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长链非编码RNA CASC2通过介导miR-135a-5p/TIMP3轴和JNK信号通路抑制高糖诱导的人肾小球系膜细胞增殖、炎症和纤维化。

Long non-coding RNA CASC2 restrains high glucose-induced proliferation, inflammation and fibrosis in human glomerular mesangial cells through mediating miR-135a-5p/TIMP3 axis and JNK signaling.

作者信息

Zhu Dongju, Wu Xiang, Xue Qian

机构信息

Department of Nephrology, The Affiliated Hospital, Panzhihua University, Panzhihua, 617000, Sichuan, China.

Department of Pediatrics, Panzhihua Central Hospital, Panzhihua, 617000, Sichuan, China.

出版信息

Diabetol Metab Syndr. 2021 Aug 26;13(1):89. doi: 10.1186/s13098-021-00709-5.

DOI:10.1186/s13098-021-00709-5
PMID:34446088
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8393478/
Abstract

BACKGROUND: Diabetic nephropathy (DN) is a common complication of diabetes. Long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is reported to exert a protective role in DN by a previous study. The working mechanism underlying the protective role of CASC2 in DN progression was further explored in this study. METHODS: The expression of CASC2 and microRNA-135a-5p (miR-135a-5p) was determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation ability was assessed by Cell Counting Kit-8 (CCK8) assay and 5-ethynyl-29-deoxyuridine (EDU) assay. Enzyme-linked immunosorbent assay (ELISA) was conducted to analyze the production of inflammatory cytokines in the supernatant. Western blot assay was performed to analyze protein expression. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the target relationship between miR-135a-5p and CASC2 or tissue inhibitors of metalloproteinase 3 (TIMP3). RESULTS: High glucose (HG) treatment reduced the expression of CASC2 in human glomerular mesangial cells (HMCs) in a time-dependent manner. CASC2 overexpression suppressed HG-induced proliferation, inflammation and fibrosis in HMCs. miR-135a-5p was validated as a target of CASC2, and CASC2 restrained HG-induced influences in HMCs partly by down-regulating miR-135a-5p. miR-135a-5p bound to the 3' untranslated region (3'UTR) of TIMP3, and CASC2 positively regulated TIMP3 expression by sponging miR-135a-5p in HMCs. miR-135a-5p silencing inhibited HG-induced effects in HMCs partly by up-regulating its target TIMP3. CASC2 overexpression suppressed HG-induced activation of Jun N-terminal Kinase (JNK) signaling partly through mediating miR-135a-5p/TIMP3 signaling. CONCLUSIONS: In conclusion, CASC2 alleviated proliferation, inflammation and fibrosis in DN cell model by sponging miR-135a-5p to induce TIMP3 expression.

摘要

背景：糖尿病肾病（DN）是糖尿病常见的并发症。先前的一项研究报道，长链非编码RNA（lncRNA）癌症易感性候选基因2（CASC2）在DN中发挥保护作用。本研究进一步探讨了CASC2在DN进展中发挥保护作用的作用机制。 方法：采用实时定量聚合酶链反应（RT-qPCR）检测CASC2和微小RNA-135a-5p（miR-135a-5p）的表达。通过细胞计数试剂盒-8（CCK8）检测和5-乙炔基-2'-脱氧尿苷（EDU）检测评估细胞增殖能力。采用酶联免疫吸附测定（ELISA）分析上清液中炎性细胞因子的产生。进行蛋白质印迹分析以分析蛋白质表达。进行双荧光素酶报告基因检测和RNA免疫沉淀（RIP）检测以验证miR-135a-5p与CASC2或金属蛋白酶组织抑制剂3（TIMP3）之间的靶向关系。 结果：高糖（HG）处理以时间依赖性方式降低人肾小球系膜细胞（HMCs）中CASC2的表达。CASC2过表达抑制HG诱导的HMCs增殖、炎症和纤维化。miR-135a-5p被验证为CASC2的靶标，并且CASC2部分通过下调miR-135a-5p抑制HG对HMCs的影响。miR-135a-5p与TIMP3的3'非翻译区（3'UTR）结合，并且CASC2通过在HMCs中海绵化miR-135a-5p正向调节TIMP3表达。miR-135a-5p沉默部分通过上调其靶标TIMP3抑制HG对HMCs的影响。CASC2过表达部分通过介导miR-135a-5p/TIMP3信号传导抑制HG诱导的Jun N末端激酶（JNK）信号传导激活。 结论：总之，CASC2通过海绵化miR-135a-5p诱导TIMP3表达减轻DN细胞模型中的增殖、炎症和纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/149056c200a2/13098_2021_709_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/ee4f21a4dcd0/13098_2021_709_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/7b7bbb8eb12e/13098_2021_709_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/3e86c65e5e8a/13098_2021_709_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/b146ff2644e7/13098_2021_709_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/d01e842b50b3/13098_2021_709_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/d7b481882949/13098_2021_709_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/149056c200a2/13098_2021_709_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/ee4f21a4dcd0/13098_2021_709_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/7b7bbb8eb12e/13098_2021_709_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/3e86c65e5e8a/13098_2021_709_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/b146ff2644e7/13098_2021_709_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/d01e842b50b3/13098_2021_709_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/d7b481882949/13098_2021_709_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9334/8393478/149056c200a2/13098_2021_709_Fig7_HTML.jpg

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引用本文的文献

[1]
Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.

Curr Mol Med. 2024-4-5

[2]
LncRNA as a regulator in the development of diabetic complications.

Front Endocrinol (Lausanne). 2024

[3]
GDF15 Interference Regulates Proliferation, Inflammation, and Autophagy of Lipopolysaccharide-induced Mesangial Cells by Inhibiting PI3K/ AKT/mTOR Signaling.

Endocr Metab Immune Disord Drug Targets. 2024

[4]
Placenta-derived exosomal miR-135a-5p promotes gestational diabetes mellitus pathogenesis by activating PI3K/AKT signalling pathway via SIRT1.

J Cell Mol Med. 2023-12

[5]
Ferroptosis: a new strategy for Chinese herbal medicine treatment of diabetic nephropathy.

Front Endocrinol (Lausanne). 2023

[6]
The role of lncRNAs in regulation of DKD and diabetes-related cancer.

Front Oncol. 2022-10-13

[7]
MicroRNA-339-5p inhibits lipopolysaccharide-induced rat mesangial cells by regulating the Syk/Ras/c-Fos pathway.

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[8]
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本文引用的文献

[1]
circRNA_010383 Acts as a Sponge for miR-135a, and Its Downregulated Expression Contributes to Renal Fibrosis in Diabetic Nephropathy.

Diabetes. 2021-2

[2]
Long non-coding RNA SNHG8 promotes prostate cancer progression through repressing miR-384 and up-regulating HOXB7.

J Gene Med. 2021-3

[3]
lncRNA MCM3AP-AS1 inhibits the progression of colorectal cancer via the miR-19a-3p/FOXF2 axis.

J Gene Med. 2021-3

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LncRNA XIST protects podocyte from high glucose-induced cell injury in diabetic nephropathy by sponging miR-30 and regulating AVEN expression.

Arch Physiol Biochem. 2023-6

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LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis.

Kidney Blood Press Res. 2020

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Loss of lncRNA MIAT ameliorates proliferation and fibrosis of diabetic nephropathy through reducing E2F3 expression.

J Cell Mol Med. 2020-11

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circ_0136666 Facilitates the Progression of Colorectal Cancer via miR-383/CREB1 Axis.

Cancer Manag Res. 2020-8-4

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Inhibition of miRNA‑135a‑5p ameliorates TGF‑β1‑induced human renal fibrosis by targeting SIRT1 in diabetic nephropathy.

Int J Mol Med. 2020-9

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CircAGFG1 drives metastasis and stemness in colorectal cancer by modulating YY1/CTNNB1.

Cell Death Dis. 2020-7-17

[10]
Identification of functional circRNA/miRNA/mRNA regulatory network for exploring prospective therapy strategy of colorectal cancer.

J Cell Biochem. 2020-12

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