Journal of cellular biochemistry
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MicroRNAs (miRNAs) are recognized as significant regulators of neuropathic pain. Moreover, neuroinflammation can contribute a lot to the progression of neuropathic pain. MiR-28-5p has been reported to be involved in many pathological diseases. ⋯ Theoverexpression of Zeb1 can disturb neuropathic pain development, which was repressed by the increase of miR-28-5p by upregulating Cox-2, IL-6, and IL-1β levels. By taking all of these together, it was indicated in our study that miR-28-5p can reduce neuropathic pain progression by targeting Zeb1 in vivo. Our data implied that miR-28-5p/Zeb1 axis can be a novel therapeutic target for neuropathic pain treatment.
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Retracted Publication
Baicalin prevents tumor necrosis factor-α-induced apoptosis and dysfunction of pancreatic β-cell line Min6 via upregulation of miR-205.
Baicalin (BAI), one major flavonoid from Scutellaria baicalensis, possesses anticancer and anti-inflammatory properties. However, the effect of BAI on diabetes mellitus has not been investigated. This study explored the antidiabetic effect of BAI on pancreatic β-cell line Min6. ⋯ Besides, the Min6 cell-protective effect of BAI was PI3K/AKT pathway and NF-κB pathway dependent. BAI activated the PI3K/AKT pathway and inhibited the NF-κB pathway by regulating miR-205. In conclusion, BAI protected Min6 cells from TNF-α-induced injury by upregulating miR-205, which acts, at least in part, via activation of the PI3K/AKT pathway and inactivation of the NF-κB pathway.
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Comparative Study
Functional comparison of high and low molecular weight basic fibroblast growth factors.
Acid-electrolyzed functional water (FW) is obtained through the electrolysis of sodium chloride solution. Stimulation of the human fibroblastic cell line HeLa by FW led to the augmented secretion of basic fibroblast growth factor (bFGF). Immunoprecipitation followed by Western blot analysis revealed that both high and low molecular weight isoforms of bFGF were secreted in response to FW treatment. ⋯ Stimulation of HeLa cells with these supernatants resulted in the augmented secretion of vascular endothelial growth factor (VEGF). To further confirm the functionality of these isoforms, an in vitro transcription/translation reaction was performed; both of the isoforms induced VEGF secretion from HeLa cells. Taken together, these results indicate that the high molecular weight 34-kDa isoform and low molecular weight 18-kDa mature bFGF isoform have identical roles in VEGF induction.
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Liver ischemia/reperfusion (I/R) injury has high mortality due to the intense inflammatory process occurs in the liver. However, the pathological mechanism underlying I/R injury is still not clear. Recent works showed that circular RNAs play critical roles in many human diseases. ⋯ To further validate bioinformatics data, two up-regulated and three down-regulated circular RNAs were confirmed in I/R models. The circularity of these differentially expressed circular RNAs was validated through gel electrophoresis and RNase R treatment. In summary, this work provides new insights into the mechanism underlying pathogenesis of liver I/R injury, providing new and potentially efficient targets against I/R injury.
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Pulmonary fibrosis (PF), characterized by the destruction of lung tissue architecture and the abnormal deposition of extracellular matrix (ECM) proteins, currently has no satisfactory treatment. The role of microRNA (miR)-21 in PF has been reported; the current study attempted to investigate a novel molecular mechanism by which miR-21 exerted its function. Consistent with previous studies, miR-21 inhibition reduced ECM protein levels in bleomycin (BLM)-induced mouse model of PF. ⋯ Regarding a novel molecular mechanism, TGFβ1 combined with TGFβ1 receptor 1 (TGFβ1RI) to activate SMAD2/3, promote SMAD4 nucleus transformation, and thus regulate miR-21 expression and ECM. SMAD3 and SMADs complex could bind to the promoter region of miR-21 to promote miR-21 expression. In conclusion, miR-21 exerts promotive effects on BLM-induced PF and TGFβ1-induced ECM in IMR-90; TGFβ1 combines with TGFβ1RI to activate SMAD2/3, promote SMAD4 nucleus transformation, promote miR-21 expression, and thus to promote BLM-induced PF and TGFβ1-induced ECM in IMR-90 cells.