The Experts below are selected from a list of 10992 Experts worldwide ranked by ideXlab platform
Yin Ding - One of the best experts on this subject based on the ideXlab platform.
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tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter mir 21 in Estrogen Deficiency induced osteoporosis
Journal of Bone and Mineral Research, 2013Co-Authors: Nan Yang, Xi Wang, Li Liao, Guang Wang, Shuli Cheng, Chenghu Hu, Liang Tang, Yin DingAbstract:Inflammatory cytokines, especially tumor necrosis factor α (TNF-α), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in Estrogen Deficiency–induced osteoporosis, but the mechanism responsible remains poorly understood. MicroRNAs (miRNAs) have been shown to regulate MSC differentiation. Here, we identified a novel mechanism whereby TNF-α, suppressing the functional axis of a key miRNA (miR-21) contributes to Estrogen Deficiency–induced osteoporosis. In this study, we screened differentially expressed miRNAs in MSCs derived from Estrogen Deficiency-induced osteoporosis and found miR-21 was significantly downregulated. miR-21 was suppressed by TNF-α during the osteogenesis of MSCs. Furthermore, miR-21 was confirmed to promote the osteoblast differentiation of MSCs by repressing Spry1, which can negatively regulate the osteogenic differentiation of MSCs. Upregulating miR-21 partially rescued TNF-α–impaired osteogenesis of MSCs. Blocking TNF-α ameliorated the inflammatory environment and significantly enhanced bone formation with increased miR-21 expression and suppressed Spry1 expression in ovariectomized (OVX) mice. Our results revealed a novel function for miR-21 and suggested that suppressed miR-21 may contribute to impaired bone formation by elevated TNF-α in Estrogen Deficiency–induced osteoporosis. This study may indicate a molecular basis for novel therapeutic strategies against osteoporosis and other inflammatory bone diseases. © 2013 American Society for Bone and Mineral Research.
Yaya Zheng - One of the best experts on this subject based on the ideXlab platform.
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gc tof ms based metabolomic profiling of Estrogen Deficiency induced obesity in ovariectomized rats
Acta Pharmacologica Sinica, 2011Co-Authors: Qi Zhang, Guangji Wang, Ying Liu, Bei Cao, Linsheng Liu, Yonglu Wang, A Jiye, Yaya ZhengAbstract:To explore the alteration of endogenous metabolites and identify potential biomarkers using metabolomic profiling with gas chromatography coupled a time-of-flight mass analyzer (GC/TOF-MS) in a rat model of Estrogen-Deficiency-induced obesity. Twelve female Sprague-Dawley rats six month of age were either sham-operated or ovariectomized (OVX). Rat blood was collected, and serum was analyzed for biomarkers using standard colorimetric methods with commercial assay kits and a metabolomic approach with GC/TOF-MS. The data were analyzed using multivariate statistical techniques. A high body weight and body mass index inversely correlated with serum estradiol (E2) in the OVX rats compared to the sham rats. Estrogen Deficiency also significantly increased serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Utilizing GC/TOF-MS-based metabolomic analysis and the partial least-squares discriminant analysis, the OVX samples were discriminated from the shams. Elevated levels of cholesterol, glycerol, glucose, arachidonic acid, glutamic acid, glycine, and cystine and reduced alanine levels were observed. Serum glucose metabolism, energy metabolism, lipid metabolism, and amino acid metabolism were involved in Estrogen-Deficiency-induced obesity in OVX rats. The series of potential biomarkers identified in the present study provided fingerprints of rat metabolomic changes during obesity and an overview of multiple metabolic pathways during the progression of obesity involving glucose metabolism, lipid metabolism, and amino acid metabolism.
Nan Yang - One of the best experts on this subject based on the ideXlab platform.
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tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter mir 21 in Estrogen Deficiency induced osteoporosis
Journal of Bone and Mineral Research, 2013Co-Authors: Nan Yang, Xi Wang, Li Liao, Guang Wang, Shuli Cheng, Chenghu Hu, Liang Tang, Yin DingAbstract:Inflammatory cytokines, especially tumor necrosis factor α (TNF-α), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in Estrogen Deficiency–induced osteoporosis, but the mechanism responsible remains poorly understood. MicroRNAs (miRNAs) have been shown to regulate MSC differentiation. Here, we identified a novel mechanism whereby TNF-α, suppressing the functional axis of a key miRNA (miR-21) contributes to Estrogen Deficiency–induced osteoporosis. In this study, we screened differentially expressed miRNAs in MSCs derived from Estrogen Deficiency-induced osteoporosis and found miR-21 was significantly downregulated. miR-21 was suppressed by TNF-α during the osteogenesis of MSCs. Furthermore, miR-21 was confirmed to promote the osteoblast differentiation of MSCs by repressing Spry1, which can negatively regulate the osteogenic differentiation of MSCs. Upregulating miR-21 partially rescued TNF-α–impaired osteogenesis of MSCs. Blocking TNF-α ameliorated the inflammatory environment and significantly enhanced bone formation with increased miR-21 expression and suppressed Spry1 expression in ovariectomized (OVX) mice. Our results revealed a novel function for miR-21 and suggested that suppressed miR-21 may contribute to impaired bone formation by elevated TNF-α in Estrogen Deficiency–induced osteoporosis. This study may indicate a molecular basis for novel therapeutic strategies against osteoporosis and other inflammatory bone diseases. © 2013 American Society for Bone and Mineral Research.
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Tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter miR-21 in Estrogen Deficiency-induced osteoporosis.
Journal of Bone and Mineral Research, 2013Co-Authors: Nan Yang, Xi Wang, Li Liao, Guang Wang, Yuanyuan Shi, Songtao Shi, Yan Cai, Shuli Cheng, Yali LiuAbstract:Inflammatory cytokines, especially tumor necrosis factor α (TNF-α), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in Estrogen Deficiency-induced osteoporosis, but the mechanism responsible remains poorly understood. MicroRNAs (miRNAs) have been shown to regulate MSC differentiation. Here, we identified a novel mechanism whereby TNF-α, suppressing the functional axis of a key miRNA (miR-21) contributes to Estrogen Deficiency-induced osteoporosis. In this study, we screened differentially expressed miRNAs in MSCs derived from Estrogen Deficiency-induced osteoporosis and found miR-21 was significantly downregulated. miR-21 was suppressed by TNF-α during the osteogenesis of MSCs. Furthermore, miR-21 was confirmed to promote the osteoblast differentiation of MSCs by repressing Spry1, which can negatively regulate the osteogenic differentiation of MSCs. Upregulating miR-21 partially rescued TNF-α-impaired osteogenesis of MSCs. Blocking TNF-α ameliorated the inflammatory environment and significantly enhanced bone formation with increased miR-21 expression and suppressed Spry1 expression in ovariectomized (OVX) mice. Our results revealed a novel function for miR-21 and suggested that suppressed miR-21 may contribute to impaired bone formation by elevated TNF-α in Estrogen Deficiency-induced osteoporosis. This study may indicate a molecular basis for novel therapeutic strategies against osteoporosis and other inflammatory bone diseases.
Qi Zhang - One of the best experts on this subject based on the ideXlab platform.
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GC-TOF/MS-based metabolomic profiling of Estrogen Deficiency-induced obesity in ovariectomized rats
Acta Pharmacologica Sinica, 2011Co-Authors: Qi Zhang, Guangji Wang, Jiye A, Ying Liu, Bei Cao, Linsheng Liu, Yonglu WangAbstract:To explore the alteration of endogenous metabolites and identify potential biomarkers using metabolomic profiling with gas chromatography coupled a time-of-flight mass analyzer (GC/TOF-MS) in a rat model of Estrogen-Deficiency-induced obesity. Twelve female Sprague-Dawley rats six month of age were either sham-operated or ovariectomized (OVX). Rat blood was collected, and serum was analyzed for biomarkers using standard colorimetric methods with commercial assay kits and a metabolomic approach with GC/TOF-MS. The data were analyzed using multivariate statistical techniques. A high body weight and body mass index inversely correlated with serum estradiol (E2) in the OVX rats compared to the sham rats. Estrogen Deficiency also significantly increased serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Utilizing GC/TOF-MS-based metabolomic analysis and the partial least-squares discriminant analysis, the OVX samples were discriminated from the shams. Elevated levels of cholesterol, glycerol, glucose, arachidonic acid, glutamic acid, glycine, and cystine and reduced alanine levels were observed. Serum glucose metabolism, energy metabolism, lipid metabolism, and amino acid metabolism were involved in Estrogen-Deficiency-induced obesity in OVX rats. The series of potential biomarkers identified in the present study provided fingerprints of rat metabolomic changes during obesity and an overview of multiple metabolic pathways during the progression of obesity involving glucose metabolism, lipid metabolism, and amino acid metabolism.
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gc tof ms based metabolomic profiling of Estrogen Deficiency induced obesity in ovariectomized rats
Acta Pharmacologica Sinica, 2011Co-Authors: Qi Zhang, Guangji Wang, Ying Liu, Bei Cao, Linsheng Liu, Yonglu Wang, A Jiye, Yaya ZhengAbstract:To explore the alteration of endogenous metabolites and identify potential biomarkers using metabolomic profiling with gas chromatography coupled a time-of-flight mass analyzer (GC/TOF-MS) in a rat model of Estrogen-Deficiency-induced obesity. Twelve female Sprague-Dawley rats six month of age were either sham-operated or ovariectomized (OVX). Rat blood was collected, and serum was analyzed for biomarkers using standard colorimetric methods with commercial assay kits and a metabolomic approach with GC/TOF-MS. The data were analyzed using multivariate statistical techniques. A high body weight and body mass index inversely correlated with serum estradiol (E2) in the OVX rats compared to the sham rats. Estrogen Deficiency also significantly increased serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol. Utilizing GC/TOF-MS-based metabolomic analysis and the partial least-squares discriminant analysis, the OVX samples were discriminated from the shams. Elevated levels of cholesterol, glycerol, glucose, arachidonic acid, glutamic acid, glycine, and cystine and reduced alanine levels were observed. Serum glucose metabolism, energy metabolism, lipid metabolism, and amino acid metabolism were involved in Estrogen-Deficiency-induced obesity in OVX rats. The series of potential biomarkers identified in the present study provided fingerprints of rat metabolomic changes during obesity and an overview of multiple metabolic pathways during the progression of obesity involving glucose metabolism, lipid metabolism, and amino acid metabolism.
Evan R Simpson - One of the best experts on this subject based on the ideXlab platform.
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Estrogen Deficiency reversibly induces telomere shortening in mouse granulosa cells and ovarian aging in vivo.
Protein & Cell, 2011Co-Authors: Sharyn Leanne Bayne, Margaret Ee Jones, Alex R Pinto, Evan R Simpson, Michelle Van Sinderen, Ann E. Drummond, Jun-ping LiuAbstract:Estrogen is implicated as playing an important role in aging and tumorigenesis of Estrogen responsive tissues; however the mechanisms underlying the mitogenic actions of Estrogen are not fully understood. Here we report that Estrogen Deficiency in mice caused by targeted disruption of the aromatase gene results in a significant inhibition of telomerase maintenance of telomeres in mouse ovaries in a tissue-specific manner. The inhibition entails a significant shortening of telomeres and compromised proliferation in the follicular granulosa cell compartment of ovary. Gene expression analysis showed decreased levels of proto-oncogene c-Myc and the telomerase catalytic subunit, telomerase reverse transcriptase (TERT), in response to Estrogen Deficiency. Estrogen replacement therapy led to increases in TERT gene expression, telomerase activity, telomere length and ovarian tissue growth, thereby reinstating ovary development to normal in four weeks. Our data demonstrate for the first time that telomere maintenance is the primary mechanism mediating the mitogenic effect of Estrogen on ovarian granulosa cell proliferation by upregulating the genes of c-Myc and TERT in vivo. Estrogen Deficiency or over-activity may cause ovarian tissue aging or tumorigenesis, respectively, through Estrogen regulation of telomere remodeling.
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Estrogen Deficiency leads to telomerase inhibition, telomere shortening and reduced cell proliferation in the adrenal gland of mice
Cell Research, 2008Co-Authors: Sharyn Bayne, Margaret Ee Jones, He Li, Alex R Pinto, Evan R SimpsonAbstract:Estrogen Deficiency mediates aging, but the underlying mechanism remains to be fully determined. We report here that Estrogen Deficiency caused by targeted disruption of aromatase in mice results in significant inhibition of telomerase activity in the adrenal gland in vivo . Gene expression analysis showed that, in the absence of Estrogen, telomerase reverse transcriptase (TERT) gene expression is reduced in association with compromised cell proliferation in the adrenal gland cortex and adrenal atrophy. Stem cells positive in c-kit are identified to populate in the parenchyma of adrenal cortex. Analysis of telomeres revealed that Estrogen Deficiency results in significantly shorter telomeres in the adrenal cortex than that in wild-type (WT) control mice. To further establish the causal effects of Estrogen, we conducted an Estrogen replacement therapy in these Estrogen-deficient animals. Administration of Estrogen for 3 weeks restores TERT gene expression, telomerase activity and cell proliferation in Estrogen-deficient mice. Thus, our data show for the first time that Estrogen Deficiency causes inhibitions of TERT gene expression, telomerase activity, telomere maintenance, and cell proliferation in the adrenal gland of mice in vivo , suggesting that telomerase inhibition and telomere shortening may mediate cell proliferation arrest in the adrenal gland, thus contributing to Estrogen Deficiency-induced aging under physiological conditions.