LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family

Abstract Background LncRNA-ATB is a long noncoding RNA (lncRNA) activated by transforming growth factor β (TGF-β) and it has important biological functions in tumours and nontumour diseases. Meanwhile, TGF-β is the most critical regulatory factor in the process of nephrotic fibrosis and calcium oxal...

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Autores principales:	Yinhui Li, Tao Ding, Haiyan Hu, Tingting Zhao, Chao Zhu, Jiarong Ding, Jihang Yuan, Zhiyong Guo
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	lncRNA-ATB EMT miR-200a Calcium oxalate monohydrate Kidney stone Calcium oxalate Therapeutics. Pharmacology RM1-950 Biochemistry QD415-436
Acceso en línea:	https://doaj.org/article/3686435078874edb8b7af8a68150cea5
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spelling	oai:doaj.org-article:3686435078874edb8b7af8a68150cea52021-11-07T12:19:14ZLncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family10.1186/s10020-021-00403-21076-15511528-3658https://doaj.org/article/3686435078874edb8b7af8a68150cea52021-11-01T00:00:00Zhttps://doi.org/10.1186/s10020-021-00403-2https://doaj.org/toc/1076-1551https://doaj.org/toc/1528-3658Abstract Background LncRNA-ATB is a long noncoding RNA (lncRNA) activated by transforming growth factor β (TGF-β) and it has important biological functions in tumours and nontumour diseases. Meanwhile, TGF-β is the most critical regulatory factor in the process of nephrotic fibrosis and calcium oxalate (CaOx) crystal-induced renal injury. The present study aimed to investigate the biological function and mechanism of lncRNA-ATB in CaOx crystal-induced renal injury. Methods The expression level of lncRNA-ATB was detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), the expression levels of epithelial-mesenchymal transition (EMT) markers, TGF-β1 and Kidney Injury Molecule-1 (KIM-1) were detected by qRT-PCR, immunofluorescence staining or western blot analysis, cell proliferation was measured with a CCK-8 kit, cell apoptosis was measured by flow cytometry and TUNEL staining, and cell injury was detected with the Cytotoxicity lactate dehydrogenase (LDH) Assay kit and the expression level of KIM-1. Results The expression levels of lncRNA-ATB and TGF-β1 were significantly increased in HK-2 cells after coincubation with calcium oxalate monohydrate (COM). COM stimulation caused significant injury in the HK-2 cells, induced cell apoptosis, inhibited cell proliferation, and induced EMT changes. After COM stimulation, the expression levels of the epithelial cell markers E-cadherin and zonula occludens (ZO)-1 in HK-2 cells significantly decreased, whereas the levels of the mesenchymal cell markers N-cadherin, vimentin and α-smooth muscle actin (α-SMA) significantly increased. Interference with lncRNA-ATB expression significantly relieved the COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT changes. The expression levels of the microRNA-200 (miR-200) family in the HK-2 cells after coincubation with COM were significantly decreased. MiR-200a mimics relieved the COM-induced cell injury, apoptosis, proliferation inhibition, and EMT changes, whereas miR-200a inhibitors abolished the lncRNA-ATB interference-induced relief of the COM-induced cell injury, apoptosis, proliferation inhibition, and EMT. Conclusion LncRNA-ATB promoted the COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT to participate in the process of CaOx crystal-induced renal injury by sponging miR-200s.Yinhui LiTao DingHaiyan HuTingting ZhaoChao ZhuJiarong DingJihang YuanZhiyong GuoBMCarticlelncRNA-ATBEMTmiR-200aCalcium oxalate monohydrateKidney stoneCalcium oxalateTherapeutics. PharmacologyRM1-950BiochemistryQD415-436ENMolecular Medicine, Vol 27, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	lncRNA-ATB EMT miR-200a Calcium oxalate monohydrate Kidney stone Calcium oxalate Therapeutics. Pharmacology RM1-950 Biochemistry QD415-436
spellingShingle	lncRNA-ATB EMT miR-200a Calcium oxalate monohydrate Kidney stone Calcium oxalate Therapeutics. Pharmacology RM1-950 Biochemistry QD415-436 Yinhui Li Tao Ding Haiyan Hu Tingting Zhao Chao Zhu Jiarong Ding Jihang Yuan Zhiyong Guo LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
description	Abstract Background LncRNA-ATB is a long noncoding RNA (lncRNA) activated by transforming growth factor β (TGF-β) and it has important biological functions in tumours and nontumour diseases. Meanwhile, TGF-β is the most critical regulatory factor in the process of nephrotic fibrosis and calcium oxalate (CaOx) crystal-induced renal injury. The present study aimed to investigate the biological function and mechanism of lncRNA-ATB in CaOx crystal-induced renal injury. Methods The expression level of lncRNA-ATB was detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), the expression levels of epithelial-mesenchymal transition (EMT) markers, TGF-β1 and Kidney Injury Molecule-1 (KIM-1) were detected by qRT-PCR, immunofluorescence staining or western blot analysis, cell proliferation was measured with a CCK-8 kit, cell apoptosis was measured by flow cytometry and TUNEL staining, and cell injury was detected with the Cytotoxicity lactate dehydrogenase (LDH) Assay kit and the expression level of KIM-1. Results The expression levels of lncRNA-ATB and TGF-β1 were significantly increased in HK-2 cells after coincubation with calcium oxalate monohydrate (COM). COM stimulation caused significant injury in the HK-2 cells, induced cell apoptosis, inhibited cell proliferation, and induced EMT changes. After COM stimulation, the expression levels of the epithelial cell markers E-cadherin and zonula occludens (ZO)-1 in HK-2 cells significantly decreased, whereas the levels of the mesenchymal cell markers N-cadherin, vimentin and α-smooth muscle actin (α-SMA) significantly increased. Interference with lncRNA-ATB expression significantly relieved the COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT changes. The expression levels of the microRNA-200 (miR-200) family in the HK-2 cells after coincubation with COM were significantly decreased. MiR-200a mimics relieved the COM-induced cell injury, apoptosis, proliferation inhibition, and EMT changes, whereas miR-200a inhibitors abolished the lncRNA-ATB interference-induced relief of the COM-induced cell injury, apoptosis, proliferation inhibition, and EMT. Conclusion LncRNA-ATB promoted the COM-induced cell injury, cell apoptosis, proliferation inhibition, and EMT to participate in the process of CaOx crystal-induced renal injury by sponging miR-200s.
format	article
author	Yinhui Li Tao Ding Haiyan Hu Tingting Zhao Chao Zhu Jiarong Ding Jihang Yuan Zhiyong Guo
author_facet	Yinhui Li Tao Ding Haiyan Hu Tingting Zhao Chao Zhu Jiarong Ding Jihang Yuan Zhiyong Guo
author_sort	Yinhui Li
title	LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
title_short	LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
title_full	LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
title_fullStr	LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
title_full_unstemmed	LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family
title_sort	lncrna-atb participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the mir-200 family
publisher	BMC
publishDate	2021
url	https://doaj.org/article/3686435078874edb8b7af8a68150cea5
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LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family

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