Long noncoding RNA MANTIS relieved the protein-bound uremic toxin-induced injury on human umbilical vein endothelial cells in chronic kidney disease and end-stage renal disease
Jiang J., Zheng D., Li Y., Liu G., Zhou H., Liu Y.
Prospective Study on Chronic Kidney Disease, published in Int J Clin Exp Pathol (2018) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Int J Clin Exp Pathol (2018)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31949698
- PMCID
- PMC6962863
- Citations
- 6
Abstract (original English)
This study aimed to explore the role of long, noncoding RNA MANTIS in regulating the protein-bound, uremic toxin-induced injury on human umbilical vein endothelial cells (HUVECs) in chronic kidney disease (CKD) and end-stage renal disease (ESRD). The MANTIS expression in patients with normal kidney function, stage 3 CKD, stage 4 CKD and ESRD was detected. In addition, HUVECs were stimulated with various concentrations of HSA-bound P-cresol (20, 40 and 80 μg/ml) and then transfected with pcDNA-MANTIS, sh-MANTIS and their controls to further investigate the effects of MANTIS overexpression and knockdown on HSA-bound P-cresol-induced HUVECs injury. Furthermore, the regulatory relationships between MANTIS and Sox18, as well as between MANTIS and p38 MAPK or p65 NF-κB pathways were elucidated. MANTIS expression was down-regulated in patients with CKD and ESRD and might be associated with disease severity. In addition, HSA-bound P-cresol induced HUVECs injury and decreased MANTIS expression. Overexpression of MANTIS relieved HSA-bound P-cresol induced HUVECs injury by increasing HUVECs viability, migration and invasion, and inhibiting cell autophagy. Moreover, the effects of MANTIS on HSA-bound P-cresol induced HUVECs injury were through positive regulation of Sox18. Besides, MANTIS overexpression markedly inhibited the activation of p38 MAPK and p65 NF-κB pathways in HSA-bound P-cre
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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