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

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 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 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.

scholarly journals Midkine Promotes the Proliferation of Airway Smooth Muscle Cells Induced by LPS Through Notch2 Pathway

2021 ◽  
Author(s):  
Qi Feng Huang ◽  
Tang Deng ◽  
Lihua Li ◽  
Jin Qian ◽  
Qi Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Airway Smooth Muscle ◽  
Airway Remodeling ◽  
Muscle Cells ◽  
Control Group ◽  
Airway Smooth Muscle Cells ◽  
Proliferation And Apoptosis

Abstract Background: Airway smooth muscle cells (ASMC) can produce a variety of cytokine during inflammation, causing changes in the components of the extracellular matrix, which are related to airway remodeling. Midkine (MK) can promote the chemotaxis of various inflammatory cells and release inflammatory factors. Whether Notch and Midkine together affect the proliferation and apoptosis of airway smooth muscle cells is unclear.Objective: To study the mechanism of Midkine on LPS-induced acute lung injury caused by airway smooth muscle cells.Methods: Airway smooth muscle cells were cultured in vitro and divided into 5 groups: control group, lipopolysaccharide group (LPS), Non-targeted siRNA group, MKsiRNA group, Notch inhibitor group (LY411575). The cell proliferation level was detected by CCK-8. The apoptosis level was detected by flow cytometry. The changes of cytokine in the Midkine/Notch2 signaling pathway were detected by Westernblot, qPCR and cellular immunofluorescence.Results: Midkine and Notch2 were highly expressed in the LPS group. MKsiRNA can effectively block the expression of Midkine induced by LPS while down-regulating the expression of Notch2. This result is the same as that of Notch inhibitor (LY411575). Exogenous Midkine promoted the proliferation of airway smooth muscle cells and reduced the rate of apoptosis in the LPS group. When the expression of Midkine was blocked, the proliferation of airway smooth muscle cells in the LPS group was significantly reduced, while apoptosis increased. Inhibiting the expression of Notch, the proliferation of airway smooth muscle cells in the LPS group decreased, and apoptosis increased.Conclusions: Midkine/Notch2 signaling pathway plays an important role in regulating airway smooth muscle cell proliferation and apoptosis in airway inflammation.

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.

scholarly journals Midazolam Inhibits the Apoptosis of Astrocytes Induced by Oxygen Glucose Deprivation via Targeting JAK2-STAT3 Signaling Pathway

2015 ◽  
Vol 35 (1) ◽  
pp. 126-136 ◽  
Author(s):  
Li Liu ◽  
Qi You ◽  
Yingfeng Tu ◽  
Quanyi Li ◽  
Lihong Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Caspase 3 ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Control Group ◽  
Protective Effects ◽  
Intrinsic Bioremediation ◽  
Proliferation And Apoptosis ◽  
Astrocytes Proliferation ◽  
Apoptotic Effects

Background: There is an increasing interest in the role of astrocytes contributing to the intrinsic bioremediation of ischemic brain injury. The purpose of this study was to disclose the effects and mechanism of midazolam (MDZ) on the proliferation and apoptosis of astrocytes under oxygen glucose deprivation (OGD) condition. Methods: The astrocytes were assigned randomly into four groups: control group, OGD group, OGD+MDZ group, and OGD+MDZ+IL-6 group. The astrocytes were treated with MDZ at dose of 10 μmol/L in OGD+MDZ group. And in OGD+MDZ+IL-6 group, the astrocytes were treated with MDZ at dose of 10μmol/L and IL-6 at dose of 50 ng/mL. MTT assay was used to assess cell proliferation, and cell apoptosis was analyzed by TUNEL apoptosis assay kit and flow cytometry. Furthermore, the expression of JAK2, p-JAK2, STAT3, p-STAT3, Bcl-2, Bax and Caspase-3 proteins were determined by western blotting assay. Results: Astrocytes proliferation was decreased obviously in OGD group, while MDZ could increase astrocytes proliferation under OGD condition. Moreover, OGD could induce apoptosis in astrocytes and MDZ could play an anti-apoptotic role. However, IL-6, a JAK2 activator, could attenuate cell proliferation and anti-apoptotic effects of MDZ in astrocytes. In addition, the expression of Bcl-2 protein in MDZ group increased markedly, while the JAK2/STAT3 signal proteins, Bax and Caspase-3 proteins decreased relative to OGD group. But IL-6 could counteract the anti-apoptotic effects of MDZ. Conclusion: Midazolam has protective effects on the proliferation and apoptosis of astrocytes via JAK2/STAT3 signal pathway in vitro. We firstly disclose the beneficial roles of midazolam in astrocytes under ischemic condition, which may be a rational treatment selection for ischemic cerebral protection.

miR-34 Promotes Autophagy and Apoptosis of Spinal Chondrocytes by Mammalian Target of Rapamycin/Phosphatidylinositol-3-Kinase/Protein Kinase B Signaling

2020 ◽  
Vol 10 (12) ◽  
pp. 1877-1883
Author(s):  
Jun Wu ◽  
Fenfen Zhao ◽  
Feng Tian ◽  
Feng Ma ◽  
Tao Guan
Keyword(s):  
Cell Proliferation ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Chondrocyte Apoptosis ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Articular Chondrocyte

Autophagy and apoptosis of chondrocytes participate in spondyloarthritis (SpA). miR-34 involves in various diseases. However, miR-34’s role in autophagy and apoptosis of spine chondrocytes remains unclear. SpA patients and normal bone and articular cartilage tissues were collected, and miR-34 level was detected by Real-time PCR. The chondrocytes of SpA patients were isolated and divided into control group, miR-34 siRNA group and miR-34 group followed by analysis of Caspase 3 activity, cell proliferation by MTT assay, expression of Bax, Bcl-2, ATG5 and Beclin1 by Real time PCR, mTOR/PI3K/AKT signaling pathway protein expression by western blot, as well as TNF-α and IL-6 secretion by ELISA. miR-34 was significantly upregulated in SpA patients compared to normal (P <0.05). miR-34 siRNA transfection into SpA chondrocytes significantly down-regulated miR-34 expression, promoted cell proliferation, decreased Caspase 3 activity and Bax expression, increased Bcl-2, ATG5 and Beclin1 expression, decreased TNF-α and IL- 6 secretion as well as increased pmTOR and pAKT expression (P <0.05). miR-34 mimics was transfected into SpA chondrocytes, which up-regulated miR-34 expression and significantly reversed the above changes (P <0.05). miR-34 is upregulated in SpA patients. Down-regulation of miR-34 inhibits articular chondrocyte apoptosis and promotes autophagy by down-regulatingmTOR/PI3K/AKT signaling pathway, thereby promoting articular chondrocyte proliferation and inhibiting joint inflammation.

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.

Effect of LncRNA BLACAT1 on the Proliferation and Apoptosis of Osteoblasts in Ankylosing Spondylitis Through Regulating RANKL/OPG Signaling Pathway

2019 ◽  
Vol 9 (9) ◽  
pp. 1279-1285
Author(s):  
Hongbin Zhu ◽  
Zongbao Gao ◽  
Tao Wang ◽  
Zhigang Lei ◽  
Maoqin Sun
Keyword(s):  
Cell Proliferation ◽  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Mrna Expression ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Stable Phase ◽  
Proliferation And Apoptosis

Ankylosing spondylitis (AS) is an autoimmune disorder. LncRNA BLACAT1 involves in several diseases such as inflammation and immune diseases, but the expression and role of LncRNA BLACAT1 in AS remains unclear. AS patients and controls were selected. LcRNA BLACAT1 expression in peripheral blood was analyzed by Real time PCR, and its correlation with CRP, ESR and AS activity was analyzed. Osteoblast hFOB 1.19 was cultured and transfected with LncRNA BLACAT1 plasmid and si-LncRNA BLACAT1, respectively followed by analysis of cell proliferation by MTT assay, apoptosis by Caspase 3, ADAMTS-4 and Runx2 mRNA expression by Real time PCR, IFN-γ and TNF-α secretion by ELISA, and as RANKL, OPG, and nerve growth factor NGF level by western blot. AS patients presented significantly elevated LcRNA BLACAT1 level than controls (P < 0.05) with higher expression in active AS patients than stable phase (P < 0.05). BLACAT1 was positively associated with CRP and disease activity index (P < 0.05). Overexpression of LncRNA BLACAT1 in osteoblast hFOB 1.19 significantly decreased cell proliferation, elevated Caspase 3 activity, increased ADAMTS-4 mRNA expression, decreased Runx2 mRNA expression, and increased IFN-γ and TNF-α sevretion, and RANKL expression, and decreased OPG and NGF expression (P < 0.05). However, the above changes were reversed by si-LncRNA BLACAT1. LncRNA BLACAT1 expression in AS patients can reflect the degree of disease activity, and its mechanism may be through regulation of RANKL/OPG signaling pathway, which affects the proliferation and apoptosis of osteoblasts in AS.

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