Ablation of interleukin-17 alleviated cardiac interstitial fibrosis and improved cardiac function via inhibiting long non-coding RNA-AK081284 in diabetic mice

Zhang, Yang; Zhang, Yiyuan; Li, Tingting; Wang, Jin; Jiang, Yuan; Zhao, Yue; Jin, Xuexin; Xue, Genlong; Yang, Ying; Zhang, Xiaofang; Sun, Yangyang; Zhang, Zhiren; Gao, Xu; Du, Zhenhong; Lu, Yanjie; Yang, Baofeng; Pan, Zhenwei

doi:10.1016/j.yjmcc.2018.01.001

Cited by 66 publications

(43 citation statements)

References 23 publications

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“…Increasing evidence suggests that lncRNAs are involved in the progression of many diseases, including organ fibrosis (26)(27)(28) found that Smad3 induced expression of lncRNA Erbb4-IR, which mediates TGF-b1-induced renal fibrosis. A recent study from our group (31) found that lncRNA AK081284 was involved in the profibrotic effects of IL-17 during cardiac fibrosis in diabetic mice. However, the role of lncRNA in lung fibrosis is poorly understood and requires further exploration.…”

Section: Discussionmentioning

confidence: 92%

lncRNA PFAL promotes lung fibrosis through CTGF by competitively binding miR‐18a

Shan

et al. 2018

FASEB j.

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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic parenchymal lung disease of unknown etiology and lacks an effective intervention. Long noncoding RNAs (lncRNAs) participate in organ fibrosis and various pulmonary diseases, but the role of lncRNAs in lung fibrosis is not fully understood. In the present study, we identified that lncRNA NONMMUT021928, designated as pulmonary fibrosis-associated lncRNA (PFAL), was up-regulated in the lungs of mice with experimental lung fibrosis, and in TGF-β1-induced fibrotic lung fibroblasts. Further study showed that overexpression of PFAL promoted cell proliferation, migration, and fibroblast-myofibroblast transition. Overexpression further resulted in extracellular matrix deposition and fibrogenesis in lung fibroblasts through regulation of microRNA-18a (miR-18a). Importantly, knockdown of PFAL alleviated lung fibrosis both in vitro and in vivo. Mechanistically, our study showed that PFAL promoted lung-fibroblast activation and fibrogenesis by acting as a competing endogenous RNA for miR-18a: forced expression of PFAL inhibited the expression and activity of miR-18a, whereas silencing of PFAL had the opposite effect. Furthermore, we found that miR-18a was decreased during lung fibrosis in vitro and in vivo, as well as in patients with IPF. Moreover, knockdown of miR-18a led to fibrogenesis in lung fibroblasts, whereas enhanced expression of miR-18a attenuated TGF-β1-induced lung fibrosis by directly targeting the regulation of connecting tissue growth factor. Taken together, these results revealed the effect and mechanism of lncRNA PFAL in pulmonary fibrosis and suggested that PFAL depletion may provide a novel strategy for the treatment of lung fibrosis.-Li, X., Yu, T., Shan, H., Jiang, H., Sun, J., Zhao, X., Su, W., Yang, L., Shan, H., Liang, H. lncRNA PFAL promotes lung fibrosis through CTGF by competitively binding miR-18a.

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Section: Discussionmentioning

confidence: 92%

lncRNA PFAL promotes lung fibrosis through CTGF by competitively binding miR‐18a

Shan

et al. 2018

FASEB j.

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“…The study of Zhuo et al showed that lncRNA H19 could silence DIRAS3 epigenetically and inhibit autophagy in diabetic cardiomyocytes . Zhang's team study showed that by inhibiting lncRNA‐AK081284, interleukin‐17 ablation reduced cardiac interstitial fibrosis and improved cardiac function in diabetic mice . Gonzalo‐Calvo et al indicated that lncRNAs are independent predictors of diastolic function and remodelling in patients with type 2 diabetes .…”

Section: Long Noncoding Rnasmentioning

confidence: 99%

“…69 Zhang's team study showed that by inhibiting lncRNA-AK081284, interleukin-17 ablation reduced cardiac interstitial fibrosis and improved cardiac function in diabetic mice. 4 Gonzalo-Calvo et al indicated that lncRNAs are independent predictors of diastolic function and remodelling in patients with type 2 diabetes. 70 Accordingly, it is of great significance to study the regulation of lncRNA in DCM.…”

Section: Long Noncoding Rnasmentioning

confidence: 99%

“…These factors affect cardiac output and eventually lead to heart failure, which is the primary cause for diabetic patients' death . Long noncoding RNAs (lncRNAs) are a class of nonprotein‐coding RNAs longer than 200 nucleotides . They have critical roles in various biological processes, including gene expression regulation, genomic imprinting, nuclear‐cytoplasmic trafficking, RNA splicing, and translational control .…”

Section: Introductionmentioning

confidence: 99%

“…They have critical roles in various biological processes, including gene expression regulation, genomic imprinting, nuclear‐cytoplasmic trafficking, RNA splicing, and translational control . Recent studies indicated that lncRNAs extensively participate in the development of diverse cardiac diseases, such as cardiac ischaemia, hypertrophy, and heart failure . To our best knowledge, the research about lncRNA in DCM is just in the beginning phase, review articles on such research are almost blank.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Long noncoding RNAs: A new player in the prevention and treatment of diabetic cardiomyopathy?

Luo

Liu

et al. 2018

Diabetes Metabolism Res

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Diabetic cardiomyopathy (DCM) can cause extensive necrosis of the heart muscle by metabolic disorders and microangiopathy, with subclinical cardiac dysfunction, and eventually progress to heart failure, arrhythmia, and cardiogenic shock; severe patients may even die suddenly. Long noncoding RNAs (lncRNAs) are a class of nonprotein-coding RNAs longer than 200 nucleotides. They have critical roles in various biological processes, including gene expression regulation, genomic imprinting, nuclear-cytoplasmic trafficking, RNA splicing, and translational control. Recent studies indicated that lncRNAs extensively participate in the development of diverse cardiac diseases, such as cardiac ischaemia, hypertrophy, and heart failure. Little is known about lncRNA in DCM. In this review, we summarize the current literature on lncRNAs in DCM studies, aiming to provide new methods for DCM's future prevention and treatment strategies.

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LncRNA HOTAIR functions as a competing endogenous RNA to upregulate SIRT1 by sponging miR‐34a in diabetic cardiomyopathy

Gao

Wang

Guo

et al. 2018

Journal Cellular Physiology

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The HOX transcript antisense RNA (HOTAIR) long noncoding RNA (lncRNA), a highly abundant and conserved imprinted gene, has been implicated in many essential biological processes and diseases. However, to date, the significance of HOTAIR in diabetic cardiomyopathy (DCM) has never been investigated. The current study was designed to determine whether DCM can be regulated by HOTAIR and to elucidate the related mechanism. In vivo, streptozotocin (STZ) was injected intraperitoneally to induce type 1 diabetes in mice. Cardiomyocyte specific HOTAIR overexpression was achieved using an adeno-associated virus system 12 weeks after STZ injection. In vitro, H9c2 were used to explore the potential molecular mechanism of HOTAIR in the regulation of high-glucose-induced cardiomyocyte injury. Luciferase reporter assay and RNA immunoprecipitation (RIP) were performed to explore the relationship between HOTAIR, microRNA-34a (miR-34a), and Sirtuin 1 (SIRT1). HOTAIR expression was significantly decreased in diabetic mice hearts. Knockdown of HOTAIR in high glucose-induced H9c2 resulted in increased oxidative injury, inflammation, and apoptosis in vitro. Cardiomyocyte-specific overexpression of HOTAIR improved cardiac function, decreased oxidative stress and inflammation, and attenuated myocyte death in mice treated with STZ. Mechanistically, the expression of SIRT1/forkhead box protein O1 was significantly increased in the HOTAIR-overexpressing hearts compared with the control hearts treated with STZ. Moreover, we found HOTAIR functioned as a molecular sponge of miR-34a in H9c2 and SIRT1 was identified as a target of miR-34a. Furthermore, the protective effects of HOTAIR on DCM was abolished in SIRT1 deficiency mice in vivo. HOTAIR protected against DCM via activation of the SIRT1 expression by sponging miR-34a.

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Ablation of interleukin-17 alleviated cardiac interstitial fibrosis and improved cardiac function via inhibiting long non-coding RNA-AK081284 in diabetic mice

Cited by 66 publications

References 23 publications

lncRNA PFAL promotes lung fibrosis through CTGF by competitively binding miR‐18a

lncRNA PFAL promotes lung fibrosis through CTGF by competitively binding miR‐18a

Long noncoding RNAs: A new player in the prevention and treatment of diabetic cardiomyopathy?

LncRNA HOTAIR functions as a competing endogenous RNA to upregulate SIRT1 by sponging miR‐34a in diabetic cardiomyopathy

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