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 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.

Bone Marrow Mesenchymal Stem Cell (BMSC)-Exosomes Overexpressing miR-141 Inhibit the Malignant Biological Behavior of Glioma Cells via Wnt Signaling

2022 ◽  
Vol 12 (4) ◽  
pp. 800-806
Author(s):  
Jing Cao ◽  
Fan Yang ◽  
Haiyan Zhou ◽  
Duojiao Fan ◽  
Hengzhou Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Wnt Signaling ◽  
Wnt Signaling Pathway ◽  
Glioma Cells ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Control Group ◽  
Mtt Method ◽  
Apoptosis Protein

Our study explores whether BMSC-exosomes overexpressing miR-141 can regulate Wnt signal to inhibit the malignant biological behavior of glioma cells. Thirty healthy mice were selected to construct a glioma mouse model and assigned randomly into the control group, miR-141 NC group, and miR-141 mimic group followed by analysis of cell proliferation, apoptosis, protein expression and mRNA expression by MTT method, flow cytometry, Western blot and RT-PCR methods. Compared with the other two groups, miR-141 mimic group showed reduced number of cell proliferation at 24 h and 48 h, decreased cell migration and invasion ability, and the increased cell apoptosis rate (P < 0.05). In miR-141 mimic group, the protein expression of miR-141 was the highest, while the protein expression of β-catenin, survivin and c-myc was the lowest (P < 0.05). In conclusion, BMSC-exosomes overexpressing miR-141 can inhibit the malignant biological behavior of GC cells possibly by inhibiting the activation of Wnt signaling pathway.

Effects of Papaya Leaf Extract (Carica papaya L.) on Cellular Proliferation and Apoptosis in Cervical Cancer Mice Model

2019 ◽  
Vol 17 (5) ◽  
pp. 265-275
Author(s):  
Y. Peristiowati ◽  
Y. Puspitasari ◽  
Indasah
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Hela Cells ◽  
Leaf Extract ◽  
Caspase 3 ◽  
Methanol Extract ◽  
Negative Control ◽  
Proliferation Index ◽  
Control Group ◽  
P53 Expression

This study is aimed at analyzing the anticancer properties of papaya leaf extract, specifically the inhibition of cell proliferation and apoptotic induction through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and p53 pathways. Twenty-five mice (Mus musculus), aged 2 months and weighing 20–30 g, was injected with 0.5 mg dexamethasone for 7 days. The mice were then injected intracutaneously with 1 ml of HeLa cells (8 × 106 HeLa cells/microliter). The mice were divided into five groups (5 each): negative control (P1) (5% CMC-Na, sodium carboxymethyl cellulose), treatment II (225 mg/kg BW (body weight) papaya leaves methanol extract), treatment III (450 mg/kg BW), treatment IV (750 mg/kg BW), and treatment PV (2 mg alcohol anticancer drug). Papaya leaf extract treatments were applied for 2 weeks. Then, the tumor tissue was isolated for hematoxylin and eosin staining. Immunohistochemical imaging was used to detect Ki-67, caspase-3, NF-κB, and p53 expression. Further analysis was undertaken using the ImmunoRatio software program. The results indicated that administration of papaya leaf methanol extract significantly increased the expression of NF-κB and p53 at a dose of 450 mg/kg BW. Our results also showed that the mice treated with 450 mg of papaya leaf extract per kg of BW (P3) had the largest increase of caspase-3 expression compared to the negative control group. Papaya leaf ethanol extract decreased the cancer cell proliferation index and increased apoptosis of cancer cells in animal models of cervical cancer; it may also work to increase NF-kB expression and expression of the p53 gene.

scholarly journals Comparison of Bax and Caspase-3 Protein Expression in Liver Cells following UVB Irradiation for 7 days and Treatment of Pimpinella alpina Molk during 7 and 15 days

2020 ◽  
Vol 19 (2) ◽  
pp. 296-303
Author(s):  
Eni Widayati ◽  
Taufiqurrachman Nasihun ◽  
Azizah Hikma Savitri ◽  
Nurina Tyagita
Keyword(s):  
Protein Expression ◽  
Caspase 3 ◽  
Medical Science ◽  
Liver Cells ◽  
Male Rats ◽  
Control Group ◽  
Sprague Dawley ◽  
Control Group Design ◽  
Uvb Irradiation ◽  
The Difference

Objective: The effect of Pimpinela alpina Molk (PaM) on decrease in Bax and Caspase-3 protein expression in liver cells apoptosis have been proven. However, the difference result between 7 and 15 days treatment duration of PaM need to be confirmed. This study aimed to confirm that treatment of PaM during 15 days is more effective decreasing Bax and Caspase-3 protein expression in liver cells following UVB irradiation. Methods: In the post test only control group design, 35 Sprague Dawley male rats, 300 gram body weight were divided into two arms, consisting of three groups respectively. First arm comprise Neg-7, PaM7-100, and PaM7-150. Second arm comprise Neg-15, PaM15-100, and PaM15-150. Nor-G was added as normal control neither exposed to UVB nor PaM treatment. In negative group was only radiated to UVB and PaM groups were exposed to UVB and treatment with 100, and 150 mg PaM per oral for 7 and 15 days respectively. At day 8 (first arm) and 16 (second arm), liver organ was taken and Bax and Caspase-3 protein expression assessed by Immunohistochemical staining method. Result: Post Hoc LSD analysis indicated that Bax and Caspase-3 protein expression in PaM15-100 and PaM15-150 was significant lower compared to that of Nor-G, PaM7-100, and PaM7-150, p < 0.05. Conclusion: Ttreatment of PaM with doses 100 and 150 mg for 15 days was better in decreasing Bax and Caspase-3 protein expression of liver cells following UVB irradiation. Bangladesh Journal of Medical Science Vol.19(2) 2020 p.296-303

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 Expression of Notch–Hif-1α signaling pathway in liver regeneration of rats

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094379
Author(s):  
Yanshan Li ◽  
Yunxiuxiu Xu ◽  
Ruomei Wang ◽  
Wenxin Li ◽  
Wenguang He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Protein Expression ◽  
Liver Regeneration ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Saline Control ◽  
Control Group ◽  
Mrna Levels ◽  
Ki 67

Objective To investigate whether the Notch–Hif-1α signaling pathway is involved in liver regeneration. Methods Rats were divided into two groups and treated with daily intraperitoneal injections of saline (control) or the gamma-secretase inhibitor, Fli-06, for 2 days. Two-thirds of the rat livers were resected and rats were later euthanized at specific time points post-resection to analyze the remnant livers. Each group's liver/body weight ratio was calculated, and immunostaining and western blotting were used to determine the cell proliferation marker, PCNA and Ki-67 expression. Real-time PCR and western blotting were used to compare the mRNA expression of Notch homolog-1 ( Notch1), hairy and enhancer of split-1 ( Hes1), and vascular endothelial growth factor ( Vegf), and the protein expression of NICD and HIF-1α, respectively. Results The liver/body weight ratios and number of Ki-67- and PCNA-positive cells were significantly lower in the experimental group than the control group, indicating lower levels of liver regeneration following the disruption of Notch signaling by Fli-06. The Hes1 and Vegf mRNA levels and NICD and HIF-1α protein expression levels were all down-regulated by Fli-06 treatment. Conclusion Notch–Hif-α signaling pathway activation plays an important role in liver regeneration, where it may contribute toward liver cell proliferation.

MK886 Induced Apoptosis in HL-60 Cells Via Inhibition mPGES-1 Expression and Down-Regulation Prostaglandin E2 Synthesize.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4824-4824
Author(s):  
Yiqing Li ◽  
Songmei Yin ◽  
Shuangfeng Xie ◽  
Danian Nie ◽  
Liping Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Prostaglandin E2 ◽  
Cell Line ◽  
Caspase 3 ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Dependent Manner ◽  
Pge2 Synthesis ◽  
Dose Dependent

Abstract Abstract 4824 Recent studies have shown that prostaglandin E2 (PGE2) may play a key role in the tumorigenesis and tumor development. Membrane-bound prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that acts downstream of cyclooxygenase (COX) and specifically catalyzes the conversion of prostaglandin H2 (PGH2) to PGE2, was over-expression in a variety of solid tumor cells and tissues such as nonsmall-cell lung cancer, colon carcinoma, gastric carcinoma and breast cancer. MK886, a small molecular inhibitor, is a reasonable potency as an inhibitor of mPGES-1 in vitro experiment. In this study, we examined effects of MK886 on expression of mPGES-1 and PGE2 synthesis in human acute myeloid leukemia cell line (HL-60), observed cell proliferation and apoptosis after 24-h treatment with MK886, and tried to explore the possible mechanisms by checking some protein belong AKT cell singling pathway such as P-AKT, Bax and Bcl-2. We found that the expression levels of mPGES-1 mRNA and protein were higher in HL-60 cells than in normal mononuclearcells (MNC). MK886 inhibited mPGES-1 mRNA and protein expression and reduced PGE2 secretion in HL-60 cells in a dose-dependent manner. The cell proliferation was inhibited and the IC50 was 132.16μmol/L. With the increase of MK886 concentration, the cell apoptosis rate assayed by flow cytometry increased and the apparent apoptotic bodies increased when staining by Hoechst 33258. After treated with MK886 for 24h, protein was extracted and assayed by western blot. The results showed that the expression levels of P-AKT, Bcl-2 and c-myc decreased while the Bax protein expression increased in a dose-dependent manner. The caspase-3 activity, determined by colorimetric detection, also increased dose-dependently. These results indicated that mPGES-1 over-expressed in leukemia cell line HL-60, MK886 could induce apoptosis in HL-60 cells via reducing mPGES-1 expression and PGE2 synthesis dose-dependently, thereby regulate the AKT pathway including Bcl-2 family and the activity of caspase-3. It suggested that mPGES-1 inhibitor might emerge as an important therapeutic tool for leukemia treatment. Disclosures: No relevant conflicts of interest to declare.

Lidocaine Inhibits Ovarian Cancer Cell Proliferation and Induces Apoptosis: An In Vitro Study

2020 ◽  
Vol 10 (5) ◽  
pp. 724-729
Author(s):  
Yaping Xu ◽  
Xiaoqin Fang ◽  
Xianjiang Wei
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Western Blot ◽  
Cancer Cell ◽  
Blot Analysis ◽  
Group Treatment ◽  
Western Blot Analysis ◽  
Ovarian Cancer Cell ◽  
Control Group

Objective: The present study aimed to explore the effects and related mechanism of lidocaine on human ovarian cancer cell lines. Methods: Human ovarian cancer cell lines (SKOV3 and ES-2) were treated with different concentrations of lidocaine for different time. We treated SKOV3 and ES-2 cells using lidocaine then used MTT assay and flow cytometry to detect the cell proliferation and cell apoptosis. In addition, we used western blot analysis to explore the protein expression of Bax and Bcl-2 in SKOV3 and ES-2 cells. Western blot analysis and qRT-PCR were performed for the detection of EMT markers (E-cadherin, N-cadherin). The protein expression levels of TRAF3 and p-p65 in SKOV3 and ES-2 cells were determined by Western blot analysis. Results: Compared to the control group, 0.5, 1, 5, and 10 mM of lidocaine significantly inhibited ovarian cancer cell proliferation at different time points, while 0.1 mM of lidocaine had no significant effect. 1, 5 mM of lidocaine induced the cell apoptosis, and observably reduced expression of Bcl-2 protein, but improved Bax expression markedly compared with the control group. Treatment of lidocaine increased E-cadherin expression, but decreased N-cadherin expression when compared with control group. Treatment of lidocaine increased TRAF3 protein expression, but decreased p-p65 protein expression in ES-2 and SKOV3 cells. Conclusion: We demonstrated that lidocaine inhibited cell proliferation, induced apoptosis, and inhibited EMT in ovarian cancer cells via regulating TRAF3/NF-κB pathway.

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