Background Undernutrition disrupts pregnant ewe's metabolic homeostasis and severely inhibits fetal growth and development.In this study,undernourished and nutrition-recovery pregnant sheep models and rumen epithe...Background Undernutrition disrupts pregnant ewe's metabolic homeostasis and severely inhibits fetal growth and development.In this study,undernourished and nutrition-recovery pregnant sheep models and rumen epithelial cells were utilized to investigate the mechanisms behind undernutrition-induced disruptions in male fetal rumen metabolism and development.Results Maternal undernutrition significantly reduced male fetal rumen weight and papilla length,width and surface area.Maternal undernutrition extremely suppressed nutrient metabolism and energy production in male fetal rumen via JAK3/STAT3 signaling to inhibit cell cycle progression and male fetal rumen development,while maternal nutritional recovery partially restored metabolic inhibition but failed to alleviate male fetal rumen development.Meanwhile,64 differentially expressed miRNAs(DEMs)were identified in male fetal rumen between undernourished ewes and controls.Novel miR-736 was overexpressed both in male fetal rumen of undernourished and nutrition-recovery models.E2F transcription factor 2(E2F2)and MYB proto-oncogene like 2(MYBL2)were the intersection of male fetal rumen differentially expressed genes(DEGs)and DEMs target genes integrated analysis and were predicted as novel miR-736 target genes.Further,we confirmed that novel miR-736 targeted and downregulated E2F2 and MYBL2 expression levels.Silencing E2F2 and MYBL2 promoted apoptosis and inhibited S-phase entry in rumen epithelial cells.Conclusions In summary,maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736,which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis,finally inhibited male fetal rumen development.This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.展开更多
目的研究linc00346和E2F2在肝癌中表达特征以及对肝癌患者预后的影响。方法从癌症基因组图集(the cancer genome atlas,TCGA)下载肝癌表达谱数据,肝癌与癌旁组织中linc00346和E2F2表达差异分析采用配对t检验,肝癌组织linc00346和E2F2共...目的研究linc00346和E2F2在肝癌中表达特征以及对肝癌患者预后的影响。方法从癌症基因组图集(the cancer genome atlas,TCGA)下载肝癌表达谱数据,肝癌与癌旁组织中linc00346和E2F2表达差异分析采用配对t检验,肝癌组织linc00346和E2F2共表达分析采用Pearson相关,linc00346和E2F2对患者预后分析采用Log-Rank检验以及Cox回归。结果肝癌组织中linc00346和E2F2表达水平分别是癌旁组织的2.24倍和3.72倍,差异均有统计学意义(均有P<0.05)。linc00346和E2F2存在共表达关系,相关系数r为0.20(P<0.001)。单因素Cox回归发现linc00346和E2F2高表达组患者死亡风险分别是低表达患者的1.77倍(95%CI:1.23~2.55)和2.19倍(95%CI:1.51~3.17)。多重Cox回归结果显示E2F2表达能够影响肝癌患者的预后。结论 linc00346和E2F2在肝癌组织中高表达,肝癌患者linc00346和E2F2高表达其预后效果差,这为探索抗肿瘤治疗提供一个新的潜在靶点,具有重要的临床意义。展开更多
目的探讨E2F转录因子2(E2F2)和多配体蛋白聚糖-4(SDC4)对急性胰腺炎患者病情评估及预后诊断的价值。方法将2018年4月至2020年4月西安市中心医院收治的45例轻症急性胰腺炎患者作为轻症组,56例重症急性胰腺炎患者为重症组;将同期20名来我...目的探讨E2F转录因子2(E2F2)和多配体蛋白聚糖-4(SDC4)对急性胰腺炎患者病情评估及预后诊断的价值。方法将2018年4月至2020年4月西安市中心医院收治的45例轻症急性胰腺炎患者作为轻症组,56例重症急性胰腺炎患者为重症组;将同期20名来我院进行健康体检者作为对照组。比较各组研究对象的一般资料及临床特征;比较三组研究对象的E2F2、SDC4 m RNA和蛋白表达水平;分析E2F2、SDC4表达水平与急性胰腺炎患者JPN评分的相关性;分析血清SDC4、E2F2水平和JPN评分对急性胰腺炎的诊断价值。结果轻症组和重症组的腹痛、恶心呕吐发生率无明显差异(P>0.05);重症组的腹胀、全身性并发症发生率高于轻症组(P<0.05);轻症组和重症组的血清淀粉酶、脂肪酶、降钙素原、乳酸脱氢酶(LDH)以及C反应蛋白(CRP)水平高于对照组(P<0.01);重症组的血清淀粉酶、脂肪酶、降钙素原、LDH、CRP水平及JPN评分高于轻症组(P<0.01)。轻症组和重症组的E2F2、SDC4 m RNA和蛋白表达水平显著高于对照组,且重症组高于轻症组(P<0.05)。E2F2和SDC4表达水平与急性胰腺炎患者JPN评分呈正相关(P<0.001);E2F2表达水平与SDC4表达水平呈正相关(P<0.001)。血清E2F2和SDC4水平对急性胰腺炎的诊断价值较高,与JPN评分相似。结论E2F2和SDC4可作为评估急性胰腺炎患者发病及预后的潜在指标。展开更多
基金supported by the National Natural Science Foundation of China(32402767)National Key Research and Development Program of China(2022YFD1301102)+3 种基金Anhui Province Natural Science Foundation Youth Project(2308085QC104)AAU Introduction of High-level Talent Funds(RC392107)Key Laboratory of Utilization of Livestock and Forage Resources in Circum-Tarim Region(Co-construction by Ministry and Province),Ministry of Agriculture and Rural Affairs(BSGJSYS202502)the China Agriculture Research System(CARS-38)。
文摘Background Undernutrition disrupts pregnant ewe's metabolic homeostasis and severely inhibits fetal growth and development.In this study,undernourished and nutrition-recovery pregnant sheep models and rumen epithelial cells were utilized to investigate the mechanisms behind undernutrition-induced disruptions in male fetal rumen metabolism and development.Results Maternal undernutrition significantly reduced male fetal rumen weight and papilla length,width and surface area.Maternal undernutrition extremely suppressed nutrient metabolism and energy production in male fetal rumen via JAK3/STAT3 signaling to inhibit cell cycle progression and male fetal rumen development,while maternal nutritional recovery partially restored metabolic inhibition but failed to alleviate male fetal rumen development.Meanwhile,64 differentially expressed miRNAs(DEMs)were identified in male fetal rumen between undernourished ewes and controls.Novel miR-736 was overexpressed both in male fetal rumen of undernourished and nutrition-recovery models.E2F transcription factor 2(E2F2)and MYB proto-oncogene like 2(MYBL2)were the intersection of male fetal rumen differentially expressed genes(DEGs)and DEMs target genes integrated analysis and were predicted as novel miR-736 target genes.Further,we confirmed that novel miR-736 targeted and downregulated E2F2 and MYBL2 expression levels.Silencing E2F2 and MYBL2 promoted apoptosis and inhibited S-phase entry in rumen epithelial cells.Conclusions In summary,maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736,which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis,finally inhibited male fetal rumen development.This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.
文摘目的:探究血清补体C1q/肿瘤坏死因子相关蛋白l(complement C1q/tumor necrosis factor-related protein 1,CTRP1)、E2F转录因子2(E2F transcription factor 2,E2F2)、C反应蛋白(C-reaction protein,CRP)水平与急性胰腺炎患者病情程度及预后的相关性。方法:急性胰腺炎患者95例,根据病情分为轻度组61例和重度组34例,以同期健康体检者95例为对照组。比较上述3组及不同预后患者血清CTRP1、E2F2、CRP水平、急性生理学与慢性健康状况评分系统Ⅱ(acute physiology and chronic health evaluation,APACHEⅡ)评分,分析血清CTRP1、E2F2、CRP水平与患者病情程度、预后及APACHEⅡ评分的相关性,血清CTRP1、E2F2、CRP水平对重度急性胰腺炎的诊断价值。结果:重度组血清CTRP1、E2F2、CRP水平及APACHEⅡ评分高于轻度组、对照组,轻度组高于对照组(均P<0.05)。预后不良患者血清CTRP1、E2F2、CRP水平高于预后良好患者(均P<0.001)。血清CTRP1、E2F2、CRP水平与急性胰腺炎患者病情程度、预后及APACHEⅡ评分呈正相关(P<0.001)。血清CTRP1、E2F2、CRP水平联合检测诊断重度急性胰腺炎算曲线下面积(area under curve,AUC)为0.843,敏感度为79.41%,特异度为80.33%,优于CTRP1、E2F2、CRP单项检测。结论:血清CTRP1、E2F2、CRP水平与急性胰腺炎患者病情程度及预后关系密切,联合检测对病情评估及预后预测具有一定价值。
文摘目的研究linc00346和E2F2在肝癌中表达特征以及对肝癌患者预后的影响。方法从癌症基因组图集(the cancer genome atlas,TCGA)下载肝癌表达谱数据,肝癌与癌旁组织中linc00346和E2F2表达差异分析采用配对t检验,肝癌组织linc00346和E2F2共表达分析采用Pearson相关,linc00346和E2F2对患者预后分析采用Log-Rank检验以及Cox回归。结果肝癌组织中linc00346和E2F2表达水平分别是癌旁组织的2.24倍和3.72倍,差异均有统计学意义(均有P<0.05)。linc00346和E2F2存在共表达关系,相关系数r为0.20(P<0.001)。单因素Cox回归发现linc00346和E2F2高表达组患者死亡风险分别是低表达患者的1.77倍(95%CI:1.23~2.55)和2.19倍(95%CI:1.51~3.17)。多重Cox回归结果显示E2F2表达能够影响肝癌患者的预后。结论 linc00346和E2F2在肝癌组织中高表达,肝癌患者linc00346和E2F2高表达其预后效果差,这为探索抗肿瘤治疗提供一个新的潜在靶点,具有重要的临床意义。
文摘目的探讨E2F转录因子2(E2F2)和多配体蛋白聚糖-4(SDC4)对急性胰腺炎患者病情评估及预后诊断的价值。方法将2018年4月至2020年4月西安市中心医院收治的45例轻症急性胰腺炎患者作为轻症组,56例重症急性胰腺炎患者为重症组;将同期20名来我院进行健康体检者作为对照组。比较各组研究对象的一般资料及临床特征;比较三组研究对象的E2F2、SDC4 m RNA和蛋白表达水平;分析E2F2、SDC4表达水平与急性胰腺炎患者JPN评分的相关性;分析血清SDC4、E2F2水平和JPN评分对急性胰腺炎的诊断价值。结果轻症组和重症组的腹痛、恶心呕吐发生率无明显差异(P>0.05);重症组的腹胀、全身性并发症发生率高于轻症组(P<0.05);轻症组和重症组的血清淀粉酶、脂肪酶、降钙素原、乳酸脱氢酶(LDH)以及C反应蛋白(CRP)水平高于对照组(P<0.01);重症组的血清淀粉酶、脂肪酶、降钙素原、LDH、CRP水平及JPN评分高于轻症组(P<0.01)。轻症组和重症组的E2F2、SDC4 m RNA和蛋白表达水平显著高于对照组,且重症组高于轻症组(P<0.05)。E2F2和SDC4表达水平与急性胰腺炎患者JPN评分呈正相关(P<0.001);E2F2表达水平与SDC4表达水平呈正相关(P<0.001)。血清E2F2和SDC4水平对急性胰腺炎的诊断价值较高,与JPN评分相似。结论E2F2和SDC4可作为评估急性胰腺炎患者发病及预后的潜在指标。
