目的探讨血清骨膜蛋白(POSTN)、微小核糖核酸-15b(miR-15b)、Clara细胞分泌蛋白16(CC16)与新生儿支气管肺发育不良(BPD)的相关性。方法选取2022年1月至2024年1月保定市妇幼保健院收治的BPD早产儿186例为BPD组,同期非BPD早产儿186例为非...目的探讨血清骨膜蛋白(POSTN)、微小核糖核酸-15b(miR-15b)、Clara细胞分泌蛋白16(CC16)与新生儿支气管肺发育不良(BPD)的相关性。方法选取2022年1月至2024年1月保定市妇幼保健院收治的BPD早产儿186例为BPD组,同期非BPD早产儿186例为非BPD组,比较两组血清POSTN、miR-15b、CC16水平,基线资料,肺功能指标。Spearman分析BPD患儿血清POSTN、miR-15b、CC16与BPD的相关性。多因素Logistic回归分析BPD患儿的影响因素。结果BPD组血清POSTN、miR-15b高于非BPD组,CC16低于非BPD组,差异有统计学意义(P<0.05)。BPD组50%潮气量时呼气流速(50%TEF)、千克体重潮气量(VT/kg)、达峰容积比(VPEF/VE)低于非BPD组,差异有统计学意义(P<0.05)。Spearman相关性分析显示,POSTN、miR-15b与5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE呈负相关,POSTN与机械通气时间、吸氧时间、最高氧浓度呈正相关,miR-15b与呼吸窘迫综合征、机械通气时间、吸氧时间、最高氧浓度呈正相关;CC16与机械通气时间、吸氧时间、最高氧浓度呈负相关,与5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE呈正相关(P<0.05)。Logistic回归分析结果显示,呼吸窘迫综合征、机械通气时间、吸氧时间、最高氧浓度、POSTN、miR-15b是BPD患儿的危险因素,5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE、CC16是BPD患儿的保护因素(P<0.05)。结论BPD患儿血清POSTN、miR-15b升高,CC16降低,其水平变化与BPD发生密切相关。展开更多
目的通过系统评价和实验验证,探讨微小RNA(miR)-15b-3p与卵巢储备功能减退(DOR)发生发展的关系。方法计算机检索PubMed、Cochrane Library、Embase、Web of Science、万方、中国知网、中国生物医学文献数据库,获取各数据库建库至2024年1...目的通过系统评价和实验验证,探讨微小RNA(miR)-15b-3p与卵巢储备功能减退(DOR)发生发展的关系。方法计算机检索PubMed、Cochrane Library、Embase、Web of Science、万方、中国知网、中国生物医学文献数据库,获取各数据库建库至2024年11月27日miRNA与DOR相关文献,根据纳入与排除标准筛选文献后,对纳入文献进行数据提取及质量评价,通过汇总、筛选、分析获得与DOR发生相关的miRNA。随后选取2024年3月至2024年12月在佛山复星禅诚医院中医妇科就诊的DOR患者和正常卵巢储备功能(NOR)患者为研究对象,检测患者血浆miR-15b-3p表达水平。结果共获得miRNA与DOR相关文献1626篇,最终纳入文献8篇,共涉及研究对象125人,其中实验组共62人,对照组共63人。8篇纳入文献共涉及10个独立研究、5种样本类型,结果共鉴定出94个miRNA至少在两项实验中差异表达。纳入文献的纽卡斯尔-渥太华量表(NOS)平均得分7.75分。临床检测结果显示,14位DOR患者和35位NOR患者血浆样本比较,DOR组患者血浆miR-15b-3p表达水平明显降低(P<0.001)。结论miR-221-3p、miR-483-3p、miR-126-5p、miR-15b-3p、miR-140-3p等miRNA在不同地区、样本来源的DOR患者中均差异表达,其中miR-15b-3p与DOR的发生发展密切相关,可能成为DOR早期检测和靶向治疗的潜在靶点。展开更多
Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was...Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion （I/R） injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation （H/R）.Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo （24.4％ ± 9.4％ vs.2.2％ ± 1.9％,P ＜ 0.01,n =5） and in vitro （14.12％ ±0.92％ vs.2.22％ ± 0.08％）.The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.展开更多
AIM To determine whether cell division cycle(Cdc)42 is regulated by microRNA(miR)-15 a in the development of pediatric inflammatory bowel disease(IBD).METHODS We cultured 293 T cells, used plasmids and performed dual-...AIM To determine whether cell division cycle(Cdc)42 is regulated by microRNA(miR)-15 a in the development of pediatric inflammatory bowel disease(IBD).METHODS We cultured 293 T cells, used plasmids and performed dual-luciferase assay to determine whether Cdc42 is a miR-15 a target gene. We cultured Caco-2 cells, and stimulated them with tumor necrosis factor(TNF)-α. We then employed lentiviruses to alter the expression of miR-15 a and Cdc42. We performed quantitative reverse transcription polymerase chain reaction(qRTPCR) and immunofluorescence to determine whether Cdc42 is regulated by miR-15 a in Caco-2 cells. Finally, we collected ileocecal tissue by endoscopy from patients and performed qRT-PCR to examine the expression of miR-15 a and Cdc42 in pediatric IBD patients.RESULTS Target Scan and dual-luciferase assay revealed thatCdc42 was a miR-15 a target gene. MiR-15 a expression increased(P = 0.0038) and Cdc42 expression decreased(P = 0.0013) in cells stimulated with TNF-α, and the expression of the epithelial junction proteins zona occludens(ZO)-1(P < 0.05) and E-cadherin(P < 0.001) decreased. Cdc42 levels decreased in miR-15 a-mimic cells(P < 0.001) and increased in miR-15 a inhibitor cells(P < 0.05). ZO-1 and E-cadherin decreased in mi R-15 a-mimic cells(P < 0.001) but not in the miR-15 a inhibitor + TNF-α cells. In Lv-Cdc42 + TNF-α cells, ZO-1 and E-cadherin expression increased compared to the Lv-Cdc42-NC + TNF-α(P < 0.05) or miR-15 a-mimic cells(P < 0.05). Fifty-four pediatric IBD patients were included in this study, 21 in the control group, 19 in the Crohn's disease(CD) active(AC) group, seven in the CD remission(RE) group, and seven in the ulcerative colitis(UC) group. MiR-15 a increased and Cdc42 decreased in the CD AC group compared to the control group(P < 0.05). miR-15 a decreased and Cdc42 increased in the CD RE group compared to the CD AC group(P < 0.05). miR-15 a was positively correlated with the Pediatric Crohn's disease Activity Index(PCDAI)(P = 0.006), while Cdc42 was negatively correlated with PCDAI(P = 0.0008). Finally, miR-15 a expression negatively correlated with Cdc42 in pediatric IBD patients(P = 0.0045).CONCLUSION Mi R-15 a negatively regulates epithelial junctions through Cdc42 in Caco-2 cells and pediatric IBD patients.展开更多
文摘目的探讨血清骨膜蛋白(POSTN)、微小核糖核酸-15b(miR-15b)、Clara细胞分泌蛋白16(CC16)与新生儿支气管肺发育不良(BPD)的相关性。方法选取2022年1月至2024年1月保定市妇幼保健院收治的BPD早产儿186例为BPD组,同期非BPD早产儿186例为非BPD组,比较两组血清POSTN、miR-15b、CC16水平,基线资料,肺功能指标。Spearman分析BPD患儿血清POSTN、miR-15b、CC16与BPD的相关性。多因素Logistic回归分析BPD患儿的影响因素。结果BPD组血清POSTN、miR-15b高于非BPD组,CC16低于非BPD组,差异有统计学意义(P<0.05)。BPD组50%潮气量时呼气流速(50%TEF)、千克体重潮气量(VT/kg)、达峰容积比(VPEF/VE)低于非BPD组,差异有统计学意义(P<0.05)。Spearman相关性分析显示,POSTN、miR-15b与5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE呈负相关,POSTN与机械通气时间、吸氧时间、最高氧浓度呈正相关,miR-15b与呼吸窘迫综合征、机械通气时间、吸氧时间、最高氧浓度呈正相关;CC16与机械通气时间、吸氧时间、最高氧浓度呈负相关,与5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE呈正相关(P<0.05)。Logistic回归分析结果显示,呼吸窘迫综合征、机械通气时间、吸氧时间、最高氧浓度、POSTN、miR-15b是BPD患儿的危险因素,5 min Apgar评分、1,25-(OH)2D3、50%TEF、VT/kg、VPEF/VE、CC16是BPD患儿的保护因素(P<0.05)。结论BPD患儿血清POSTN、miR-15b升高,CC16降低,其水平变化与BPD发生密切相关。
文摘目的通过系统评价和实验验证,探讨微小RNA(miR)-15b-3p与卵巢储备功能减退(DOR)发生发展的关系。方法计算机检索PubMed、Cochrane Library、Embase、Web of Science、万方、中国知网、中国生物医学文献数据库,获取各数据库建库至2024年11月27日miRNA与DOR相关文献,根据纳入与排除标准筛选文献后,对纳入文献进行数据提取及质量评价,通过汇总、筛选、分析获得与DOR发生相关的miRNA。随后选取2024年3月至2024年12月在佛山复星禅诚医院中医妇科就诊的DOR患者和正常卵巢储备功能(NOR)患者为研究对象,检测患者血浆miR-15b-3p表达水平。结果共获得miRNA与DOR相关文献1626篇,最终纳入文献8篇,共涉及研究对象125人,其中实验组共62人,对照组共63人。8篇纳入文献共涉及10个独立研究、5种样本类型,结果共鉴定出94个miRNA至少在两项实验中差异表达。纳入文献的纽卡斯尔-渥太华量表(NOS)平均得分7.75分。临床检测结果显示,14位DOR患者和35位NOR患者血浆样本比较,DOR组患者血浆miR-15b-3p表达水平明显降低(P<0.001)。结论miR-221-3p、miR-483-3p、miR-126-5p、miR-15b-3p、miR-140-3p等miRNA在不同地区、样本来源的DOR患者中均差异表达,其中miR-15b-3p与DOR的发生发展密切相关,可能成为DOR早期检测和靶向治疗的潜在靶点。
文摘Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion （I/R） injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation （H/R）.Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo （24.4％ ± 9.4％ vs.2.2％ ± 1.9％,P ＜ 0.01,n =5） and in vitro （14.12％ ±0.92％ vs.2.22％ ± 0.08％）.The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.
基金Supported by the National Natural Science Foundation of Shanghai,No.201540068
文摘AIM To determine whether cell division cycle(Cdc)42 is regulated by microRNA(miR)-15 a in the development of pediatric inflammatory bowel disease(IBD).METHODS We cultured 293 T cells, used plasmids and performed dual-luciferase assay to determine whether Cdc42 is a miR-15 a target gene. We cultured Caco-2 cells, and stimulated them with tumor necrosis factor(TNF)-α. We then employed lentiviruses to alter the expression of miR-15 a and Cdc42. We performed quantitative reverse transcription polymerase chain reaction(qRTPCR) and immunofluorescence to determine whether Cdc42 is regulated by miR-15 a in Caco-2 cells. Finally, we collected ileocecal tissue by endoscopy from patients and performed qRT-PCR to examine the expression of miR-15 a and Cdc42 in pediatric IBD patients.RESULTS Target Scan and dual-luciferase assay revealed thatCdc42 was a miR-15 a target gene. MiR-15 a expression increased(P = 0.0038) and Cdc42 expression decreased(P = 0.0013) in cells stimulated with TNF-α, and the expression of the epithelial junction proteins zona occludens(ZO)-1(P < 0.05) and E-cadherin(P < 0.001) decreased. Cdc42 levels decreased in miR-15 a-mimic cells(P < 0.001) and increased in miR-15 a inhibitor cells(P < 0.05). ZO-1 and E-cadherin decreased in mi R-15 a-mimic cells(P < 0.001) but not in the miR-15 a inhibitor + TNF-α cells. In Lv-Cdc42 + TNF-α cells, ZO-1 and E-cadherin expression increased compared to the Lv-Cdc42-NC + TNF-α(P < 0.05) or miR-15 a-mimic cells(P < 0.05). Fifty-four pediatric IBD patients were included in this study, 21 in the control group, 19 in the Crohn's disease(CD) active(AC) group, seven in the CD remission(RE) group, and seven in the ulcerative colitis(UC) group. MiR-15 a increased and Cdc42 decreased in the CD AC group compared to the control group(P < 0.05). miR-15 a decreased and Cdc42 increased in the CD RE group compared to the CD AC group(P < 0.05). miR-15 a was positively correlated with the Pediatric Crohn's disease Activity Index(PCDAI)(P = 0.006), while Cdc42 was negatively correlated with PCDAI(P = 0.0008). Finally, miR-15 a expression negatively correlated with Cdc42 in pediatric IBD patients(P = 0.0045).CONCLUSION Mi R-15 a negatively regulates epithelial junctions through Cdc42 in Caco-2 cells and pediatric IBD patients.
文摘目的 探究新生儿早发型败血症(EONS)患者血清miR-16a,miR-15b水平表达与临床诊断及预后评估价值研究。方法 选取2020年10月~2023年10月首都医科大学附属北京儿童医院保定医院新生儿科收治的114例确诊为EONS患儿为EONS组,同期选择在该院体检健康的新生儿114例为对照组。对所有EONS患儿进行为期6个月的随访,其中预后不良组34例和预后良好组80例。入院当日6h内采取血清使用实时荧光定量PCR(qRT-PCR)检测miR-16a,miR-15b相对表达水平。受试者工作特征(ROC)曲线分析血清miR-16a,miR-15b对EONS的诊断以及预后评估价值。多因素Logistic回归分析影响EONS预后不良的因素。结果 与对照组相比,EONS组患儿出生时体质量(3.44±0.35kg/m^(2)vs 3.89±0.40kg/m^(2))显著降低,病理学黄疸(35/114 vs 1/114)发生率升高,差异具有统计学意义(t=9.040,χ2=35.922,均P<0.05)。与对照组相比,EONS组患儿血清miR-16a(1.15±0.16 vs 1.01±0.11),miR-15b(1.18±0.15 vs 1.02±0.13)水平显著升高,差异具有统计学意义(t=7.699,8.606,均P<0.05)。血清miR-16a,miR-15b联合诊断EONS的ROC曲线下面积(AUC)高于miR-16a,mi R-15b单独诊断,差异具有统计学意义(Z=2.619,2.157,均P<0.05)。与预后良好组相比,预后不良组出生时体质量显著降低,血清miR-16a,miR-15b水平显著升高,差异具有统计学意义(t=6.724,5.434,6.308,均P<0.05)。血清miR-16a,miR-15b二者联合对EONS预后评估的AUC高于miR-16a,miR-15b单独评估,差异具有统计学意义(Z=2.364,2.073,均P<0.05)。出生时体质量、miR-16a,miR-15b表达水平是EONS预后不良的影响因素(Wald χ^(2)=33.459,16.146,49.797,均P<0.05)。结论 EONS患儿血清中miR-16a,miR-15b呈高表达,二者对EONS有一定的诊断及预后评估价值。
