Circ_0116061 regulated the proliferation, apoptosis, and inflammation of osteoarthritis chondrocytes through regulating the miR-200b-3p/SMURF2 axis

Abstract Background Circular RNA (circRNA) has been shown to be associated with osteoarthritis (OA) progression. Circ_0116061 has been found to be highly expressed in OA cartilage tissues, but its role and mechanism in OA progression remain unclear. Methods Expression levels of circ_0116061, microRNA (miR)-200b-5p, and Smad ubiquitin regulatory factor 2 (SMURF2) were detected using quantitative real-time PCR. The proliferation and apoptosis of cells were measured using cell counting kit 8 (CCK8) assay, colony formation assay, and flow cytometry. Furthermore, the protein levels of proliferation-related marker, apoptosis-related markers, inflammatory factors, and SMURF2 were tested using western blot (WB) analysis. In addition, the interaction between miR-200b-3p and circ_0116061 or SMURF2 was examined using dual-luciferase reporter assay and biotin-labeled RNA pull-down assay. Results Circ_0116061 and SMURF2 were highly expressed, and miR-200b-3p was lowly expressed in OA cartilage tissues. Knockdown of circ_0116061 could promote the proliferation and inhibit the apoptosis and inflammation of OA chondrocytes. MiR-200b-3p could be sponged by circ_0116061, and its inhibitor could reverse the regulation of circ_0116061 silencing on the biological functions of OA chondrocytes. SMURF2 was a target of miR-200b-3p, and its expression was positively regulated by circ_0116061. Silencing of SMURF2 also could enhance the proliferation and suppress the apoptosis and inflammation of OA chondrocytes. Furthermore, the regulation of circ_0116061 silencing on the biological functions of OA chondrocytes also could be reversed by SMURF2 overexpression. Conclusion Our data showed that circ_0116061 might regulate the miR-200b-3p/SMURF2 axis to promote the progression of OA.

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Knockdown of Circ_SLC39A8 protects against the progression of osteoarthritis by regulating miR-591/IRAK3 axis

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02323-7 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Jizhe Yu ◽

Yushuang Qin ◽

Naxin Zhou

Keyword(s):

Cell Viability ◽

Molecular Mechanisms ◽

Interleukin 1 ◽

Cell Counting ◽

Luciferase Reporter ◽

Circular Rnas ◽

Oa Chondrocytes ◽

Polymerase Chain ◽

Apoptosis And Inflammation ◽

The Relationship

Abstract Background The dysregulation of circular RNAs (circRNAs) has been identified in various human diseases, including osteoarthritis (OA). The purpose of this study was to identify the role and mechanism of circ_SLC39A8 in regulating the progression of OA. Methods The expression levels of circ_SLC39A8, miR-591, and its potential target gene, interleukin-1-receptor-associated kinase 3 (IRAK3), were identified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The relationship between miR-591 and circ_SLC39A8 or IRAK3 was predicted by bioinformatics tools and verified by dual-luciferase reporter. Results Circ_SLC39A8 and IRAK3 were upregulated and miR-591 was downregulated in OA cartilage tissues. Knockdown of circ_SLC39A8 inhibited apoptosis and inflammation in OA chondrocytes, while these effects were reversed by downregulating miR-591. Promotion cell viability effects of miR-591 were partially reversed by IRAK3 overexpression. Conclusion Our findings indicated that knockdown of circ_SLC39A8 delayed the progression of OA via modulating the miR-591-IRAK3 axis, providing new insight into the molecular mechanisms of OA pathogenesis.

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CircSMAD4 alleviates high glucose-induced inflammation, extracellular matrix deposition and apoptosis in mouse glomerulus mesangial cells by relieving miR-377-3p-mediated BMP7 inhibition

Diabetology & Metabolic Syndrome ◽

10.1186/s13098-021-00753-1 ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Rina Wu ◽

Zheli Niu ◽

Guangwei Ren ◽

Lin Ruan ◽

Lijun Sun

Keyword(s):

Extracellular Matrix ◽

High Glucose ◽

Mesangial Cells ◽

Circular Rna ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Protein Levels ◽

Matrix Deposition

Abstract Background Diabetic nephropathy (DN) is a common complication of diabetes mellitus. Accumulating studies suggest that the deregulation of circular RNA (circRNA) is involved in DN pathogenesis. This study aimed to investigate the role of circSMAD4 in DN models. Methods Mice were treated with streptozotocin to establish DN models in vivo. Mouse glomerulus mesangial cells (SV40-MES13) were treated with high glucose to establish DN models in vitro. The expression of circSMAD4, miR-377-3p and bone morphogenetic protein 7 (BMP7) mRNA was measured by quantitative real-time PCR (qPCR). The releases of inflammatory factors were examined by ELISA. The protein levels of fibrosis-related markers, apoptosis-related markers and BMP7 were checked by western blot. Cell apoptosis was monitored by flow cytometry assay. The predicted relationship between miR-377-3p and circSMAD4 or BMP7 was validated by dual-luciferase reporter assay or pull-down assay. Results CircSMAD4 was poorly expressed in DN mice and HG-treated SV40-MES13 cells. HG induced SV40-MES13 cell inflammation, extracellular matrix (ECM) deposition and apoptosis. CircSMAD4 overexpression alleviated, while circSMAD4 knockdown aggravated HG-induced SV40-MES13 cell injuries. MiR-377-3p was targeted by circSMAD4, and miR-377-3p enrichment partly reversed the effects of circSMAD4 overexpression. BMP7 was a target of miR-377-3p, and circSMAD4 regulated BMP7 expression by targeting miR-377-3p. MiR-377-3p overexpression aggravated HG-induced injuries by suppressing BMP7. Conclusion CircSMAD4 alleviates HG-induced SV40-MES13 cell inflammation, ECM deposition and apoptosis by relieving miR-377-3p-mediated inhibition on BMP7 in DN progression.

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Circ_0007841 promotes the progression of multiple myeloma via miR-338-3p/BRD4 axis

10.21203/rs.3.rs-17503/v1 ◽

2020 ◽

Author(s):

Yan Wang ◽

Quande Lin ◽

Chunge Song ◽

Ruojin Ma ◽

Xiaojie Li

Keyword(s):

Cell Cycle ◽

Multiple Myeloma ◽

Plasma Cells ◽

Circular Rna ◽

Cell Counting ◽

Luciferase Reporter ◽

Serine Threonine Kinase ◽

Western Blot Assay ◽

Protein Levels ◽

Proliferation And Metastasis

Abstract Background The pathogenesis of multiple myeloma (MM) is not completely known. Herein, we explored the function and the working mechanism of circular RNA circ_0007841 in MM progression. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the expression of circ_0007841, microRNA-338-3p (miR-338-3p) and bromodomain containing 4 (BRD4). The proliferation and metastasis of MM cells were examined by cell counting kit-8 (CCK8) assay and transwell assays. Flow cytometry was conducted to assess the cell cycle and the apoptosis of MM cells. The targets of circ_0007841 and miR-338-3p were predicted by circinteractome and targetscan softwares, and these predictions were confirmed by dual-luciferase reporter assay and RNA-pull down assay. The protein levels of BRD4, phosphorylated-phosphatidylinositol 3-kinase (p-PI3K), PI3K, p-AKT serine/threonine kinase (p-AKT) and AKT were measured by Western blot assay. Exosomes were extracted using Exosome isolation kit. Results Circ_0007841 was highly expressed in bone marrow (BM)-derived plasma cells of MM patients and MM cells than that in healthy volunteers and normal plasma cells nPCs. Circ_0007841 promoted the proliferation, cell cycle and metastasis and impeded the apoptosis of MM cells. MiR-338-3p was a direct target of circ_0007841 in MM cells. Circ_0007841 accelerated the progression of MM through targeting miR-338-3p. BRD4 could directly bind to miR-338-3p in MM cells. MiR-338-3p exerted an anti-tumor role through targeting BRD4. Circ_0007841 promoted the activation of PI3K/AKT signaling via miR-338-3p/BRD4 axis. Exosomes generated from mesenchymal stromal cells (MSCs) elevated the malignant behaviors of MM cells via circ_0007841. Conclusion Circ_0007841 acted as an oncogene to promote the proliferation, cell cycle and motility and restrain the apoptosis of MM cells through sequestering miR-338-3p to up-regulate the expression of BRD4.

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Circ_0124644 Serves as a ceRNA for miR-590-3p to Promote Hypoxia-Induced Cardiomyocytes Injury via Regulating SOX4

Frontiers in Genetics ◽

10.3389/fgene.2021.667724 ◽

2021 ◽

Vol 12 ◽

Author(s):

Juan Tan ◽

Weinan Pan ◽

Huilin Chen ◽

Yafang Du ◽

Peiyong Jiang ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Cell Cycle Progression ◽

Circular Rna ◽

Suppressive Effect ◽

Cell Counting ◽

Luciferase Reporter ◽

Protein Levels ◽

Stress Markers ◽

Transcription Factor 4

Circular RNA (circRNA) is an important factor for regulating the progression of many cardiovascular diseases, including acute myocardial infarction (AMI). However, the role of circ_0124644 in AMI progression remains unclear. Hypoxia was used to induce cardiomyocytes injury. The expression of circ_0124644, microRNA (miR)-590-3p, and SRY-box transcription factor 4 (SOX4) mRNA was measured by qRT-PCR. Cell counting kit 8 (CCK8) assay and flow cytometry were utilized to detect cell viability, cell cycle progression, and apoptosis. The protein levels of apoptosis markers and SOX4 were determined by western blot (WB) analysis, and the levels of oxidative stress markers were assessed using commercial Assay Kits. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were employed to confirm the interaction between miR-590-3p and circ_0124644 or SOX4. Circ_0124644 was upregulated in AMI patients and hypoxia-induced cardiomyocytes. Hypoxia could inhibit cardiomyocytes viability, cell cycle process, and promote apoptosis and oxidative stress, while silencing circ_0124644 could alleviate hypoxia-induced cardiomyocytes injury. In terms of mechanism, circ_0124644 could target miR-590-3p. MiR-590-3p overexpression could relieve hypoxia-induced cardiomyocytes injury. Also, the suppressive effect of circ_0124644 knockdown on hypoxia-induced cardiomyocytes injury could be reversed by miR-590-3p inhibitor. Moreover, SOX4 was found to be a target of miR-590-3p, and its overexpression also could reverse the regulation of miR-590-3p on hypoxia-induced cardiomyocytes injury. Circ_0124644 silencing could alleviate hypoxia-induced cardiomyocytes injury by regulating the miR-590-3p/SOX4 axis, suggesting that it might be a target for alleviating AMI.

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Long non-coding RNA DANCR regulates proliferation and apoptosis of chondrocytes in osteoarthritis via miR-216a-5p-JAK2-STAT3 axis

Bioscience Reports ◽

10.1042/bsr20181228 ◽

2018 ◽

Vol 38 (6) ◽

Cited By ~ 14

Author(s):

Lei Zhang ◽

Pin Zhang ◽

Xiangyi Sun ◽

Liwu Zhou ◽

Jianning Zhao

Keyword(s):

Underlying Mechanism ◽

Joint Disease ◽

Cell Counting ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Protein Coding ◽

Stat3 Signaling Pathway ◽

Rna Immunoprecipitation ◽

Oa Chondrocytes ◽

Novel Target

Osteoarthritis (OA) is one of the most common chronic joint disease. Long non-coding RNAs (lncRNAs) have been confirmed to play important roles in a variety of diseases including OA. However, the underlying mechanism of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) in OA has not been well elucidated. The expression of DANCR in cartilage tissues from OA patients was detected using quantitative real-time PCR. After cell transfection, the effects of DANCR inhibition on the proliferation, apoptosis and inflammatory factors of OA chondrocytes were detected using Cell Counting Kit-8 assay and flow cytometry assay. Novel target of DANCR was then identified through bioinformatics analysis and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The expression of DANCR was significantly increased in OA patients. Function assays demonstrated that DANCR suppression inhibited the proliferation, inflammation, and promoted apoptosis of chondrocytes cells. Additionally, DANCR regulated survival of OA chondrocytes through acting as a competitive endogenous RNA for miR-216a-5p. Furthermore, JAK2 was a direct target of miR-216a-5p, and DANCR regulated the JAK2/STAT3 signal pathway through miR-216a-5p in OA chondrocytes. In the present study, we concluded that DANCR promoted the proliferation, inflammation, and reduced cell apoptosis in OA chondrocytes through regulating miR-216a-5p/JAK2/STAT3 signaling pathway, indicating DANCR might be a useful biomarker and potential therapeutic target for OA treatment.

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Circular RNA circ_0128846 promotes the progression of osteoarthritis by regulating miR-127-5p/NAMPT axis

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02428-z ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Chao Liu ◽

Ping Cheng ◽

Jianjun Liang ◽

Xiaoming Zhao ◽

Wei Du

Keyword(s):

Western Blot ◽

Cell Viability ◽

Circular Rna ◽

Cell Counting ◽

Luciferase Reporter ◽

Circular Rnas ◽

Western Blot Assay ◽

Nicotinamide Phosphoribosyltransferase ◽

Ecm Degradation ◽

Oa Chondrocytes

Abstract Background Mounting evidence indicates that circular RNAs (circRNAs) participate in the occurrence and development of various diseases, including osteoarthritis (OA). However, the effects and molecular mechanism of circ_0128846 in OA have not been reported. Methods The expression levels of circ_0128846, microRNA-127-5p (miR-127-5p), and nicotinamide phosphoribosyltransferase (NAMPT) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was examined by flow cytometry and western blot assay. Inflammatory response and cartilage extracellular matrix (ECM) degradation were evaluated by western blot assay. The relationship between miR-127-5p and circ_0128846 or NAMPT was predicted by bioinformatics tools and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. Results Circ_0128846 and NAMPT were upregulated and miR-127-5p was downregulated in OA cartilage tissues. Knockdown of circ_0128846 increased cell viability and inhibited apoptosis, inflammation and ECM degradation in OA chondrocytes, while these effects were reversed by downregulating miR-127-5p. Moreover, circ_0128846 positively regulated NAMPT expression by sponging miR-127-5p. Furthermore, miR-127-5p promoted cell viability and suppressed apoptosis, inflammation, and ECM degradation in OA chondrocytes by directly targeting NAMPT. Conclusion Circ_0128846 knockdown might inhibit the progression of OA by upregulating miR-127-5p and downregulating NAMPT, offering a new insight into the potential application of circ_0128846 in OA treatment.

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Hsa_circ_0004674 promotes osteosarcoma doxorubicin resistance by regulating the miR-342-3p/FBN1 axis

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02631-y ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Yumei Bai ◽

Yanghua Li ◽

Juan Bai ◽

Yumei Zhang

Keyword(s):

Animal Experiments ◽

Circular Rna ◽

Suppressive Effect ◽

Cell Counting ◽

Luciferase Reporter ◽

Protein Levels ◽

Promising Target ◽

Fibrillin 1

Abstract Background The occurrence of chemoresistance is a common problem in tumor treatment. Circular RNA (circRNA) has been confirmed to be related to tumor chemoresistance. However, the role and the underlying molecular mechanism of hsa_circ_0004674 in the chemoresistance of osteosarcoma (OS) are still unclear. Methods The expression of hsa_circ_0004674, miR-342-3p, and fibrillin-1 (FBN1) was determined by qRT-PCR. Cell counting kit 8 assay was used to evaluate the doxorubicin (DXR) resistance of cells. The proliferation and apoptosis of cells were measured using colony formation assay and flow cytometry. Western blot analysis was utilized to examine the protein levels of resistance markers, Wnt/β-catenin pathway markers and FBN1. The interaction between miR-342-3p and hsa_circ_0004674 or FBN1 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. Moreover, animal experiments were performed to assess the effect of hsa_circ_0004674 silencing on the DXR sensitive of OS in vivo. Results The upregulated hsa_circ_0004674 was found in DXR-resistant OS tissues and cells. Knockdown of hsa_circ_0004674 could inhibit the DXR resistance of OS cells in vitro and promote the DXR sensitive of OS tumors in vivo. In addition, we discovered that hsa_circ_0004674 could sponge miR-342-3p, and miR-342-3p could target FBN1. MiR-342-3p inhibitor could reverse the inhibition effect of hsa_circ_0004674 knockdown on the DXR resistance of OS cells. Similarly, the suppressive effect of miR-342-3p on the DXR resistance of OS cells also could be reversed by FBN1 overexpression. Furthermore, we revealed that hsa_circ_0004674 silencing inhibited the activity of Wnt/β-catenin pathway by the miR-342-3p/FBN1 axis. Conclusion Hsa_circ_0004674 facilitated the DXR resistance of OS through Wnt/β-catenin pathway via regulating the miR-342-3p/FBN1 axis, suggesting that hsa_circ_0004674 was a promising target for the chemoresistance of OS.

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LncRNA MEG3 Protects Chondrocytes From IL-1β-Induced Inflammation via Regulating miR-9-5p/KLF4 Axis

Frontiers in Physiology ◽

10.3389/fphys.2021.617654 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yijiang Huang ◽

Daosen Chen ◽

Zijian Yan ◽

Jingdi Zhan ◽

Xinghe Xue ◽

...

Keyword(s):

Inflammatory Response ◽

Cartilage Damage ◽

Protective Role ◽

Cell Counting ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Enzyme Linked Immunosorbent Assay ◽

Klf4 Expression ◽

And Migration ◽

Apoptosis And Inflammation

BackgroundOsteoarthritis (OA) is a chronic degenerative disease of the joints characterized by articular cartilage damage, subchondral bone remodeling, osteophyte formation, and inflammatory changes. This work aims to investigate the protective role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) against the apoptosis of chondrocytes.MethodsChondrocyte cell lines, CHON-001, and ATDC5 were treated with different doses of interleukin-1β (IL-1β) to mimic the inflammatory response during OA pathogenesis. Quantitative real-time polymerase chain reaction was performed to measure MEG3, miR-9-5p, and Krüppel-like factor 4 (KLF4) mRNA expression levels. MEG3 and KLF4 overexpression plasmids, MEG3 shRNA, miR-9-5p mimics, and miR-9-5p inhibitors were transfected into the cells. Cell counting kit-8, wound healing assay, and flow cytometry were conducted to determine cell viability, migration, and apoptotic rate. Dual-luciferase reporter assay was adopted to verify the targeting relationships among MEG3, miR-9-5p, and KLF4. Western blot was used to detect KLF4 protein expression. Enzyme-linked immunosorbent assay was employed to measure the levels of inflammatory factors.ResultsMEG3 expression in chondrocytes was down-regulated by the stimulation of IL-1β, and MEG3 negatively regulated miR-9-5p expression but positively regulated KLF4 expression. MEG3 overexpression strengthened the viability and migration of CHON-001 and ATDC5 cells but restrained the apoptosis and inflammatory response, while MEG3 knockdown had opposite effects. miR-9-5p inhibition or KLF4 overexpression could counteract the effects of MEG3 knockdown on chondrocytes. Besides that, MEG3 was proved to be a molecular sponge for miR-9-5p, and KLF4 was verified as the target of miR-9-5p.ConclusionMEG3 can promote chondrocyte proliferation and migration and inhibit apoptosis and inflammation by sponging miR-9-5p to induce KLF4 expression, which provides a promising therapy target for OA treatment.

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CircHIPK3 knockdown suppresses E2F3 expression to inhibit the viability and promote the apoptosis of lens epithelial cells in age-related cataract by sponging miR-499a-5p

Archives of Medical Science ◽

10.5114/aoms/138262 ◽

2021 ◽

Author(s):

Qichao Han ◽

Rong Zhang ◽

Lan Ma ◽

Li Shao ◽

Meiyan Feng

Keyword(s):

Epithelial Cells ◽

Cell Viability ◽

Circular Rna ◽

Cell Counting ◽

Luciferase Reporter ◽

Lens Epithelial Cells ◽

Protein Levels ◽

Age Related ◽

Anterior Lens Capsule ◽

E2f Transcription Factor

IntroductionCircular RNA (circRNA) is considered to be a vital regulator of disease progression, including age-related cataract (ARC). However, the molecular mechanism of circHIPK3 in ARC progression has not been fully elucidated.Material and methodsThe expression levels of circHIPK3, miR-499a-5p and E2F transcription factor 3 (E2F3) were measured by quantitative real-time PCR. Cell counting kit 8 assay and flow cytometry were performed to detect cell viability and apoptosis, respectively. Western blot analysis was employed to test the protein levels of apoptosis-related markers and E2F3. Biotin-labeled RNA pull-down assay was used to select miRNAs that could be targeted by circHIPK3, and dual-luciferase reporter assay was performed to confirm the interaction between miR-499a-5p and circHIPK3 or E2F3.ResultsCircHIPK3 is a stable circRNA that is significantly under-expressed in the anterior lens capsule tissues of ARC patients. Knockdown of circHIPK3 suppressed SRA01/04 cell viability and accelerated apoptosis. Moreover, miR-499a-5p could be targeted by circHIPK3, and its inhibitor reversed the effect of circHIPK3 silencing on cell viability and apoptosis. Furthermore, E2F3 was a target of miR-499a-5p, and its overexpression reversed the effect of miR-499a-5p on the viability and apoptosis of SRA01/04 cells. In addition, circHIPK3 positively regulated E2F3 expression by sponging miR-499a-5p.ConclusionsCircHIPK3 knockdown inhibited viability and enhanced apoptosis of lens epithelial cells to promote ARC progression by regulating miR-499a-5p/E2F3 axis.

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Regulation of the miR-19b-mediated SOCS6-JAK2/STAT3 pathway by lncRNA MEG3 is involved in high glucose-induced apoptosis in hRMECs

Bioscience Reports ◽

10.1042/bsr20194370 ◽

2020 ◽

Vol 40 (7) ◽

Author(s):

Fan Xiao ◽

Lan Li ◽

Jing-Song Fu ◽

Yu-Xiang Hu ◽

Rong Luo

Keyword(s):

Cell Viability ◽

High Glucose ◽

Caspase 3 ◽

Signalling Pathway ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Protein Levels ◽

Induced Apoptosis ◽

Apoptosis And Inflammation ◽

Stat3 Signalling

Abstract Objective: Diabetic retinopathy (DR) is one of the most severe and common complications of diabetes mellitus. The present study aimed to investigate the molecular mechanism of MEG3, miR-19b and SOCS6 in human retinal microvascular endothelial cells (hRMECs) under high glucose conditions. Methods: HRMECs were cultured in 5 or 30 mM D-glucose medium. qRT-PCR and Western blotting were used to determine the mRNA expression and protein levels. MTT assay and flow cytometry analysis were performed to detect the viability and apoptosis of hRMECs, respectively. TNF-α, IL-6 and IL-1β levels in cell supernatants were detected by ELISA. The activity of caspase-3/7 was also determined. A luciferase reporter assay was performed to confirm the targeting relationship between miR-19b and SOCS6, as well as MEG3 and miR-19b. Results: Our study demonstrated that miR-19b was increased and SOCS6 was decreased in HG-induced hRMECs. Knockdown of SOCS6 inhibited cell viability and reversed the promotion of cell viability induced by knockdown of miR-19b. Additionally, miR-19b directly targeted and negatively regulated SOCS6. Moreover, miR-19b promoted the cell apoptosis rate and caspase-3/7 activity and increased inflammatory factors through the SOCS6-mediated JAK2/STAT3 signalling pathway. In addition, MEG3 attenuated HG-induced apoptosis of hRMECs by targeting the miR-19b/SOCS6 axis. Conclusion: These findings indicate that MEG3 inhibited HG-induced apoptosis and inflammation by regulating the miR-19b/SOCS6 axis through the JAK2/STAT3 signalling pathway in hRMECs. Thus, these findings might provide a new target for the treatment of DR.

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