Effect of MiR-21 on Regulating the Proliferation of Synovial Fibroblasts in Rheumatoid Arthritis

2020 ◽  
Vol 10 (7) ◽  
pp. 1052-1058
Author(s):  
Zhichao Li ◽  
Jin Wang ◽  
Jing Yang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Mrna Level ◽  
Synovial Fibroblasts ◽  
Control Group ◽  
Spearman Correlation ◽  
Qrt Pcr ◽  
Relationship Of ◽  
The Relationship

Background: This study investigated whether miR-21 regulates the expression of STAT3 and affects FLS cells. Methods: MiR-21 and STAT3 mRNA level was assessed by qRT-PCR and STAT3 and p-STAT3 level was evaluated by Western blot. Spearman correlation was used to analyze the relationship between miR-21 and STAT3 mRNA expression in synovial tissue of RA patients. FLS cells were treated with IL-17A, and the cells without treatment was included as the control group. Under IL-17A treatment, FLS cells were divided into 2 groups: miR-NC group and miR-21 mimic group. MiR-21, STAT3, p-STAT3 expression were detected and compared. EdU staining was used to detect cell proliferation and flow cytometry was used to measure cell apoptosis. Results: There was a target relationship of miR-21 with STAT3 mRNA. IL-17A treatment significantly downregulated miR-21 in FLS cells, upregulated STAT3 and p-STAT3 and enhanced cell proliferation. Transfection of miR21 mimic significantly downregulated STAT3 and p-STAT3 in FLS cells, reduced cell proliferation and increased cell apoptosis. Conclusion: MiR-21 overexpression down-regulates STAT3, inhibits FLS cell proliferation and promotes apoptosis, indicating that it might be a therapeutic target for treating RA.

scholarly journals Adipocytokines in early rheumatoid arthritis: relationship to pro- and anti-inflammatory markers

2019 ◽  
Vol 56 (6) ◽  
pp. 697-702
Author(s):  
L. V. Kondratyeva ◽  
T. V. Popkova ◽  
Yu. N. Gorbunova
Keyword(s):  
Rheumatoid Arthritis ◽  
Early Rheumatoid Arthritis ◽  
Control Group ◽  
Disease Modifying Antirheumatic Drugs ◽  
Erythrocyte Sedimentation ◽  
Anti Inflammatory ◽  
The One ◽  
Relationship Of ◽  
The Relationship ◽  
Citrullinated Peptide

Objective: to clarify the relationship of adiponectin and leptin to the signs of disease activity and the levels of pro- and anti-inflammatory cytokines in patients with early rheumatoid arthritis (RA).Subjects and methods. The investigation enrolled 27 RA patients who met the 2010 ACR/EULAR classification criteria and had never received glucocorticoids (GCs) or disease-modifying antirheumatic drugs. The median age of the patients was 56 [46; 64] years; the duration of the disease was 8 [6; 15] months. All the patients had moderate or high RA activity according to DAS28. The majority of the patients were seropositive for rheumatoid factor (88.9%) or anticyclic citrullinated peptide antibodies (96.3%). A control group included 30 gender-, age-, and body mass index (BMI)-matched people without inflammatory arthritis. Enzyme immunoassay was used to estimate the concentrations of adiponectin and leptin; XMAP multiplex assay was applied to measure the levels of interleukin-1β (IL-1β), IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12, IL-13, IL-15, IL-17 and macrophage inflammation proteins (MIP), such as MIP-1α and MIP-1β.Results and discussion. In RA patients, adiponectin concentrations were higher (p<0.001) and leptin levels and leptin/adiponectin (L/A) ratios were lower than those in the controls (p=0.04 and p<0.001, respectively). In RA, there were direct correlations of leptin levels with concentration of IL-17 (r=0.4; p=0.03), IL-4 (r=0.39; p=0.04) and erythrocyte sedimentation rate (ESR) (r=0.3; p=0.05), as well as relationships of L/A ratios to ESR (r=0.38; p=0.05) and the levels of CRP (r=0.4; p=0.04) and MIP-1β (r=0.55; p=0.03). An increase in adiponectin concentrations was associated with a decrease in MIP-1β levels (r=-0.63; p<0.01). In patients with BMI ≥25 kg/m2, leptin concentrations were comparable in RA patients and controls (p=0.1); the differences in adiponectin levels and L/A ratios remained in both cases (p<0.001). This subgroup of patients with RA showed significant correlations between leptin and IL-17 levels (r=0.52; p=0.03), adiponectin and MIP-1β concentrations (r=-0.59; p=0.01), L/A ratios and MIP-1β levels (r=0.55; p=0.02).Conclusion. In early RA, there was a lower leptin synthesis and a higher adiponectin production. The correlations between the levels of adipocytokines, IL-17, and MIP1β, on the one hand, suggest that adipose tissue has an impact on systemic inflammation and, on the other, confirm that proinflammatory cytokines are involved in the development of insulin resistance and obesity.

scholarly journals Osteoporosis in Rheumatoid Arthritis: Dangerous Liaisons

2020 ◽  
Vol 7 ◽  
Author(s):  
Irene Llorente ◽  
Noelia García-Castañeda ◽  
Cristina Valero ◽  
Isidoro González-Álvaro ◽  
Santos Castañeda
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Remodeling ◽  
Bone Destruction ◽  
Synovial Fibroblasts ◽  
Mineral Density ◽  
Tnf Α ◽  
Activated T Lymphocytes ◽  
Inflammatory State ◽  
Relationship Of ◽  
The Relationship

Osteoporosis has been classically considered a comorbidity of rheumatoid arthritis (RA). However, recent advances in the pathogenesis of osteoporosis in RA have shown a close interplay between cells of the immune system and those involved in bone remodeling, introducing new actors into the classic route in which osteoclast activation is related to the RANK/RANKL/OPG pathway. In fact, the inflammatory state in early stages of RA, mediated by interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor (TNF)-α has the ability to activate and differentiate osteoclasts not only through their relationship with RANKL, but also through the Wnt/DKK1/sclerostin pathway, leading to bone loss. The role of synovial fibroblasts and activated T lymphocytes in the expression of the RANKL system and its connection to bone destruction is also depicted. In addition, autoantibodies such as rheumatoid factor and anti-citrullinated protein antibodies are other pathogenic mechanisms for the development of bone erosions and systemic osteoporosis in RA, even before the onset of arthritis. The aim of this review is to unravel the relationship between different factors involved in the development of osteoporosis in RA patients, both the classic factors and the most novel, based on the relationship of autoantibodies with bone remodeling. Furthermore, we propose that bone mineral density measured by different techniques may be helpful as a biomarker of severity in early arthritis patients.

scholarly journals MicroRNA-3666 Regulates Thyroid Carcinoma Cell Proliferation via MET

2016 ◽  
Vol 38 (3) ◽  
pp. 1030-1039 ◽  
Author(s):  
Gang Wang ◽  
Chengzhong Cai ◽  
Lei Chen
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Thyroid Carcinoma ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Bioinformatics Analyses ◽  
Survival And Growth ◽  
Relationship Of ◽  
The Relationship

Background/Aims: Thyroid carcinoma (TC) is a highly lethal malignant cancer and its carcinogenesis remains undetermined. Dysregulation of microRNAs (miRNAs) is well known to be involved in the development of various cancers, including TC, whereas a role of miR-3666 in the pathogenesis of TC has not been appreciated. Methods: We analyzed the levels of MET and miR-3666 in TC tissue and the relationship of miR-3666 levels with patients' prognosis. We then overexpressed miR-3666 by miRNA mimics transfection and inhibited miR-3666 by miRNA antisense transfection in TC cells. Cell survival and growth were analyzed by CCK-8 assay and MTT assay, respectively. Cell apoptosis and proliferation were analyzed by flow cytometry. Bioinformatics analyses were applied to predict miR-3666 targets, which was then confirmed using luciferase reporter assay. Results: We detected significantly higher levels of MET, and significantly lower levels of miR-3666 in TC tissue, compared to the adjacent non-tumor tissue. Moreover, the low miR-3666 levels were associated with poor survival of the patients. Overexpression of miR-3666 significantly inhibited cell growth, while depletion of miR-3666 increased cell growth in TC cells. Moreover, the effects of miR-3666 on cell growth appeared to result from alteration in cell proliferation, rather than changes in cell apoptosis. MiR-3666 was found to bind to the 3'-UTR of MET mRNA to inhibit its translation in TC cells. Conclusion: Reduced miR-3666 levels in TC tissue may promotes TC growth, possibly through MET-mediated cell proliferation.

scholarly journals Kruppel-like factor 4 upregulates the resistance to apoptosis induced by tumor necrosis factor α in synovial fibroblasts with rheumatoid arthritis

2021 ◽  
Vol 19 ◽  
pp. 205873922110317
Author(s):  
Chenghong Ni ◽  
Shiyi Zeng ◽  
Chen Zhang ◽  
Kehan Lao ◽  
Jifeng Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Cell Apoptosis ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Caspase 3 ◽  
Synovial Fibroblasts ◽  
Factor Α ◽  
Necrosis Factor

Objective The objective is to examine the effect of tumor necrosis factor α (TNFα) on apoptosis and proliferation of rheumatoid arthritis synovial fibroblasts (RASFs) and to elucidate the regulatory roles of Kruppel-like factor 4 (KLF4) in TNFα-induced RASF apoptosis. Methods Changes in cell proliferation were measured using an 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, and changes in cell apoptosis were detected by flow cytometry and Hoechst 33258 staining. Changes in the apoptosis-related protein caspase-3 and the apoptosis-related genes bcl-2/bax were measured by western blot and real-time PCR, respectively Results TNFα stimulation increased cell proliferation ( p < 0.05), decreased cell apoptosis ( p < 0.05), declined caspase-3 expression ( p < 0.05), and upregulated bcl-2/bax level ( p < 0.05) in RASFs. KLF4 gene silencing decreased cell proliferation ( p < 0.05), increased cell apoptosis ( p < 0.05), upregulated caspase-3 expression ( p < 0.05), and downregulated bcl-2/bax level ( p < 0.05) induced by TNFα in RASFs. Conclusions TNFα caused a decrease in RASF apoptosis, and KLF4 promoted resistance to TNFα-induced apoptosis and cell proliferation.

Lidocaine Protects Endometriosis by Inducing Apoptosis of Endometrial Stromal Cells

2020 ◽  
Vol 10 (6) ◽  
pp. 845-851
Author(s):  
Ping Li ◽  
Qian Zhang ◽  
Tao Li ◽  
Haibo Wang ◽  
Xia Ji ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Stromal Cells ◽  
Blot Analysis ◽  
Protein Level ◽  
Cell Apoptosis ◽  
Western Blot Analysis ◽  
Control Group ◽  
Endometrial Stromal Cells ◽  
Qrt Pcr

Objective: This study aimed to explore the effects of lidocaine on ectopic endometrial stromal cells and the underlying mechanisms in endometriosis. Methods: Ectopic endometrial stromal cells (ESCs), which were separated from endometriotic tissues, were subjected to various concentrations of lidocaine for different time. After the treatment of lidocaine, MTT assay was applied to assess the cell proliferation of ESCs, and cell apoptosis was analyzed by flow cytometry. Meanwhile, we detected the protein level of pro-caspse3 and cleaved-caspase3 protein in ESCs by Western blot analysis. The invasion and migration capability of ESCs was also detected by transwell assay. Western blot analysis and qRT-PCR were performed for the detection of EMT markers (E-cadherin, N-cadherin and MMP-9). Similarly, the expression levels of β-catenin, cyclin D1 and c-myc in ESCs were determined by Western blot analysis and qRT-PCR. Results: 0.5, 1, 5 and 10 mM of lidocaine obviously inhibited the cell proliferation of ESCs at different time points compared with the control group, while no significant effect was observed in 0.1 mM lidocaine treated cells. Lidocaine dose-dependently increased cell apoptosis, reduced the protein level of pro-caspse3 protein, but improved cleaved-caspase3 protein level in ESCs. Moreover, lidocaine dose-dependently decreased the migration and invasion capabilities of ESCs. In addition, compared to the control group, lidocaine enhanced the level of E-cadherin, and reduced the level of N-cadherin and MMP-9 in ESCs. Lidocaine suppressed the level of β-catenin, cyclin D1 and c-myc in ESCs in a dose-dependent manner. Conclusion: We demonstrated that lidocaine protected endometriosis by inducing the apoptosis of ESCs via regulating Wnt/β-catenin pathway.

Curcumin Affects Parkinson Protein 7 (PARK7; DJ-1) Expression and Regulates Proliferation and Apoptosis of Breast Cancer Cells by Up-Regulating miR-203

2021 ◽  
Vol 11 (12) ◽  
pp. 2484-2490
Author(s):  
Lu Wang ◽  
Jianglun Shen ◽  
Ning Li ◽  
Yang Zhang ◽  
Feng Hu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Breast Cancer Cells ◽  
Mrna Level ◽  
Akt Pathway ◽  
Pathway Activity ◽  
Qrt Pcr ◽  
Pten Mrna

PTEN can inhibit PI3 K/AKT signaling pathway and DJ-1 negatively regualtes PTEN. Curcumin (Cur) regulates PTEN-PI3 K/AKT pathway. Bioinformatics analysis showed a targeting relationship between miR-203 and DJ-1, but it is unclear whether Cur regulates DJ-1-PTEN/PI3 K/AKT pathway through miR-203. We assessed Cur’s role in breast cancer cells. MCF-10A and MDA-MB-231 cells were cultured and expression of miR-203, DJ-1 and PTEN mRNA was measured by qRT-PCR. MDA-MB-231 cells were treated with 0, 10 μM Cur followed by analysis cell proliferation by CCK-8 assay, cell apoptosis by flow cytometry, miR-203, DJ-1 and PTEN mRNA level by qRT-PCR. MDA-MB-231 cells were divided into 3 groups: 0 μM, 10 μM Cur+miR-NC treatment group, 10 μM+miR-203 inhibitor group to measure cell apoptosis and proliferation. Compared with MCF-10A cells, miR-203 and DJ-1 mRNA in MDA-MB-231 cells was significantly upregulated and PTEN mRNA expression was decreased. Cur treatment significantly decreased cell proliferation, promoted caspase-3 activity and cell apoptosis, as well as elevated miR-203 and PTEN mRNA level and decreased DJ-1 mRNA level. miR-203 inhibitor transfection can antagonize Cur’s effect on upregulation of miR-203, increase DJ-1 expression, decrease PTEN expression, enhance PI3 K/AKT pathway activity, and antagonize Cur’s anti-tumor effect. Curcumin increases miR-203 expression, down-regulates DJ-1 expression, affects PTEN-PI3 K/AKT pathway activity, and play an anti-tumor effect through inhibiting breast cancer cell proliferation and promoting apoptosis.

scholarly journals Hh pathway expression in the blood, synovial cells and chondrocytes of different rheumatoid arthritis models

2021 ◽  
Vol 18 (3) ◽  
pp. 499-504
Author(s):  
Yingyi Wu ◽  
Guangxia Yang ◽  
Jing Fei ◽  
Yang Huang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Proliferation ◽  
Articular Cartilage ◽  
Protein Expression ◽  
Cell Apoptosis ◽  
Fluorescein Isothiocyanate ◽  
Control Group ◽  
Cartilage Cell ◽  
Expression Levels ◽  
Articular Cartilage Cell

Purpose: To investigate the effect of the hedgehog (Hh) pathway inhibitor, cyclopamine, and activator purmorphamine on articular cartilage cell proliferation. Methods: Rats were subjected to AA and CIA models. Secondary paw swelling was measured at 12, 15, 18, 21, 24, 27, and 30 days. The rats were sacrificed on day 30. Tissues from the cartilage and knee joints were collected. Cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay while cell apoptosis was determined by annexin V-fluorescein isothiocyanate/propidium iodide assay. Protein expression levels of Shh, Ptch1 and Gli1 were determined by Western blotting. Results: Compared with the control group, arthritis index and secondary foot swelling of the adjuvant arthritis (AA) and collagen-induced arthritis (CIA) groups deteriorated significantly (p < 0.05). MTT data revealed that cyclopamine promoted articular cartilage cell proliferation of the AA and CIA groups. The cell proliferation rates of AA and CIA groups were significantly higher than that of control group (p < 0.05). Flow cytometry showed that the cell apoptosis rates of AA and CIA groups were significantly lower than that of control group (p < 0.05). Compared with control, cyclopamine decreased the protein expression levels of sonic Hh, patched homologue 1 and glioma-associated oncogene homologue, but the effect of purmorphamine was the reverse. Conclusion: Hh pathway inhibitor (cyclopamine) and activator (purmorphamine) affect the expression of Hh pathway. Disruption of the Hh pathway may be of potential therapeutic significance in protecting articular cartilage from rheumatoid arthritis.

scholarly journals MiR-140-3p inhibits the cell viability and promotes apoptosis of synovial fibroblasts in rheumatoid arthritis through targeting sirtuin 3

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Beibei Zu ◽  
Lin Liu ◽  
Jingya Wang ◽  
Meirong Li ◽  
Junxia Yang
Keyword(s):  
Rheumatoid Arthritis ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Pearson Correlation ◽  
Fibrous Tissue ◽  
Synovial Fibroblasts ◽  
Cell Counting ◽  
Sirtuin 3 ◽  
Fibrous Tissues

Abstract Background Synovial fibroblasts (SFs) with the abnormal expressions of miRNAs are the key regulator in rheumatoid arthritis (RA). Low-expressed miR-140-3p was found in RA tissues. Therefore, we attempted to investigate the effect of miR-140-3p on SFs of RA. Methods RA and normal synovial fibrous tissue were gathered. The targets of miR-140-3p were found by bioinformatics and luciferase analysis. Correlation between the expressions of miR-140-3p with sirtuin 3 (SIRT3) was analyzed by Pearson correlation analysis. After transfection, cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry. The expressions of miR-140-3p, SIRT3, Ki67, Bcl-2, Bax, and cleaved Caspase-3 were detected by RT-qPCR or western blot. Results Low expression of miR-140-3p and high expression of SIRT3 were found in RA synovial fibrous tissues. SIRT3 was a target of miR-140-3p. SIRT3 expression was negatively correlated to the expression of miR-140-3p. MiR-140-3p mimic inhibited the MH7A cell viability and the expressions of SIRT3, Ki67, and Bcl-2 and promoted the cell apoptosis and the expressions of Bax and cleaved Caspase-3; miR-140-3p inhibitor showed an opposite effect to miR-140-3p mimic on MH7A cells. SIRT3 overexpression not only promoted the cell viability and inhibited cell apoptosis of MH7A cells but also reversed the effect of miR-140-3p mimic had on MH7A cells. Conclusions The results in this study revealed that miR-140-3p could inhibit cell viability and promote apoptosis of SFs in RA through targeting SIRT3.

scholarly journals METTL14 promotes tumorigenesis by regulating lncRNA OIP5-AS1/miR-98/ADAMTS8 signaling in papillary thyroid cancer

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Xiaoping Zhang ◽  
Dan Li ◽  
Chengyou Jia ◽  
Haidong Cai ◽  
Zhongwei Lv ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Papillary Thyroid ◽  
Qrt Pcr ◽  
The Relationship

Abstract Background Papillary thyroid cancer (PTC) is the most common type of cancer of the endocrine system. Long noncoding RNAs (lncRNAs) are emerging as a novel class of gene expression regulators associated with tumorigenesis. Through preexisting databases available for differentially expressed lncRNAs in PTC, we uncovered that lncRNA OIP5-AS1 was significantly upregulated in PTC tissues. However, the function and the underlying mechanism of OIP5-AS1 in PTC are poorly understood. Methods Expression of lncRNA OIP5-AS1 and miR-98 in PTC tissue and cells were measured by quantitative real-time PCR (qRT-PCR). And expression of METTL14 and ADAMTS8 in PTC tissue and cells were measured by qRT-PCR and western blot. The biological functions of METTL14, OIP5-AS1, and ADAMTS8 were examined using MTT, colony formation, transwell, and wound healing assays in PTC cells. The relationship between METTL14 and OIP5-AS1 were evaluated using RNA immunoprecipitation (RIP) and RNA pull down assay. And the relationship between miR-98 and ADAMTS8 were examined by luciferase reporter assay. For in vivo experiments, a xenograft model was used to investigate the effects of OIP5-AS1 and ADAMTS8 in PTC. Results Functional validation revealed that OIP5-AS1 overexpression promotes PTC cell proliferation, migration/invasion in vitro and in vivo, while OIP5-AS1 knockdown shows an opposite effect. Mechanistically, OIP5-AS1 acts as a target of miR-98, which activates ADAMTS8. OIP5-AS1 promotes PTC cell progression through miR-98/ADAMTS8 and EGFR, MEK/ERK pathways. Furthermore, RIP and RNA pull down assays identified OIP5-AS1 as the downstream target of METTL14. Overexpression of METTL14 suppresses PTC cell proliferation and migration/invasion through inhibiting OIP5-AS1 expression and regulating EGFR, MEK/ERK pathways. Conclusions Collectively, our findings demonstrate that OIP5-AS1 is a METTL14-regulated lncRNA that plays an important role in PTC progression and offers new insights into the regulatory mechanisms underlying PTC development.

scholarly journals MiR-206 regulates the progression of osteoporosis via targeting HDAC4

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Zhiyuan Lu ◽  
Dawei Wang ◽  
Xuming Wang ◽  
Jilong Zou ◽  
Jiabing Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Diagnostic Value ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Control Group ◽  
Luciferase Reporter Gene ◽  
Mineral Density ◽  
Gene Assay

Abstract Background More and more studies have confirmed that miRNAs play an important role in maintaining bone remodeling and bone metabolism. This study investigated the expression level of miR-206 in the serum of osteoporosis (OP) patients and explored the effect and mechanism of miR-206 on the occurrence and development of osteoporosis. Methods 120 postmenopausal women were recruited, including 63 cases with OP and 57 women without OP. The levels of miR-206 were determined by qRT-PCR technology. Spearman correlation coefficient was used to evaluate the correlation of miR-206 with bone mineral density (BMD). An ROC curve was used to evaluate the diagnostic value of miR-206 in osteoporosis. The effects of miR-206 on cell proliferation and cell apoptosis of hFOBs were measured by CCK-8 assay and flow cytometry, respectively. Luciferase reporter gene assay was used to confirm the interaction of miR-206 and the 3′UTR of HDAC4. Results Serum miR-206 had low expression level in osteoporosis patient group compared with control group. The expression level of serum miR-206 had diagnostic value for osteoporosis, and the serum miR-206 levels were positively correlated with BMD. The down-regulated miR-206 could inhibit cell proliferation and promote cell apoptosis. Luciferase analysis indicated that HDAC4 was the target gene of miR-206. Conclusions MiR-206 could be used as a new potential diagnostic biomarker for osteoporosis, and in in vitro cell experiments, miR-206 may regulate osteoblast cell proliferation and apoptosis by targeting HDAC4.

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