Function and potential mechanism of microvesicles (MVs) containing microRNA34a in renal interstitial fibrosis were investigated. A rat model of renal interstitial fibrosis was established by unilateral ureteral ligation (UUO). Rat proximal tubular epithelial cell line (NRK-52E) was used to explore the effect of MVs containing microRNA-34a on tubular epithelial cells during fibrosis, which were secreted by tubulointerstitial fibroblasts. Regardless of the UUO renal interstitial fibrosis model, or the TGF-β1-treated renal tubular epithelial cells, microRNA-34a was increased in the MVs secreted by tubulointerstitial fibroblasts. miR-34a could be transmitted through the damaged tubule basement membrane to proximal tubular epithelial cells, where it induced apoptosis of renal tubular epithelial cells by inhibiting the expression of Bcl-2, further aggravating renal interstitial fibrosis. MicroRNA-34a secreted by damaged renal interstitial fibroblasts can promote renal tubular epithelial cell apoptosis and participate in renal interstitial fibrosis by inhibiting Bcl-2.
Radiation therapy has been widely used for the treatment of various types of cancer; however, it may cause neuroinflammation during the pathological process of the disease. Astrocytes, the most abundant cell type in the central nervous system, have been confirmed to play vital roles in various diseases. Connexin (Cx)43, the main Cx type in astrocytes, which has been identified as a direct target gene of microRNA (miR)-206, was found to be involved in diseases pathologies in regions with astrocytes. The aim of the present study was to investigate the mechanism through which γ-radiation may cause astrocyte neuroinflammation and determine the specific mechanism underlying the effects of miR-206 in irradiation-induced HA-1800 cells. A dual-luciferase reporter system was used to predict and verify the target binding site between Cx43 and miR-206. HA-1800 cell viability and apoptosis were determined using a MTT assay and flow cytometry, respectively. In addition, the HA-1800 cells were induced by γ-radiation, then the protein and mRNA expression levels of Cx43, miR-206 and cleaved-caspase-3 were determined using western blot and reverse transcription-quantitative PCR analyses, respectively. ELISA was also performed to evaluate the concentrations of different inflammatory cytokines (TNF-α, IL-β, IL-6 and IFN-γ). The dual-luciferase reporter system indicated that Cx43 was a direct target of miR-206. miR-206 mimics increased the expression level of miR-206 in the astrocytes. Irradiation suppressed cell proliferation, increased apoptotic cells and enhanced cleaved-caspase-3 expression and inflammatory cytokines secretion in astrocytes. Furthermore, miR-206 was found to be downregulated and its expression was inversely associated with that of Cx43 in γ-radiation-induced astrocytes.Overexpression of miR-206 enhanced miR-206 and suppressed Cx43 expression, while Cx43 was upregulated in HA-1800 cells transfected with miR-206 mimic + Cx43-plasmid. However, the expression level of miR-206 was not significantly different in the Cx43-plasmid transfected group. In addition, it was found that miR-206 mimics relieved irradiation-induced neuroinflammation, which was confirmed by increased cell viability, and reduced cell apoptosis and cleaved caspase-3 protein expression, as well as decreased inflammatory cytokine secretion. Furthermore, all the effects of miR-206 mimics on γ-radiation-induced astrocytes were reversed by Cx43-plasmid. In summary, the results of the present study indicated that miR-206 may relieve irradiation-induced neural damage by regulating Cx43, which may provide a novel research direction and a potential therapeutic target for the clinical treatment of inflammation-associated neuronal injury following irradiation.
Background: Early diagnosis and timely treatment are crucial for breast cancer patients. Objectives: This study aimed to investigate the diagnostic value of full-field digital mammography (FFDM), digital breast tomosynthesis (DBT), and magnetic resonance imaging (MRI) for breast cancer. Patients and Methods: This study was performed on 210 patients diagnosed with breast cancer and benign breast lesions (n = 105) by FFDM, DBT, MRI, and pathological examination from January 2019 to December 2020. The patients’ imaging and clinical data were retrospectively analyzed. The lesions were evaluated according to the breast imaging-reporting and data system, with pathological diagnosis as the gold standard. The diagnostic efficiency of the examination methods was analyzed by plotting the receiver operating characteristic (ROC) curves. The DBT and MRI results were finally compared. Results: In 210 patients, 105 benign and 105 malignant lesions were detected. The area under the ROC curve (AUC) of FFDM, DBT, MRI, FFDM + DBT, and FFDM + MRI was 0.734, 0.857, 0.883, 0.865, and 0.924, respectively. Based on the results, the AUC values were significantly higher for DBT, MRI, FFDM + DBT, and FFDM + MRI compared to FFDM (P < 0.05), while similar values were reported for the former methods (P > 0.05). The diagnostic sensitivity of MRI was higher than that of DBT and FFDM; the sensitivity of DBT was higher than that of FFDM; and the specificity and positive predictive value were higher for DBT compared to MRI and FFDM. Conclusion: Compared to FFDM, DBT and FFDM + DBT could significantly improve the diagnostic efficiency of breast cancer; the diagnostic efficiency of these modalities was comparable to that of MRI and FFDM + MRI. The sensitivity of DBT was lower than that of MRI and higher than that of FFDM, while its specificity and positive predictive value were higher than those of MRI. Overall, FFDM + DBT and FFDM + MRI are conducive to early diagnosis.
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