Spinal cord injury (SCI) is a neurological disease commonly caused by traumatic events on spinal cords. MiRNA-92a-3p is reported to be down-regulated after SCI. Our study investigated the effects of up-regulated miR-92a-3p on SCI and the underlying mechanisms. SCI mice model was established to evaluate the functional recovery of hindlimbs of mice through open-field locomotion and scored by Basso, Beattie, and Bresnahan (BBB) locomotion scale. Apoptosis of spinal cord cells was determined by flow cytometry. The effects of miR-92a-3p on SCI were detected by intrathecally injecting miR-92a-3p agomiR (agomiR-92) into the mice prior to the establishment of SCI. Phosphatase and tensin homolog (PTEN) was predicted as a target of miR-29a-3p by TargetScan. We further assessed the effects of agomiR-92 or/and overexpressed PTEN on apoptosis rates and apoptotic protein expressions in SCI mice. Moreover, the activation of protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling was determined by Western blot. The results showed that compared with the sham-operated mice, SCI mice had much lower BBB scores, and theapoptosis rate of spinal cord cells was significantly increased. After SCI, the expression of miR-92a-3p was down-regulated, and increased expression of miR-92a-3p induced by agomiR-92 further significantly increased the BBB score and decreased apoptosis. PTEN was specifically targeted by miR-92a-3p. In addition, the phosphorylation levels of Akt and mTOR were up-regulated under the treatment of agomiR-92. Our data demonstrated that the neuroprotective effects of miR-92a-3p on spinal cord safter SCI were highly associated with the activation of the PTEN/AKT/mTOR pathway.
Objective Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction in OA chondrocytes induced by interleukin-1β (IL-1β). Methods The quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II, and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The expressions of aggrecan and collagen II in the chondrocyte were detected by Western blot. The levels of tumor necrosis factor–α (TNF-α), IL-8, IL-6, MMP-13, MMP-9, MMP-3, and prostaglandin E2 (PGE2) in chondrocyte were determined by enzyme-linked immunosorbernt assay. Bioinformatics, dual luciferin gene reporting, RNA pulldown, and Northern blot were used to determine the interaction between LINC01534 and miR-140-5p. Results The results showed that LINC01534 was upregulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly downregulated the expression of matrix metalloproteinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also significantly inhibited the productions of proinflammatory factors NO, PGE2, TNF-α, IL-6, and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was confirmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion Therefore, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.
SummaryParagonimus proliferus (P. proliferus), one of 46 Paragonimus species registered in the National Center for Biotechnology Information database, may be much more widely distributed in Southeast Asia than previously thought, as its reported natural foci have increased in the past decades. However, very little is known about its molecular biology, especially at the transcriptome level. For the first time, the transcriptome of this species was sequenced and compared with four other common Paragonimus species, namely Paragonimus skrjabini, Paragonimus kellicotti, Paragonimus miyazakii, and Paragonimus westermani, to predict homologous genes and differentially expressed homologous genes to explore interspecies differences of Paragonimus proliferus.A total of 7393 genes were found to be significantly differentially expressed. Of these, 49 were considered to be core genes because they were differentially expressed in all four comparison groups. Annotations revealed that these genes were related mainly to “duplication, transcription, or translation”, energy or nutrient metabolism, and parasitic growth, proliferation, motility, invasion, adaptation to the host, or virulence. Interestingly, a majority (5601/7393) of the identified genes, and in particular the core genes (48/49), were expressed at lower levels in P. proliferus. The identified genes may play essential roles in the biological differences between Paragonimus species. This work provides fundamental background information for further research into the molecular biology of P. proliferus.
Backgrounds: Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction and inflammation in OA chondro-cytes induced by IL-1β. Methods: The quantitative Real-Time PCR (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The ex-pressions of aggrecan and collagen II in the chondrocyte were detected by Western Blot. The levels of TNF-α, IL-8, IL-6, MMP-13, MMP-9, MMP-3 and prostaglandin E2 (PGE2) in chondrocyte were determined by ELISA. Bioinformatics, dual luciferin gene reporting, RNA pulldown and Northern Blot were used to determine the interac-tion between LINC01534 and miR-140-5p. Results: The results showed that LINC01534 was up-regulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly down-regulated the expression of matrix metallopro-teinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also sig-nificantly inhibited the productions of pro-inflammatory factors NO, PGE2, TNF-α, IL-6 and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was con-firmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on inflammation and abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion: Therefor, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.
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