemia‐induced pyroptosis via the miR‐185‐5p/PAK2 axis in cardiomyocytes

Shi

Wang

et al. 2022

J Cellular Molecular Medi

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Coronary heart disease (CHD) remains a major cause of morbidity and mortality worldwide, which is responsible for nearly 1.8 million deaths in Europe, and similarly 1.7 million deaths in China annually. 1,2 Acute myocardial infarction (AMI), the worst outcome of CHD, accounts for many of these deaths. 3 Despite there has been a dramatic improvement in the overall mortality rate of AMI due to the advances in pharmacological therapy and reperfusion strategies over the past two decades, 4 quite a number of survivors eventually suffer from chronic heart failure, a long-term condition which leads to frequent hospitalizations, low quality of life and huge economic

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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LncRNA FAF attenuates hypoxia/ischaemia‐induced pyroptosis via the miR‐185‐5p/PAK2 axis in cardiomyocytes

Shi

Wang

et al. 2022

J Cellular Molecular Medi

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“…Co-regulates the transcription of target genes with other transcription factors [36]. Many articles indicate that repress the TGF-β1 channel can inhibit broblasts functions [37][38][39].…”

Section: Discussionmentioning

confidence: 99%

Mycophenolate mofetil reduces epidural fibrosis by regulating TGF-β1/Smad2/3 axis to repress the proliferation, migration and differentiation of fibroblasts

Zhu¹,

Zhang²,

Zhang³

et al. 2020

Preprint

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Background Excessive fibroblasts proliferation is believed as a major reason in the process of epidural fibrosis, which is known as a troublesome complication of lumbar laminectomy clinically. Mycophenolate mofetil (MMF) is a kind of immunosuppressant, previous studies had shown that it has the function of preventing fibrosis, but the role and mechanism are still unclear. In this study, we determined the repressed effect of MMF on fibroblasts proliferation, migration and differentiation in surgical-induced epidural fibrosis and the underlying mechanism. Methods In vitro, the impacts of MMF on cell viability were measured by cell counting kit-8 (CCK-8) assay and the fibroblasts proliferation rates were determined by using EdU incorporation, cell cycle assays and western blot. Additionally, the impacts of MMF on fibroblasts migration and differentiation were analyzed by cell wound scratch assay, transwell assay, immunofluorescence analysis and western blot. In vivo, we built epidural fibrosis models in rats and locally applied MMF. Histological and immunohistochemical staining were used to determine the effect of MMF on reducing epidural fibrosis and fibroblasts functions. Results CCK-8 assay demonstrated that MMF repressed fibroblasts proliferation in a time- and a dose-dependent manner. EdU incorporation assay and cell cycle analysis proved the inhibition effect of MMF on the proliferation of fibroblasts. Cell wound scratch assay, transwell assay and immunofluorescence proved the inhibition effect of MMF on the migration and differentiation of fibroblasts. Western blotting analysis proved that MMF inhibited the expression of TGF-β1, p-Smad2 and p-Smad3. The expression of proliferation proteins, migration proteins and differentiation proteins were downregulated. In addition, histological and immunohistochemical stain showed that MMF reduces epidural fibrosis by repressing the proliferation, migration and differentiation of fibroblasts. Conclusion MMF could inhibit the proliferation, migration and differentiation of fibroblasts, it reduced surgical-induced epidural fibrosis as well. TGF-β1/Smad2/3 axis may be the latent mechanism in MMF reduced epidural fibrosis. It might provide a new notion for mitigating surgery-induced epidural fibrosis.

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New developments in the biology of fibroblast growth factors

Ornitz

Itoh

2022

WIREs Mechanisms of Disease

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The fibroblast growth factor (FGF) family is composed of 18 secreted signaling proteins consisting of canonical FGFs and endocrine FGFs that activate four receptor tyrosine kinases (FGFRs 1-4) and four intracellular proteins (intracellular FGFs or iFGFs) that primarily function to regulate the activity of voltagegated sodium channels and other molecules. The canonical FGFs, endocrine FGFs, and iFGFs have been reviewed extensively by us and others. In this review, we briefly summarize past reviews and then focus on new developments in the FGF field since our last review in 2015. Some of the highlights in the past 6 years include the use of optogenetic tools, viral vectors, and inducible transgenes to experimentally modulate FGF signaling, the clinical use of small molecule FGFR inhibitors, an expanded understanding of endocrine FGF signaling, functions for FGF signaling in stem cell pluripotency and differentiation, roles for FGF signaling in tissue homeostasis and regeneration, a continuing elaboration of mechanisms of FGF signaling in development, and an expanding appreciation of roles for FGF signaling in neuropsychiatric diseases.

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LncRNA FAF inhibits fibrosis induced by angiotensinogen II via the TGFβ1-P-Smad2/3 signalling by targeting FGF9 in cardiac fibroblasts

Cited by 16 publications

References 22 publications

LncRNA FAF attenuates hypoxia/ischaemia‐induced pyroptosis via the miR‐185‐5p/PAK2 axis in cardiomyocytes

LncRNA FAF attenuates hypoxia/ischaemia‐induced pyroptosis via the miR‐185‐5p/PAK2 axis in cardiomyocytes

Mycophenolate mofetil reduces epidural fibrosis by regulating TGF-β1/Smad2/3 axis to repress the proliferation, migration and differentiation of fibroblasts

New developments in the biology of fibroblast growth factors

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