lncRNA HOTAIR upregulates autophagy to promote apoptosis and senescence of nucleus pulposus cells

Zhan, Shengfeng; Wang, Kun; Xiang, Qian; Song, Yu; Li, Shuai; Liang, Hang; Luo, Rongjin; Wang, Bingjin; Liao, Zhiwei; Zhang, Yukun; Yang, Cao

doi:10.1002/jcp.29129

Cited by 50 publications

(48 citation statements)

References 59 publications

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“…Accumulating evidence suggests that lncRNAs play a critical role in IVDD progression through modulating various cellular processes, such as autophagy, senescence, proliferation, and ECM synthesis (33,34). A previous study demonstrated that lncRNA FAM83H-AS1 contributes to NP cell growth through the regulation of the Notch signaling pathway (31).…”

Section: Discussionmentioning

confidence: 99%

LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

Jiang¹,

Chen²

2020

Ann Transl Med

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Background: Intervertebral disc degeneration (IVDD) is regarded as the leading cause of low back pain, resulting in disability and a heavy burden on public health. Several studies have unveiled that long noncoding RNAs (lncRNAs) play a key role in the pathogenesis and progression of IVDD. In this study, we aimed to investigate the biological function and latent molecular mechanism of the lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) in IVDD development.Methods: Firstly, we established an IVDD model in rats using advanced glycation end products (AGEs) intradiscal injection. Subsequently, gain-of-function assays were conducted to investigate the role of FAM83H-AS1 in the progression of IVDD. Bioinformatics analysis, RNA pull down assay and rescue experiments were employed to shed light on the molecular mechanism underlying FAM83H-AS1 involving in IVDD.Results: Our findings verified that AGEs treatment aggravated IVDD damage, and FAM83H-AS1 was downregulated in the IVDD group. Additionally, overexpression of FAM83H-AS1 contributed to the growth of nucleus pulposus (NP) cells and ameliorated IVDD injury. It was revealed that FAM83H-AS1 possessed the speculated binding sites of miR-22-3p. More importantly, we confirmed that FAM83H-AS1 functioned as a sponge of miR-22-3p in IVDD. Lastly, we demonstrated that miR-22-3p mediated the impact of FAM83H-AS1 on cell proliferation, ECM degradation, and inflammation. Conclusions:Our study indicated that FAM83H-AS1 relieved IVDD deterioration through sponging miR-22-3p, and provides novel insights into the mechanisms underlying FAM83H-AS1 in IVDD progression.

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Section: Discussionmentioning

confidence: 99%

LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

Jiang¹,

Chen²

2020

Ann Transl Med

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“…The role of long-chain non-coding RNA (lnc RNA) has attracted widespread attention [33]. LncRNAs have been reported in nervous system disorders, metabolic diseases, reproductive development and cardiovascular diseases [34]. Recent study has con rmed that lncRNA may play an important role in cardiac regeneration and repair as a potential target of treatment [35].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SUMO1P3 Aggravates Doxorubicin-Induced Cardiomyocyte Apoptosis by Targeting miR-93-5p / Bin1

Lin

2021

Preprint

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Background/AimsNon-coding RNA plays a critical role in myocardial apoptosis induced by doxorubicin (DOX). However, the specific function of Long noncoding RNA (lncRNA) small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is unclear. The purpose of this study was to determine the role of lncRNA SUMO1P3 in myocardial apoptosis induced by DOX. MethodsQRT-PCR were used to detect the expression levels of SUMO1P3 and miR-93-5p in DOX-treated primary cardiomyocytes and rat models. QRT-PCR and Western blot were used to detect the expression levels of Bin1 in DOX-treated primary cardiomyocytes and rat models. The relationship between SUMO1P3, miR-93-5p and Bin1 was analyzed using bioinformatics analysis and Luciferase reporter assay. The effects of DOX on the viability and apoptosis of cardiomyocytes were evaluated by flow cytometry and CCK-8. The effects of SUMO1P3 on cardiomyocyte apoptosis were analyzed by TUNEL staining and echocardiography. ResultsIn DOX-treated primary cardiomyocytes and rat models, the expression levels of SUMO1P3 and Bin1 were significantly increased, while the expression levels of miR-93-5p were significantly reduced. MiR-93-5p was a direct target gene of SUMO1P3, and Bin1 was a direct target gene of miR-93-5p. In addition, miR-93-5p reversed the protective effect of SUMO1P3 knockout on cardiomyocytes by inhibiting the expression of Bin1. ConclusionSUMO1P3 inhibited DOX-induced cardiomyocyte apoptosis through miR-93-5p/Bin1 axis.

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“…Low levels of ERS often lead to autophagy; however, under high levels of ERS, autophagy is transiently activated and then accompanied by the activation of apoptosis, along with rapid inhibition of autophagy (Holczer et al, 2015). Additionally, autophagy or proteins involved in the process of autophagy may drive the activation of apoptosis and necrosis by breaking down indispensable components of the cells, which in turn facilitates cell death (Zhan et al, 2020). 3-methyladenine (3-MA), the PI3K inhibitor, was the first identified, and is the most widely used, autophagy inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Cucurbitacin E Induces Autophagy-Involved Apoptosis in Intestinal Epithelial Cells

et al. 2020

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Apoptosis plays a crucial role in maintaining the structural and functional integrity of the intestinal epithelial barrier. Autophagy mediates injury to and repair of the intestinal epithelial barrier through multiple pathways in pathophysiological conditions. Our earlier study has found that cucurbitacin E (CuE) regulates the proliferation, migration, and permeability of human intestinal epithelial cells (IECs); however, its effects and mechanisms on apoptosis and autophagy are still unclear. This study reported CuE induced apoptosis and promoted autophagy of IECs in a concentration-dependent manner. The results showed that CuE could inhibit the expression of apoptosis-related protein Bcl-2 and drove activation of caspase-3 and cleavage of its substrate poly (ADP-ribose) polymerase. CuE also facilitated the expression of endoplasmic reticulum stress-related proteins, CHOP and Grp78, and autophagy-related proteins, Beclin1 and LC3, while inhibiting the phosphorylation of AKT and mammalian target of rapamycin (mTOR). An autophagy inhibitor, 3-methyladenine, reduced CuE-induced apoptosis. These results suggest that CuE may induce apoptosis and autophagy in IECs via the PI3K/AKT/mTOR signaling pathway and that autophagy following endoplasmic reticulum stress participates in the pro-apoptotic process induced by CuE.

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lncRNA HOTAIR upregulates autophagy to promote apoptosis and senescence of nucleus pulposus cells

Cited by 50 publications

References 59 publications

LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition

LncRNA SUMO1P3 Aggravates Doxorubicin-Induced Cardiomyocyte Apoptosis by Targeting miR-93-5p / Bin1

Cucurbitacin E Induces Autophagy-Involved Apoptosis in Intestinal Epithelial Cells

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