Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1
BACKGROUND: MicroRNAs (miRNAs) contribute to the progression of chronic kidney disease (CKD) by regulating renal homeostasis. This study explored the effects of miR-181a on CKD through the Toll-like receptor (TLR)/nuclear factor-kappa B (NF-κB) pathway by binding to CRY1.
METHODS: Seventy male rats were selected and assigned into specific groups: miR-181a mimic, miR-181a inhibitor, and siRNA against CRY1, with each group undergoing different treatments to investigate many different outcomes. First, 24-h urinary protein was measured. ELISA was used to determine the serum levels of SOD, ROS, MDA, IL-1β, IL-6, and TNF-α. Biochemical tests for renal function were performed to measure albumin, uric acid, and urea in urine and urea nitrogen and creatinine in serum. The glomerulosclerosis index (GSI) and renal tubular epithelial (RTE) cell apoptosis were detected using PASM staining and TUNEL staining, respectively. Finally, RT-qPCR and western blot were done to determine miR-181a, CRY1, TLR2, TLR4, and NF-κB expression.
RESULTS: CRY1 is the target gene of miR-181a, according to a target prediction program and luciferase assay. Rats diagnosed with CKD presented increases in 24-h urinary protein; GSI; RTE cell apoptosis rate; serum ROS, MDA, IL-1β, IL-6, and TNF-α; and CRY1, TLR2, TLR4, and NF-κB expression, as well as decreases in SOD level and miR-181a expression. Following transfection with either the miR-181a mimic or si-CRY1, 24-h urinary protein, renal damage, GSI, and cell apoptosis rate were all decreased. In addition, the overexpression of miR-181a or inhibition of CRY1 alleviated the degree of kidney injury through suppression of the TLR/NF-κB pathway.
CONCLUSION: miR-181a alleviates both GS and RTE injury in CKD via the down-regulation of the CRY1 gene and the TLR/NF-κB pathway.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2018 |
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| Erschienen: |
2018 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
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| Enthalten in: |
Molecular medicine (Cambridge, Mass.) - 24(2018), 1 vom: 18. Sept., Seite 49 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Liu, Lei [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 17.01.2019 Date Revised 17.01.2019 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1186/s10020-018-0045-2 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM288779282 |
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| 100 | 1 | |a Liu, Lei |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Over-expressed microRNA-181a reduces glomerular sclerosis and renal tubular epithelial injury in rats with chronic kidney disease via down-regulation of the TLR/NF-κB pathway by binding to CRY1 |
| 264 | 1 | |c 2018 | |
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| 500 | |a Date Completed 17.01.2019 | ||
| 500 | |a Date Revised 17.01.2019 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND: MicroRNAs (miRNAs) contribute to the progression of chronic kidney disease (CKD) by regulating renal homeostasis. This study explored the effects of miR-181a on CKD through the Toll-like receptor (TLR)/nuclear factor-kappa B (NF-κB) pathway by binding to CRY1 | ||
| 520 | |a METHODS: Seventy male rats were selected and assigned into specific groups: miR-181a mimic, miR-181a inhibitor, and siRNA against CRY1, with each group undergoing different treatments to investigate many different outcomes. First, 24-h urinary protein was measured. ELISA was used to determine the serum levels of SOD, ROS, MDA, IL-1β, IL-6, and TNF-α. Biochemical tests for renal function were performed to measure albumin, uric acid, and urea in urine and urea nitrogen and creatinine in serum. The glomerulosclerosis index (GSI) and renal tubular epithelial (RTE) cell apoptosis were detected using PASM staining and TUNEL staining, respectively. Finally, RT-qPCR and western blot were done to determine miR-181a, CRY1, TLR2, TLR4, and NF-κB expression | ||
| 520 | |a RESULTS: CRY1 is the target gene of miR-181a, according to a target prediction program and luciferase assay. Rats diagnosed with CKD presented increases in 24-h urinary protein; GSI; RTE cell apoptosis rate; serum ROS, MDA, IL-1β, IL-6, and TNF-α; and CRY1, TLR2, TLR4, and NF-κB expression, as well as decreases in SOD level and miR-181a expression. Following transfection with either the miR-181a mimic or si-CRY1, 24-h urinary protein, renal damage, GSI, and cell apoptosis rate were all decreased. In addition, the overexpression of miR-181a or inhibition of CRY1 alleviated the degree of kidney injury through suppression of the TLR/NF-κB pathway | ||
| 520 | |a CONCLUSION: miR-181a alleviates both GS and RTE injury in CKD via the down-regulation of the CRY1 gene and the TLR/NF-κB pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CRY1 gene | |
| 650 | 4 | |a Chronic kidney disease | |
| 650 | 4 | |a Glomerular sclerosis | |
| 650 | 4 | |a MicroRNA-181a | |
| 650 | 4 | |a Renal tubular epithelial injury | |
| 650 | 4 | |a The TLR/NF-κB pathway | |
| 650 | 7 | |a Cry1 protein, rat |2 NLM | |
| 650 | 7 | |a Cryptochromes |2 NLM | |
| 650 | 7 | |a MIRN181 microRNA, rat |2 NLM | |
| 650 | 7 | |a MicroRNAs |2 NLM | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a Tlr2 protein, rat |2 NLM | |
| 650 | 7 | |a Tlr4 protein, rat |2 NLM | |
| 650 | 7 | |a Toll-Like Receptor 2 |2 NLM | |
| 650 | 7 | |a Toll-Like Receptor 4 |2 NLM | |
| 700 | 1 | |a Pang, Xin-Lu |e verfasserin |4 aut | |
| 700 | 1 | |a Shang, Wen-Jun |e verfasserin |4 aut | |
| 700 | 1 | |a Xie, Hong-Chang |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jun-Xiang |e verfasserin |4 aut | |
| 700 | 1 | |a Feng, Gui-Wen |e verfasserin |4 aut | |
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