ABSTRACT
OBJECTIVE: The long non-coding ribonucleic acid (lncRNA)-myocardial infarction associated transcript (MIAT) has been demonstrated to serve as a key regulator in various physiological and pathological processes. This study aims to explore whether lncRNA-MIAT regulates the expression of micro RNA (miR)-29a to affect kidney's injury in sepsis rats. MATERIALS AND METHODS: A total of 30 healthy male Sprague-Dawley (SD) rats were randomly divided into experimental group and control group. Rats in the experimental group were injected with lipopolysaccharide (LPS) through the tail vein to prepare the model of sepsis-induced kidney injury, while those in the control group with the equal volume of normal saline. After the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in rats were determined to ascertain successful modeling, fluorescence quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to measure the expression levels of the lncRNA-MIAT and miR-29a messenger RNAs (mRNAs) in renal tissues. The normal rat kidney epithelial (NRK-52E) cell line was cultured in vitro, and the model was established in vitro via LPS to study the influences of lncRNA-MIAT and miR-29a on the kidney injury in sepsis rats. Moreover, cell apoptosis was detected using Western blotting. RESULTS: According to the results of the rat in vivo experiment and NRK-52E cell line in vitro experiment, the model of kidney injury was established successfully, and compared with the control group, experiment group had significantly raised SCr and BUN levels (p<0.01) and a remarkably increased lincRNA-MIAT gene expression level (p<0.01), but a substantially decreased miR-29a gene expression level (p<0.01). Additionally, when the expression of lncRNA-MIAT was up-regulated, the expression of miR-29a was prominently decreased (p<0.01), but that of the cell apoptosis gene cysteine-aspartic proteases (Caspase)-8 protein was remarkably increased (p<0.01). However, the expression of Caspase-8 protein was significantly lowered (p<0.01) once the expression of miR-29a was up-regulated. CONCLUSIONS: LncRNA-MIAT may bind to miR-29a to participate in sepsis-related kidney injury.
Subject(s)
Acute Kidney Injury/metabolism , MicroRNAs/genetics , RNA, Long Noncoding/metabolism , Sepsis/metabolism , Acute Kidney Injury/chemically induced , Acute Kidney Injury/pathology , Animals , Apoptosis , Cells, Cultured , Disease Models, Animal , Injections, Intravenous , Lipopolysaccharides/administration & dosage , Male , MicroRNAs/analysis , MicroRNAs/metabolism , RNA, Long Noncoding/genetics , Rats , Rats, Sprague-Dawley , Sepsis/chemically induced , Sepsis/pathologyABSTRACT
OBJECTIVE: To investigate the influences of micro ribonucleic acid (miR)-205 on renal injury in sepsis rats through the high-mobility group box 1 (HMGB1)-phosphatase and tensin homolog deleted on chromosome ten (PTEN) signaling pathway. MATERIALS AND METHODS: A rat model of sepsis-induced renal injury was established by cecal ligation and perforation. The rats were randomly divided into 3 groups, namely the Sham group, the Model group, and the miR-205 group. Hematoxylin and eosin (HE) staining was applied to examine the pathological renal morphology. The enzyme-linked immunosorbent assay (ELISA) was adopted to measure the serum levels of Caspase-3 and Bcl-2-associated X protein (Bax) in rats. Cell apoptosis rate in the renal tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Finally, the protein levels of phosphorylate-HMGB1 (p-HMGB1) and p-PTEN in the renal tissues were determined using the Western blotting (WB) assay. RESULTS: Compared with those in the Sham group, the pathological morphology of the renal tissues was poor in Model group. The serum levels of Caspase-3 and Bax, the apoptosis rate, and the protein levels of p-HMGB1 and p-PTEN were remarkably enhanced in the Model group compared to the Sham group. In comparison with those in Model group, the pathological changes in renal morphology, apoptosis-related indexes, and protein levels of p-HMGB1 and p-PTEN were alleviated in the miR-205 group. CONCLUSIONS: MiR-205 agonist can improve the pathological morphology in the sepsis rats with renal injury, improve renal cell apoptosis, and inhibit the protein levels of HMGB1 and PTEN in renal tissues. MiR-205 alleviates sepsis-induced renal injury through the HMGB1-PTEN signaling pathway.
Subject(s)
Acute Kidney Injury/metabolism , HMGB1 Protein/metabolism , MicroRNAs/metabolism , PTEN Phosphohydrolase/metabolism , Sepsis/metabolism , Signal Transduction , Acute Kidney Injury/pathology , Animals , Apoptosis , Cell Proliferation , Disease Models, Animal , HMGB1 Protein/analysis , Male , PTEN Phosphohydrolase/analysis , Phosphorylation , Rats , Rats, Sprague-Dawley , Sepsis/pathologyABSTRACT
In this work, we measured the time evolution of the transmission features of 10-100 keV protons transmitted through nanocapillaries in a polycarbonate (PC) membrane. After reaching equilibrium, transmitted particles with an incident energy of 100 keV were located around the direction along the incident beam but not along the capillary axis, indicating that the transport mechanism of the 100 keV ion was distinct from that of keV-energy ions. The simulation results indicated that charge-patch-assisted collective scatterings on the surface are the main transport mechanism for the hundred-keV ions in nanocapillaries. This scenario fills in the gap in the previous understanding of ion transmission in nanocapillaries from keV to MeV energies.
