Main conclusion The molecular mechanism underlying white petal color in Brassica napus was revealed by transcriptomic and metabolomic analyses. Abstract Rapeseed (Brassica napus L.) is one of the most important oilseed crops worldwide, but the mechanisms underlying flower color in this crop are known less. Here, we performed metabolomic and transcriptomic analyses of the yellow-flowered rapeseed cultivar ‘Zhongshuang 11’ (ZS11) and the white-flowered inbred line ‘White Petal’ (WP). The total carotenoid contents were 1.778-fold and 1.969-fold higher in ZS11 vs. WP petals at stages S2 and S4, respectively. Our findings suggest that white petal color in WP flowers is primarily due to decreased lutein and zeaxanthin contents. Transcriptome analysis revealed 10,116 differentially expressed genes with a fourfold or greater change in expression (P-value less than 0.001) in WP vs. ZS11 petals, including 1,209 genes that were differentially expressed at four different stages and 20 genes in the carotenoid metabolism pathway. BnNCED4b, encoding a protein involved in carotenoid degradation, was expressed at abnormally high levels in WP petals, suggesting it might play a key role in white petal formation. The results of qRT-PCR were consistent with the transcriptome data. The results of this study provide important insights into the molecular mechanisms of the carotenoid metabolic pathway in rapeseed petals, and the candidate genes identified in this study provide a resource for the creation of new B. napus germplasms with different petal colors.
Carotenoid cleavage dioxygenase (CCD), a key enzyme in carotenoid metabolism, cleaves carotenoids to form apo-carotenoids, which play a major role in plant growth and stress responses. CCD genes had not previously been systematically characterized in Brassica napus (rapeseed), an important oil crop worldwide. In this study, we identified 30 BnCCD genes and classified them into nine subgroups based on a phylogenetic analysis. We identified the chromosomal locations, gene structures, and cis-promoter elements of each of these genes and performed a selection pressure analysis to identify residues under selection. Furthermore, we determined the subcellular localization, physicochemical properties, and conserved protein motifs of the encoded proteins. All the CCD proteins contained a retinal pigment epithelial membrane protein (RPE65) domain. qRT-PCR analysis of expression of 20 representative BnCCD genes in 16 tissues of the B. napus cultivar Zhong Shuang 11 ('ZS11') revealed that members of the BnCCD gene family possess a broad range of expression patterns. This work lays the foundation for functional studies of the BnCCD gene family.
Vascular smooth muscle cell (VSMC) hyperproliferation is the main pathological process in various cardiovascular diseases, such as vascular restenosis. This process may be repressed by RING finger protein 10 (RNF10) in metabolic syndrome (MetS) rats. The aim of this study is to evaluate the inhibitory effects and molecular mechanisms of RNF10 on VSMC hyperproliferation. Neointimal hyperplasia in MetS and high‐glucose‐induced VSMC hyperproliferation were measured after infection with adenoviruses encoding RNF10 (Ad‐RNF10), short hairpin RNF10 (Ad‐shRNF10), or green fluorescent protein (Ad‐GFP). In vivo and in vitro, we found that overexpression of RNF10 significantly affected neointima formation and VSMC proliferation, and displayed further inhibitory activity by promoting mesenchyme homeobox 2 (Meox2) and suppressing activating protein 1 (AP‐1). In contrast, Ad‐shRNF10 had an opposite effect on neointimal hyperplasia and VSMC hyperproliferation in vivo and in vitro. Our study indicated that RNF10 inhibited the hyperproliferation with the activities of Meox2 and AP‐1 proteins. RNF10 may be a next drug target for treating vascular restenosis and other related cardiovascular diseases. © 2018 IUBMB Life, 71(5):632–642, 2019
Background: Postoperative atrial fibrillation (POAF) occurs commonly after cardiac surgery. Studies suggest that corticosteroid can reduce the incident of POAF. However, the results remain controversial. This meta-analysis aimed to evaluate the efficacy and safety corticosteroid on the prevention of POAF following cardiac surgery. Methods: Randomized controlled trials were identified through a systematic literature search. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. Primary outcome was the incidence of POAF as well as length of hospital stay and intensive care unit stay, wound and other infection, mortality, duration of ventilation, myocardial infarction, gastrointestinal complications, high blood sugar, stroke, and postoperative bleeding. Results: Fourteen studies with 13,803 patients were finally involved in the present study. Overall, corticosteroid significantly decreased the risk of POAF (relative risk [RR], 0.7; 95% confidence interval [CI], 0.55–0.89; P = .003). There were no significant differences in the incidence of length of intensive care unit stay (RR, −2.32; 95% CI, −5.44 to 0.80; P = .14) and hospital stay (RR, −0.43; 95% CI, −0.84 to −0.02; P = .04), infections (RR, 1.01; 95% CI, 0.83–1.23; P = .9), mortality (RR, 0.87; 95% CI, 0.71–1.06; P = .16), duration of ventilation (RR, −0.29; 95% CI, −0.65 to 0.07; P = .12), gastrointestinal complications (RR, 1.26; 95% CI, 0.91–1.76; P = .16), high blood sugar (RR, 1.98; 95% CI, 0.91–4.31; P = .09), stroke (RR, 0.9; 95% CI, 0.69–1.18; P = .45), postoperative bleeding (RR −44.54; 95% CI, −115.28 to 26.20; P = .22) and myocardial infarction (RR, 1.71; 95% CI, 0.96–1.43; P = .12). Conclusion: Our review suggests that the efficacy of corticosteroid might be beneficial to POAF development in patients undergoing cardiac surgery. The strength of this association remains uncertain because of statistical and clinical heterogeneity among the included studies.
Background The age‐related trends in the predictive ability of carotid intima‐media thickness (CIMT) for cardiovascular risk remain unclear. We aimed to identify the age‐related trends in the predictive value of CIMT for cardiovascular death. Methods and Results In a prospective cohort of adults aged 35 to 75 years without history of cardiovascular disease who were enrolled between 2014 and 2020, we measured CIMT at baseline and collected the vital status and cause of death. We divided the study population into 4 age groups (35–44, 45–54, 55–64, and 65–75 years). Competing risk models were fitted to estimate the associations between CIMT and cardiovascular death. The added values of CIMT in prediction were assessed by the differences of the Harrell's concordance index and the net reclassification improvement index. We included 369 478 adults and followed them for a median of 4.7 years. A total of 4723 (1.28%) cardiovascular deaths occurred. After adjusting for the traditional risk factors, the hazard ratios for CIMT mean per SD decreased with age, from 1.27 (95% CI, 1.17–1.37) in the 35 to 44 years age group to 1.14 (95% CI, 1.10–1.19) in the 65 to 75 years age group ( P for interaction <0.01). Meanwhile, the net reclassification improvement indexes for CIMT mean were attenuated with age, from 22.60% (95% CI, 15.56%–29.64%) in the 35 to 44 years age group to 7.00% (95% CI, −6.82% to 20.83%) in the 65 to 75 years age group. Similar results were found for maximum CIMT in all age groups. Conclusions CIMT may improve cardiovascular risk prediction in the young and middle‐aged populations, rather than those aged ≥55 years.
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