PDF(Pubmed)
Abstract：
UNASSIGNED: Mesenchymal stem cells can develop into osteoblasts, making them a promising cell-based osteoporosis treatment. Despite their therapeutic potential, their molecular processes are little known. Bioinformatics and experimental analysis were used to determine the molecular processes of bone marrow mesenchymal stem cell (BMSC) therapy for postmenopausal osteoporosis (PMO).
UNASSIGNED: We used weighted gene co-expression network analysis (WGCNA) to isolate core gene sets from two GEO microarray datasets (GSE7158 and GSE56815). GeneCards found PMO-related genes. GO, KEGG, Lasso regression, and ROC curve analysis refined our candidate genes. Using the GSE105145 dataset, we evaluated KLF2 expression in BMSCs and examined the link between KLF2 and PIK3CA using Pearson correlation analysis. We created a protein-protein interaction network of essential genes involved in osteoblast differentiation and validated the functional roles of KLF2 and PIK3CA in BMSC osteoblast differentiation in vitro.
UNASSIGNED: We created 6 co-expression modules from 10 419 differentially expressed genes (DEGs). PIK3CA, the key gene in the PI3K-Akt pathway, was among 197 PMO-associated DEGs. KLF2 also induced PIK3CA transcription in PMO. BMSCs also expressed elevated KLF2. BMSC osteoblast differentiation involved the PI3K-Akt pathway. In vitro, KLF2 increased PIK3CA transcription and activated the PI3K-Akt pathway to differentiate BMSCs into osteoblasts.
UNASSIGNED: BMSCs release KLF2, which stimulates the PIK3CA-dependent PI3K-Akt pathway to treat PMO. Our findings illuminates the involvement of KLF2 and the PI3K-Akt pathway in BMSC osteoblast development, which may lead to better PMO treatments.
UNASSIGNED: We used weighted gene co-expression network analysis (WGCNA) to isolate core gene sets from two GEO microarray datasets (GSE7158 and GSE56815). GeneCards found PMO-related genes. GO, KEGG, Lasso regression, and ROC curve analysis refined our candidate genes. Using the GSE105145 dataset, we evaluated KLF2 expression in BMSCs and examined the link between KLF2 and PIK3CA using Pearson correlation analysis. We created a protein-protein interaction network of essential genes involved in osteoblast differentiation and validated the functional roles of KLF2 and PIK3CA in BMSC osteoblast differentiation in vitro.
UNASSIGNED: We created 6 co-expression modules from 10 419 differentially expressed genes (DEGs). PIK3CA, the key gene in the PI3K-Akt pathway, was among 197 PMO-associated DEGs. KLF2 also induced PIK3CA transcription in PMO. BMSCs also expressed elevated KLF2. BMSC osteoblast differentiation involved the PI3K-Akt pathway. In vitro, KLF2 increased PIK3CA transcription and activated the PI3K-Akt pathway to differentiate BMSCs into osteoblasts.
UNASSIGNED: BMSCs release KLF2, which stimulates the PIK3CA-dependent PI3K-Akt pathway to treat PMO. Our findings illuminates the involvement of KLF2 and the PI3K-Akt pathway in BMSC osteoblast development, which may lead to better PMO treatments.
摘要：
■间充质干细胞可以发育成成骨细胞，使它们成为一种有前途的基于细胞的骨质疏松症治疗方法。尽管它们具有治疗潜力，它们的分子过程鲜为人知。生物信息学和实验分析用于确定骨髓间充质干细胞（BMSC）治疗绝经后骨质疏松症（PMO）的分子过程。
■我们使用加权基因共表达网络分析（WGCNA）从两个GEO微阵列数据集（GSE7158和GSE56815）中分离核心基因集。GeneCards发现了与PMO相关的基因。GO,KEGG,套索回归，和ROC曲线分析完善了我们的候选基因。使用GSE105145数据集，我们评估了BMSCs中KLF2的表达，并使用Pearson相关分析检查了KLF2和PIK3CA之间的联系。我们创建了参与成骨细胞分化的必需基因的蛋白质-蛋白质相互作用网络，并验证了KLF2和PIK3CA在体外BMSC成骨细胞分化中的功能作用。
■我们从10419个差异表达基因（DEGs）中创建了6个共表达模块。PIK3CA,PI3K-Akt通路的关键基因,是197个与PMO相关的DEG之一。KLF2还在PMO中诱导PIK3CA转录。BMSC还表达升高的KLF2。BMSC成骨细胞分化涉及PI3K-Akt途径。体外，KLF2增加PIK3CA转录并激活PI3K-Akt通路以将BMSCs分化为成骨细胞。
■BMSCs释放KLF2，刺激PIK3CA依赖性PI3K-Akt途径治疗PMO。我们的发现阐明了KLF2和PI3K-Akt通路在BMSC成骨细胞发育中的参与。这可能会导致更好的PMO治疗。
■我们使用加权基因共表达网络分析（WGCNA）从两个GEO微阵列数据集（GSE7158和GSE56815）中分离核心基因集。GeneCards发现了与PMO相关的基因。GO,KEGG,套索回归，和ROC曲线分析完善了我们的候选基因。使用GSE105145数据集，我们评估了BMSCs中KLF2的表达，并使用Pearson相关分析检查了KLF2和PIK3CA之间的联系。我们创建了参与成骨细胞分化的必需基因的蛋白质-蛋白质相互作用网络，并验证了KLF2和PIK3CA在体外BMSC成骨细胞分化中的功能作用。
■我们从10419个差异表达基因（DEGs）中创建了6个共表达模块。PIK3CA,PI3K-Akt通路的关键基因,是197个与PMO相关的DEG之一。KLF2还在PMO中诱导PIK3CA转录。BMSC还表达升高的KLF2。BMSC成骨细胞分化涉及PI3K-Akt途径。体外，KLF2增加PIK3CA转录并激活PI3K-Akt通路以将BMSCs分化为成骨细胞。
■BMSCs释放KLF2，刺激PIK3CA依赖性PI3K-Akt途径治疗PMO。我们的发现阐明了KLF2和PI3K-Akt通路在BMSC成骨细胞发育中的参与。这可能会导致更好的PMO治疗。
