Winter rapeseed is susceptible to low temperature during winter in Northwest China, which could lead to a severe reduction of crop production. The freezing temperature could stress the whole plant, especially the leaf, and ultimately harm the survival rate of winter rapeseed. However, the molecular mechanism underlying freezing tolerance is still unclear in winter rapeseed. In this study, a comprehensive investigation of winter rapeseed freezing tolerance was conducted at the levels of transcript, protein, and physiology and biochemistry, using a pair of freezing-sensitive and freezing-resistant cultivars NQF24 and 17NTS57. There were 4,319 unique differentially expressed genes (DEGs) and 137 unique differentially abundant proteins (DAPs) between two cultivars identified in leaf under freezing stress. Function enrichment analysis showed that most of the enriched DEGs and DAPs were involved in plant hormone signal transduction, alpha-linolenic/linoleic acid metabolism, peroxisome, glutathione metabolism, fatty acid degradation, and secondary metabolite biosynthesis pathways. Based on our findings, it was speculated that freezing tolerance formation is caused by increased signal transduction, enhanced biosynthesis of protein, secondary metabolites, and plant hormones, elevated energy supply, greater reactive oxygen species scavenging, and lower lipid peroxidation as well as stronger cell stability in leaf under freezing stress. These results provide a comprehensive profile of leaf response under freezing stress, which have potential to be used as selection indicators of breeding programs to improve freezing tolerance in rapeseed.

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Two winter rapeseed cultivars, “NS” (cold tolerant) and “NF” (cold sensitive), were used to reveal the morphological, physiological, and proteomic characteristics in leaves of plants after treatment at -4°C for 12 h(T1) and 24 h(T2), and at room temperature(T0), to understand the molecular mechanisms of cold tolerance. Antioxidant activity and osmotic adjustment ability were higher, and plasma membrane injury was less obvious, in NS than in NF under cold stress. We detected different abundant proteins (DAPs) related to cold tolerance in winter rapeseed through data-independent acquisition (DIA). Compared with NF, A total of 1,235 and 1,543 DAPs were identified in the NSs under T1 and T2, respectively. Compared with NF, 911 proteins were more abundant in NS only after cold treatment. Some of these proteins were related to ROS scavenging through four metabolic pathways: lysine degradation; phenylalanine, tyrosine, and tryptophan; flavonoid biosynthesis; and ubiquinone and other terpenoid-quinone biosynthesis. Analysis of these proteins in the four candidate pathways revealed that they were rapidly accumulated to quickly enhance ROS scavenging and improve the cold tolerance of NS. These proteins were noticeably more abundant during the early stage of cold stress, which was critical for avoiding ROS damage.

Atherosclerosis (AS) is a cardiovascular disease caused by multiple factors, leading to high mortality and morbidity in aged people. Some long noncoding RNAs have been reported to be associated with AS progression. However, the roles of OIP5-AS1 in AS development are still little known. In this study, the levels of OIP5-AS1 and miR-26a-5p in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs) were determined by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 assay and flow cytometric analysis, respectively. The protein levels of proliferating cell nuclear antigen, B-cell lymphoma-2, cleaved caspase 3, inflammatory cytokines (IL-6 and IL-1β), protein kinase B (AKT), p-AKT, p65, p-p65, IκBα, and p-IκBα were detected by Western blot analysis. The targeting relationship between OIP5-AS1 and miR-26a-5p was verified by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. As a result, the expression of OIP5-AS1 was upregulated and miR-26a-5p was downregulated in ox-LDL–treated HUVECs. MiR-26a-5p was identified as a direct target of OIP5-AS1. OIP5-AS1 knockdown reversed the inhibitory effect on cell proliferation and the promotional effects on apoptosis and inflammation induced by ox-LDL treatment in HUVECs. Interestingly, the effects caused by OIP5-AS1 knockdown were further attenuated by miR-26a-5p inhibition. Furthermore, OIP5-AS1 knockdown blocked the AKT/NF-κB pathway by regulating miR-26a-5p expression. In conclusion, OIP5-AS1 knockdown promoted cell proliferation and suppressed apoptosis and inflammatory response in ox-LDL–treated HUVECs by targeting miR-26a-5p through blocking the AKT/NF-κB pathway, indicating a promising strategy for AS treatment.