Effect of Simvastatin on Bone Marrow Mesenchymal Stem Cells in Osteoporosis Rats

2019 ◽  
Vol 9 (9) ◽  
pp. 1311-1316
Author(s):  
Yuechuang Liang ◽  
Liang Ma ◽  
Yu Wu ◽  
Youwei Tian ◽  
Dongyue Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Lipid Lowering ◽  
Control Group ◽  
Activity Increase ◽  
Promote Cell Proliferation ◽  
Alp Activity ◽  
The Difference

Osteoporosis (OP) is a common and frequently-occurring disease in orthopedics. BMSCs play a role in OP. Simvastatin (SVA) is a commonly used lipid-lowering drug, but its role in OP remains unclear. Our study intends to assess SVA’s effect on BMSCs in osteoporosis rats. SD rats were randomly and equally divided into control group and OP group. BMSCs in control group and OP group were cultured in vitro treated with 5 μM and 10 μM SVA followed by analysis of cell proliferation by MTT assay, apoptosis activity by Caspase 3 activity, Wnt5/TGF-β signaling pathway protein expression by Western blot, ALP activity; Runx2 and OC expression by Real time PCR as well as BMP-2 and TGF-β secretion by ELISA. OP rat BMSCs showed significantly inhibited cell proliferation, increased Caspase 3 activity, decreased Wnt5, Runx2 and OC expression and ALP activity, as well as reudced BMP-2 and TGF-β secretion (P < 0.05). SVA can promote cell proliferation, inhibit Caspase 3 activity, increase Wnt5, Runx2 and OC expression and ALP activity, as well as promote BMP-2 and TGF-β secretion in OP rat BMSCs. Compared with OP group, the difference was statistically significant with more significant changes with increasing concentration (P < 0.05). Simvastatin activates Wnt5/TGF-β signaling pathway, regulates BMSCs proliferation and apoptosis and promotes their differentiation into osteogenic direction in OP rats.

Effect of Silent Information Regulator on the Survival and Osteogenic Differentiation of Inflammatory Bone Marrow Mesenchymal Stem Cells by Regulating NF-κB Signaling Pathway

2020 ◽  
Vol 10 (1) ◽  
pp. 121-126
Author(s):  
Wenkun Lu ◽  
Tao Wang ◽  
Xunjian Gao ◽  
Fuqiang Yang ◽  
Jianjian Ge
Keyword(s):  
Cell Proliferation ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Adipogenic Differentiation ◽  
Control Group ◽  
Promote Cell Proliferation ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells ◽  
Inflammation Group

Osteogenic differentiation of BMSCs is beneficial for osteoarthritis (OA) treatment. Silent information regulator (SIRT1) plays a role in endocrine diseases and aging-related diseases. However, the role of SIRT1 in OA has not yet been elucidated. Rat BMSCs were isolated and divided into control group, inflammation group (BMSCs were cultured with IL-6), SIRT1 group (SIRT1 agonist Resveratrol was added under the action of IL-6) followed by analysis of cell proliferation by MTT assay, Caspase 3 activity, ALP activity, expression of osteogenic genes Runx2 and OC and adipogenic differentiation gene PPARγ2 by Real time PCR, NF-κB expression by western blot and secretion of TNF-α and IL-6 by ELISA. In inflammation group, SIRT1 expression was significantly decreased, cell proliferation was significantly inhibited, and Caspase 3 activity was increased. Meanwhile, ALP activity, Runx2 and OC expression was decreased, PPARγ2 and NF-κB expression was increased, along with elevated TNF-α and IL-6 secretion compared to control (P < 0.05). Resveratrol can significantly promote the expression of SIRT1 in BMSCs of inflammation group, promote cell proliferation, decrease Caspase 3 activity, and increase Runx2 and OC expression. In addition, it decreased PPARγ2 and NF-κB expression and reduced the secretion of TNF-α and IL-6 (P < 0.05). The expression of SIRT1 was decreased in BMSCs under inflammation. SIRT1 overexpression in BMSCs under inflammation inhibits inflammation, promotes proliferation and osteogenic differentiation of BMSCs through regulating NF-κB signaling pathway.

MiR-144-3p Regulates Lipopolysaccharide-Stimulated Chondrocyte Biological Behavior via Wingless-Related Integration Site/Beta-Catenin

2021 ◽  
Vol 11 (8) ◽  
pp. 1612-1617
Author(s):  
Nanxin Zhang ◽  
Kuangda Li ◽  
Qiong Han ◽  
Maohou Wu ◽  
Qiang Li
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Caspase 3 ◽  
Biological Behavior ◽  
Cartilage Tissue ◽  
Control Group ◽  
Beta Catenin ◽  
Activity Increase ◽  
Signaling Protein ◽  
Promote Cell Proliferation

Osteoarthritis (OA) gradually affects all joint tissues. Chondrocytes participate in osteoarthritis. However, the role and mechanism of MiR-144-3p on chondrocytes during the development of OA has not been elucidated. OA patients and normal bone and articular cartilage tissues were collected to measure MiR-144-3p level by Real-time PCR. Chondrocytes were divided into control group, LPS group (1 μg/ml lipopolysaccharide (LPS) was added to establish an osteoarthritis (OA) stimulation model, and MiR-144-3p inhibitor group which was transfected with MiR-144-3p inhibitor followed by analysis of cell proliferation by MTT, Caspase 3 activity, Wnt/β-catenin signaling protein expression by Western blot and TNF-α and IL-6 secretion by ELISA. MiR-144-3p was significantly upregulated in OA patients (P <0.05). In LPS group, MiR-144-3p was significantly upregulated, chondrocyte proliferation decreased, Caspase 3 activity increased, Wnt/β-catenin signaling protein decreased, and TNF-α and IL-6 secretion increased (P <0.05). MiR-144-3p inhibitor transfection can significantly down-regulate MiR-144-3p, promote cell proliferation, reduce Caspase 3 activity, increase Wnt/β-catenin signaling protein expression, and reduce TNF-α and IL-6 secretion (P <0.05). MiR-144-3p is upregulated in osteoarthritis cartilage tissue. Inhibition of MiR-144-3p can inhibit articular chondrocytes apoptosis under inflammatory condition, promote cell proliferation, and alleviate joint inflammation by regulating Wnt/β-catenin signaling pathway.

Effect of 25-Hydroxycholesterol on the Differentiation of Bone Marrow Mesenchymal Stem Cells Through Wnt5/TGF-β Signaling Pathway

2019 ◽  
Vol 9 (11) ◽  
pp. 1583-1588
Author(s):  
Shaoting Li ◽  
Jinhe Zhou ◽  
Zhiqing Ye ◽  
Shenglin Wu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Control Group ◽  
Nodule Formation ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) can be multi-directionally differentiated and are widely used in tissue engineering. 25-hydroxycholesterol (25-HC) can induce osteogenesis and is involved in osteogenic formation. However, the role of 25-hydroxycholesterol in BMSCs is unclear. Rat BMSCs were isolated and divided into control group and 25-HC treatment (2 and 4 μM) group. Cell proliferation was detected by MTT assay. Caspase-3 and ALP activity was analyzed. Real time PCR was done to analyze Runx2, OPN, FABP4 and PPARγ2 expression. Red staining detects the calcified nodule formation. Wnt5 level was detected by western blot and TGF-β secretion was analyzed by ELISA. 25-HC treatment significantly inhibited cell proliferation, increased Caspase 3 activity, decreased ALP activity and the expression of Runx2 and OPN, increased expression of FABP4 and PPARγ2, decreased formation of calcified nodules, secretion of TGF-β and reduced expression of Wnt5 compared to control group (P < 0.05), and the above changes were significant with the increase of the concentration of 25-HC (P < 0.05). 25-hydroxycholesterol regulates the proliferation and apoptosis of BMSCs by regulating Wnt5/TGF-β signaling pathway, inhibiting the differentiation of BMSCs into osteogenic direction and promoting its adipogenic differentiation.

Effect of LncRNA DGCR5 on Bone Marrow Mesenchymal Stem Cells of Osteoporosis Rats Through Regulation of ERK/P38 Signaling Pathway

2019 ◽  
Vol 9 (11) ◽  
pp. 1589-1594
Author(s):  
Xu Tong ◽  
Renjian Zheng ◽  
Linjing Shu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Control Group ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation plays an important role in Osteoporosis (OP). LncRNA DGCR5 participates in OP development. However, LncRNA DGCR5's effect on BMSCs in osteoporosis rats and related mechanisms have not been elucidated. SD rats were divided into control group and OP group. Rat BMSCs were cultured and transfected with LncRNA DGCR5 siRNA followed by analysis of LncRNA DGCR5 expression by Real time PCR, cell proliferation by MTT assay, Caspase 3 activity, of ERK/P38 signaling pathway protein expression by Western blot, ALP activity, and the osteogenic genes Runx2 and OC expression by Real time PCR. LncRNA DGCR51 expression was increased in BMSCs of OP rats. Compared with control group, cell proliferation was significantly inhibited, Caspase 3 activity was increased, p-ERK1/2 and p-P38 were downregulated, ALP activity, Runx2 and OC expression was decreased (P < 0.05). DGCR51 siRNA transfection into OP rat BMSCs significantly reduced DGCR51 expression, promoted cell proliferation, decreased Caspase 3 activity, increased p-ERK1/2 and p-P38 expression, increased ALP activity, Runx2 and OC expression compared to OP group (P < 0.05). LncRNA DGCR51 expression is increased in OP rat BMSCs. Down-regulation of LncRNA DGCR51 promoted the activation of ERK/P38 signaling pathway, thereby inhibiting the apoptosis of BMSCs and promoting proliferation and osteogenic differentiation of BMSC in OP rats.

Long Noncoding RNA Metastasis-Associated Lung Carcinoma Transcript 1 (MALAT1) Inhibits Bone Marrow Mesenchymal Stem Cell Formation Through Regulating Smad/Runx2 Signaling Pathway

2020 ◽  
Vol 10 (5) ◽  
pp. 730-736
Author(s):  
Qingyun Pan ◽  
Biao Dong ◽  
Yong He ◽  
Xiaohui Wang
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Control Group ◽  
Alp Activity ◽  
Lncrna Malat1 ◽  
Sirna Group

Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is controlled by elaborate genetic programs. lncRNA MALAT1 plays an important role in many diseases. However, the role of lncRNA MALAT1 in BMSCs remains unclear. Isolated Rat BMSCs were cultured and randomly divided into control group, MALAT1 group and MALAT1 siRNA group, in which lncRNA MALAT1 plasmid and lncRNA MALAT1 siRNA were transfected into BMSCs followed by analysis of lncRNA MALAT1 expression by real time PCR, cell proliferation by MTT assay, Caspase 3 activity, ALP activity was analyzed, calcified nodules by alizarin red staining, expression of Smad1 and Smad7 by Western blot as well as Runx2 expression by real time PCR. In MALAT1 group, MALAT1 expression was significantly increased along with significantly inhibited cell proliferation, increased Caspase 3 activity, decreased ALP activity and calcified nodules, reduced expression of Smad1, Smad7 and Runx2 compared with control group (P < 0 05). MALAT1 expression in MALAT1 siRNA group was decreased with significantly promoted cell proliferation, decreased Caspase 3 activity, increased ALP activity and calcified nodules, as well as significantly elevated expression of Smad1, Smad7 and Runx2 compared with control group (P < 0 05). Up-regulation of lncRNA MALAT1 expression inhibits the Smad/Runx2 signaling pathway, thereby inhibiting BMSCs proliferation and osteogenesis. Down-regulation of lncRNA MALAT1 expression promotes Smad/Runx2 signaling pathway activation, inhibits BMSCs apoptosis, promotes proliferation and osteogenic differentiation.

Effect of LncRNA Cancer Upregulated Drug Resistant (CUDR) on Osteoarthritis Chondrocyte Proliferation and Apoptosis by Regulating NF-κB Signaling Pathway

2020 ◽  
Vol 10 (12) ◽  
pp. 1871-1876
Author(s):  
Shaohua Liu ◽  
Guanming Zhou ◽  
Xicong Chen ◽  
Huiliang Zeng ◽  
Jian Cai
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Articular Chondrocytes ◽  
The Body ◽  
Cartilage Tissue ◽  
Control Group ◽  
Promote Cell Proliferation ◽  
Proliferation And Apoptosis ◽  
Oa Chondrocytes

Osteoarthritis (OA) is a common and frequently-occurring disorder in orthopedics. LncRNA CUDR involves in several physiological and pathological activities of the body. However, the role and mechanism of LncRNA CUDR in OA has not been elucidated. Cartilage tissue from OA patients and normal bone and joints were collected to detect LncRNA CUDR level by Real-time PCR. Chondrocytes from OA patients were isolated and divided into control group, LncRNA CUDR siRNA group, and LncRNA CUDR group followed by analysis of cell proliferation by MTT assay, Caspase 3 activity, NF-κB expression by Western blot, secretion of TNF-α and IL-6 by ELISA. LncRNA CUDR was significantly higher in OA patients than controls (P <0.05). LncRNA CUDR siRNA transfection into OA chondrocytes can significantly down-regulate LncRNA CUDR expression, promote cell proliferation, and reduce Caspase 3 activity, NF-κB level, as well as TNF-α and IL-6 secretion (P <0.05). Transfection of pcDNALncRNA CUDR plasmid into OA chondrocytes could up-regulate the expression of LncRNA CUDR and significantly reverse the above changes (P <0.05). LncRNA CUDR expression is increased in OA patients. Down-regulating LncRNA CUDR can inhibit the apoptosis and promote proliferation of articular chondrocytes and inhibit arthritis by down-regulating the NF-κB signaling pathway

scholarly journals HPV-18 E6 Oncoprotein and Its Spliced Isoform E6*I Regulate the Wnt/β-Catenin Cell Signaling Pathway through the TCF-4 Transcriptional Factor

2018 ◽  
Vol 19 (10) ◽  
pp. 3153 ◽  
Author(s):  
J. Muñoz-Bello ◽  
Leslie Olmedo-Nieva ◽  
Leonardo Castro-Muñoz ◽  
Joaquín Manzo-Merino ◽  
Adriana Contreras-Paredes ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Transcriptional Activation ◽  
Target Genes ◽  
Promote Cell Proliferation ◽  
E6 And E7 ◽  
Hpv 18

The Wnt/β-catenin signaling pathway regulates cell proliferation and differentiation and its aberrant activation in cervical cancer has been described. Persistent infection with high risk human papillomavirus (HR-HPV) is the most important factor for the development of this neoplasia, since E6 and E7 viral oncoproteins alter cellular processes, promoting cervical cancer development. A role of HPV-16 E6 in Wnt/β-catenin signaling has been proposed, although the participation of HPV-18 E6 has not been previously studied. The aim of this work was to investigate the participation of HPV-18 E6 and E6*I, in the regulation of the Wnt/β-catenin signaling pathway. Here, we show that E6 proteins up-regulate TCF-4 transcriptional activity and promote overexpression of Wnt target genes. In addition, it was demonstrated that E6 and E6*I bind to the TCF-4 (T cell factor 4) and β-catenin, impacting TCF-4 stabilization. We found that both E6 and E6*I proteins interact with the promoter of Sp5, in vitro and in vivo. Moreover, although differences in TCF-4 transcriptional activation were found among E6 intratype variants, no changes were observed in the levels of regulated genes. Furthermore, our data support that E6 proteins cooperate with β-catenin to promote cell proliferation.

Effect of SRY-Related High Mobility Group Box 9 on Extracellular Signal-Regulated Kinase/p38 Signaling Pathway in Glioma

2021 ◽  
Vol 11 (1) ◽  
pp. 171-175
Author(s):  
Tianlong Quan ◽  
Chunhua Zhang ◽  
Xin Song ◽  
Lu Wang
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Invasion ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
High Mobility ◽  
Negative Control ◽  
Glioma Cell Line ◽  
High Mobility Group ◽  
Control Group

As a common malignant tumor in neurosurgery, glioma is characterized as high incidence rate, easy to invade, metastasize and recurrent. It is difficult to treat and has a poor prognosis. The gliomas pathogenesis is complex and has not been fully resolved. Therefore, finding effective molecular targets for glioma is beneficial to improve therapeutic effect. The SRY-related high mobility group box 9 (SOX9) gene involves in mammalian development and is significantly increased in glioma. However, SOX9’s role in gliomas is unclear. The glioma cell line U87 was assigned into control group, scramble group that was transfected with siRNA negative control, and SOX9 siRNA group that was transfected with SOX9 siRNA followed by analysis of SOX9 mRNA and protein level by qPCR and Western blot, cell proliferation by MTT assay, cell apoptosis by Caspase 3 activity assay, cell invasion by Transwell assay, and MMP-9 level by ELISA. SOX9 siRNA transfection significantly downregulated SOX9 mRNA and protein expressions, inhibited U87 cell proliferation, enhanced Caspase 3 activity, suppressed cell invasion of U87, decreased the secretion of MMP-9 in the supernatant, and reduced ERK1/2 and P38 phosphorylation levels (P < 0.05). SOX9 can regulate the progression of glioma by regulating ERK/P38 signaling pathway, promoting cell apoptosis, inhibiting cell proliferation, and restraining cell invasion.

Effect of Tumor Growth Factor-β on Osteogenesis in Osteoporosis Rats by Regulating Bone Morphogenetic Protein Signaling Pathway

2020 ◽  
Vol 10 (12) ◽  
pp. 1884-1890
Author(s):  
Jing Tian ◽  
Qianying Zhao ◽  
Dapeng Zhou ◽  
Bing Xie
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Bmp Signaling ◽  
Control Group ◽  
Protein Signaling ◽  
Alp Activity ◽  
Tissue Repair And Regeneration ◽  
Tumor Growth Factor ◽  
Morphogenetic Protein ◽  
Proliferation And Differentiation

The balance of osteoblasts and osteoclasts is critical for bone formation and remodeling and imbalance causes osteoporosis (OP). TGF-β regulates bone tissue repair and regeneration, but TGF-β’s role in osteogenesis in OP has not been elucidated. OVX-induced OP rat models were constructed and rat BMSCs were isolated and assigned into control group, OP group, and TGF-β group (transfected with TGF-β1 plasmid followed by analysis of cell proliferation by MTT assay, RUNX2 and OPN expression by Real time PCR, ALP activity and secretion of TGF-β, BMP-2 and BMP-9 by ELISA. In addition, RANKL was added to induce BMSCs differentiation into to osteoclasts which were transfected with TGF-β1 followed by analysis of cell proliferation, c-Fos and TRAP expression and secretion of BMP-2 and BMP-9. OP group rats had significantly reduced secretion of TGF-β1, BMP-2 and BMP-9, reduced cell proliferation, decreased RUNX2 and OPN expression and ALP activity (P <0.05). Transfection of TGF-β1 in BMSCs of OP group rats could significantly reverse the above changes (P <0.05). TGF-β1 significantly inhibited osteoclast proliferation, decreased expression of c-Fos and TRAP, and increased secretion of BMP-2 and BMP-9 (P <0.05). TGF-β1 level in OP is decreased. Up-regulating TGF-β promotes osteoblast differentiation in OP rats by regulating BMP signaling pathway, and inhibits osteoclast proliferation and differentiation.

scholarly journals MiRNA-21 Regulates Bronchial Epithelial Cell Proliferation by Activating Tgfβ1/Smad Signaling Pathway and Its Correlation with Asthma Severity in Children

2021 ◽  
Author(s):  
Yang Kang ◽  
Minghui Bai ◽  
Liling Deng ◽  
Linbo Fan ◽  
Xing Wang
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Bronchial Epithelial Cell ◽  
Control Group ◽  
Healthy Children ◽  
Bronchial Epithelial ◽  
Smad Signaling ◽  
Smad Signaling Pathway ◽  
Tgf Β1

Background: This research was designed to probe into the role of miRNA-21 in the pathogenesis of childhood asthma and its correlation with the severity. Methods: Fifty-four children with bronchial asthma admitted to the Third Affiliated Hospital of Qiqihar Medical University from Jun 2018 to Dec 2019 were included. Forty nine healthy children underwent physical examination at this time period were also enrolled. The miR-21 expression in peripheral blood serum was analyzed by qRT-PCR. The relationship between the expression and severity of asthma in children was explored by Spearman correlation analysis and ROC curve. Bronchial epithelial cell lines were cultured in vitro and divided into blank control group, negative control group and miR-21 inhibition and activation group. The changes of cell proliferation after treatment were detected by CCK-8 test in different groups. The expression of TGF-β1/Smad signaling pathway protein in cells was assessed by Western blot (WB). Results: Compared with that of healthy children, the miR-21 expression in peripheral blood serum of asthmatic children was higher (P<0.001). MiR-21 expression was positively correlated with the severity of illness (r=0.853, P<0.001). The results of cell experiments in vitro signified that miR-21 can promote the proliferation of bronchial epithelial cells, and may be involved in regulating the expression of TGF-β1/ Smad3 signaling pathway, thus affecting cell proliferation. Conclusion: miRNA-21 regulates the proliferation of bronchial epithelial cells by activating TGFβ1/Smad signaling pathway. And it is positively correlated with the severity of asthma in children.

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