scholarly journals Mechanical Overload Regulates Osteoblast Proliferation, Differentiation And Mineralization Through Wnt/Β-Catenin Signaling Pathway

2021 ◽  
Author(s):  
Yaru Fan ◽  
Yingbin Yan ◽  
Han Liu ◽  
Rui Luo ◽  
Hao Liu ◽  
...  
Keyword(s):  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Marker Gene ◽  
Control Group ◽  
Marker Genes ◽  
Osteoblast Proliferation ◽  
Alizarin Red ◽  
Mechanical Overload

Abstract Objectives: To study the effect of mechanical overload stimulation on proliferation, differentiation and mineralization of osteoblast and the underlying mechanisms.Methods: MC3T3-E1 cells were divided into overload group and control group. Four-point bending loading device was used to exert mechanical overload stimulation on MC3T3-E1 cells for a certain time. The proliferation of osteoblasts was detected by MTT colorimetric assay. Real-time PCR and Western Blot were used to detect the transcription and expression of osteoblast marker genes and proteins. The specific fluorescent dyes were used to label the actin filament and the nucleus, and the changes of cytoskeleton were observed under laser scanning confocal microscope. The mineralization of osteoblasts was evaluated by the number of calcium nodules formed by alizarin red staining. Results: Compared with the control group, the mechanical overload group significantly inhibited the proliferation of osteoblasts (p <0.05). Real-time PCR and Western Blot showed that the expression of osteoblast differentiation marker gene and protein was inhibited by mechanical overload stimulation. Under laser confocal microscopy, the overload group cell shrinkage deformation was observed, also the microfilament arrangement disorder, the skeleton arrangement loose, the direction difference and the skeleton breakage, but the nucleus does not have obvious change. Alizarin red staining showed that mechanical overload inhibited the formation of calcium nodules in osteoblasts. The expression of β-catenin protein in Wnt signaling pathway was inhibited by overload mechanical stimulation under immunofluorescence microscopy.Conclusion: Mechanical overload stimulation reduces the expression of Runx 2 by affecting the classical Wnt/β-catenin signaling pathway, thus it was inhibited osteoblast proliferation, differentiation and mineralization.

scholarly journals Astragaloside positively regulated osteogenic differentiation of pre-osteoblast MC3T3-E1 through PI3K/Akt signaling pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Wei Bing Jing ◽  
Hongjuan Ji ◽  
Rui Jiang ◽  
Jinlong Wang
Keyword(s):  
Western Blot ◽  
Osteogenic Differentiation ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Akt Signaling ◽  
Calcium Deposition ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Western Blot Assay

Abstract Background Osteoporosis is a widespread chronic disease characterized by low bone density. There is currently no gold standard treatment for osteoporosis. The aim of this study was to explore the role and mechanism of Astragaloside on osteogenic differentiation of MC3T3-E1 cells. Methods MC3T3-E1 cells were divided into control and different dose of Astragaloside (10, 20, 40, 50, and 60 μg/ml). Then, ALP and ARS staining were performed to identify the effects of Astragaloside for early and late osteogenic capacity of MC3T3-E1 cells, respectively. Real-time PCR and western blot were performed to assess the ALP, OCN, and OSX expression. PI3K/Akt signaling pathway molecules were then assessed by Western blot. Finally, PI3K inhibitor, LY294002, was implemented to assess the mechanism of Astragaloside in promoting osteogenic differentiation of MC3T3-E1 cells. Results Astragaloside significantly increased the cell viability than the control group. Moreover, Astragaloside enhanced the ALP activity and calcium deposition than the control groups. Compared with the control group, Astragaloside increased the ALP, OCN, and OSX expression in a dose-response manner. Western blot assay further confirmed the real-time PCR results. Astragaloside could significantly increase the p-PI3K and p-Akt expression than the control group. LY294002 partially reversed the promotion effects of Astragaloside on osteogenic differentiation of MC3T3-E1 cells. LY294002 partially reversed the promotion effects of Astragaloside on ALP, OCN, and OSX of MC3T3-E1 cells. Conclusion The present study suggested that Astragaloside promoted osteogenic differentiation of MC3T3-E1 cells through regulating PI3K/Akt signaling pathway.

scholarly journals Effects of rutin on osteoblast MC3T3-E1 differentiation, ALP activity and Runx2 protein expression

2021 ◽  
Vol 65 (1) ◽  
Author(s):  
Xin-Wei Liu ◽  
Bin Ma ◽  
Ying Zi ◽  
Liang-Bi Xiang ◽  
Tian-Yu Han
Keyword(s):  
Western Blot ◽  
Osteogenic Differentiation ◽  
Real Time ◽  
Real Time Pcr ◽  
Osteoblastic Differentiation ◽  
Control Group ◽  
Alizarin Red ◽  
Wide Range ◽  
Osteogenic Induction ◽  
Orthopedic Diseases

As a flavonoid, rutin has been found to have a wide range of biological functions, such as resisting inflammation and oxidation, and preventing cerebral hemorrhage and hypertension. It has been found to play an important role in osteoporosis and other orthopedic diseases in recent years. MC3T3-E1 cells were randomly divided into a control group, a rutin-1 group (0.01 mmol/L), a rutin-2 group (0.05 mmol/L) and a rutin-3 group (0.1 mmol/L). Osteogenic differentiation of cells was induced by osteogenic induction fluid. The control group was treated with the maximum dose of drug solvent. 2~3 days later, the solvent was replaced with fresh osteogenic induction fluid containing rutin. After a certain period of routine culture, the cells were collected for subsequent experiments. The expression of Runx2 gene in cells in all groups was detected by Real-time PCR; the expression of Runx2 protein was detected by Western blot and immunocytochemistry; the activity of ALP was detected by reagent kit method; osteogenic differentiation was analyzed by alizarin red staining. The results of Real-time PCR showed that, compared with the control group, the treatment of cells with rutin can significantly increase the expression of Runx2 gene (p<0.05); the higher the concentration, the higher the expression of Runx2 gene, and significant differences were found among groups in which different concentrations were used (p<0.05); the results of Western blot and IHC showed that the expression trend of Runx2 protein in each group was consistent with PCR results. In drug treatment groups, the activity of ALP was significantly higher than that in the control group (p<0.05); there were significant differences among groups in which different concentrations were used (p<0.05). The results of alizarin red staining showed that calcified nodules were formed in all groups and that the area of calcified nodules formed in groups treated with rutin was greater than that in the control group; the greater the concentration, the larger the area. Rutin can promote osteoblastic differentiation; and the greater the concentration, the more effective it is.

miR-184 Inhibits Inflammation Through Targeting Toll-Like Receptor 4 (TLR4)/NLR Family Pyrin Domain Containing 3 (NLRP3) Signaling Pathway in Neonatal Purulent Meningitis

2020 ◽  
Vol 10 (4) ◽  
pp. 569-575
Author(s):  
Jiang Wu ◽  
Shixiong Yang ◽  
Jin Shi ◽  
Yibing Shi
Keyword(s):  
Cell Proliferation ◽  
Cerebrospinal Fluid ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Caspase 1 ◽  
Purulent Meningitis ◽  
Inflammation Group

Neonatal purulent meningitis (NPM) leads to higher mortality and neurological sequelae rates. miR184 involves in inflammation and tumor, but the role of miR-184 in NPM remains unclear. NPM patients and non-intracranial infected neonates were collected and miR-184 expression in cerebrospinal fluid was assessed by real-time PCR. The Neuro-2a cell line was cultured and divided into control group, inflammation group (treated with LPS), and miR-184 inhibitor group, which was transfected with miR-184 inhibitor on the basis of inflammation followed by analysis of miR-184 and TLR4 expression by Real time PCR, Caspase 3 activity, cell proliferation by MTT assay, secretion of IL-1β and IL-6 by ELISA, NLRP3 expression by real time PCR and western blot, and Caspase-1 p20 and NF- B level by western blot. miR-184 expression level was significantly increased in cerebrospinal fluid of NPM group (P < 0 05) and also elevated in inflammation group along with significantly inhibited cell proliferation was inhibited, increased Caspase 3 activity, IL-1β and IL-6 secretion, and decreased TLR4, NLRP3, Caspase-1 p20 and NFκ- B expression (P < 0 05). miR-184 inhibitor significantly down-regulated miR-184 expression in the inflammation group, promoted cell proliferation, decreased Caspase 3 activity, IL-1β and IL-6 secretion, and increased TLR4, NLRP3, Caspase1 p20 and NF- κB expression (P < 0 05). miR-184 expression is increased in neonatal purulent meningitis and it can inhibit inflammation by targeting TLR4/NLRP3 signaling pathway, leading to amelioration of the progression of neonatal purulent meningitis.

miR-184 Inhibits Hypertrophic Scar Through Regulating Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway

2020 ◽  
Vol 10 (1) ◽  
pp. 133-138
Author(s):  
Peng Zhao ◽  
Junxia Qin ◽  
Lili Liang ◽  
Xinzhong Zhang
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Hypertrophic Scar ◽  
Scar Tissue ◽  
Akt Signaling ◽  
Scar Formation ◽  
Akt Signaling Pathway

Hypertrophic scar (HS) is a process of tissue repair and healing, and excessive fibrosis of local tissue leads to scar formation. During HS formation, fibroblasts (Fb) proliferate, synthesize and secrete and promote HS development. miR-184 regulates skin formation and tissue development. However, miR-184’s role in HS remains unclear. miR-184 expression in HS patients and normal healthy (Control) tissues was measured by real-time PCR. pAKT expression was analyzed by Western blot. Fb cells from human HS were cultured and divided into 2 groups, siRNA NC group and miR-184 siRNA group followed by analysis of miR-184 expression by real time PCR, cell proliferation by MTT assay, secretion of inflammatory factors IL-1β and IL-6 by ELISA, as well as expression of pAKT and AKT by western blot. Compared with control group, miR-184 and pAKT expression was significantly increased in the HS group. Transfection of miR-184 siRNA into Fb significantly downregulated miR-184 expression, inhibited cell proliferation, promoted Caspase 3 activity, decreased IL-1β and IL-6 secretion, and reduced pAKT level (P < 0.05). miR-184 expression is increased in hypertrophic scar tissue. Down-regulation of miR-184 expression in proliferative scar tissue fibroblasts can down-regulate PI3K/AKT signaling pathway, inhibit inflammation, promote apoptosis, inhibit fibroblast proliferation, and regulate hypertrophic scar formation.

scholarly journals Liraglutide Exerts Antidiabetic Effect via PTP1B and PI3K/Akt2 Signaling Pathway in Skeletal Muscle of KKAy Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Wenjun Ji ◽  
Xinlin Chen ◽  
Juan Lv ◽  
Meng Wang ◽  
Shuting Ren ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Glucose Transporter ◽  
Tyrosine Phosphatase ◽  
Gene Expressions ◽  
Protein Levels ◽  
Kkay Mice

Background. Liraglutide (a glucagon-like peptide 1 analog) was used for the treatment of type 2 diabetes (T2DM) which could produce glucose-dependent insulin secretion.Aim. The aim was to investigate whether liraglutide could improve myofibril and mitochondria injury in skeletal muscle and the mechanisms in diabetic KKAy mice.Method. We divided the male KKAy mice into 2 groups: liraglutide group (250 μg/kg/day liraglutide subcutaneous injection) and model group; meanwhile, the male C57BL/6J mice were considered as the control. After 6 weeks, the ultrastructure of skeletal muscle was observed by electron microscope. The gene expressions of protein tyrosine phosphatase 1B (PTP1B), phosphatidylinositol 3-kinase (PI3K), and glucose transporter type 4 (GLUT4) were determined by real-time PCR. The protein levels of the above molecules and phospho-Akt2 (p-Akt2) were measured by Western blot.Results. Liraglutide significantly ameliorated the injury of mitochondria by increasing the number (+441%) and the area (+113%) of mitochondria and mitochondrial area/100 µm2(+396%) in skeletal muscle of KKAy mice. The results of real-time PCR and Western blot showed that liraglutide downregulated PTP1B while it upregulated PI3K and GLUT4 (P<0.01). The protein level of p-Akt2/Akt2 was also increased (P<0.01).Conclusion. These results revealed that liraglutide could improve myofibril and mitochondria injury in skeletal muscle against T2DM via PTP1B and PI3K/Akt2 signaling pathway.

scholarly journals EGFL6 Modulates WNT Signaling to Drive Esophageal Cancer Metastasis and Proliferation

2020 ◽  
Author(s):  
Yanhong Wang ◽  
Jing Kang ◽  
Jihua Tian ◽  
Hongyan Jia ◽  
Juanjuan Wang ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Expression Level ◽  
Marker Genes ◽  
Invasion And Migration ◽  
Ec Cells

Abstract Background Esophageal cancer (EC) is the sixth deadliest cancer in the world. There has been no breakthrough in the research on EC in the past few decades. Epidermal growth factor-like protein 6 (EGFL6), as a member of the epidermal growth factor superfamily, plays an important role in the occurrence and development of some tumors. However, the role of EGFL6 in the EC has never explored. Methods Immunohistochemical staining was used to evaluate the expression level of EGEC6 protein in human EC and its adjacent non-tumor tissues, and analyzed the correlation between the expression level of EGFL6 protein and clinical pathological indexes and survival rate. In vitro, by constructing EGFL6 silence and overexpressed EC cells,used CCK-8, clone formation, wound healing assays, transwell experiment and flow cytometry to explore the effects of EGFL6 on the proliferation, invasion, migration and apoptosis of EC. By using real-time PCR or western blot to detect the related marker genes of epithelial-mesenchymal transformation (EMT), tumor stem cells (TSCs) and Wnt/β-catenin. In vivo, established a nude mouse EC transplantation tumor model. Results The results showed that the expression level of EGFL6 in EC is significantly higher than that in adjacent non-tumor tissues, and is related to poor prognosis of patients. In vitro, CCK-8, clone formation, wound healing assays, transwell experiment and flow cytometry results show that EGFL6 overexpression can promotes proliferation, invasion and migration of EC cells and inhibits apoptosis. EGFL6 silencing inhibits proliferation, invasion and migration of EC cells and promotes apoptosis. Real-time PCR and Western-blot detection of EMT-related markers found that EGFL6 can induce EC cells EMT. Real-time PCR detection of esophageal cancer stem cell-related genes showed that EGFL6 may maintain the expression of esophageal cancer stem cell-like cell population. Western-blot detection of Wnt/β-catenin signaling marker genes showed that EGFL6 participated in the expression of Wnt/β-catenin signaling pathway. In vivo experiments found that knockout of EGFL6 could inhibit the formation of subcutaneous tumors in nude mice. Conclusion Taken together, our study identified a novel role and mechanism of EGFL6 in EC and provided epigenetic therapeutic strategies for the treatment of EC.

scholarly journals Sclerostin/Receptor Related Protein 4 and Ginkgo Biloba Extract Alleviates β-Glycerophosphate-Induced Vascular Smooth Muscle Cell Calcification By Inhibiting Wnt/β-Catenin Pathway

2019 ◽  
Vol 47 (Suppl. 1) ◽  
pp. 17-23 ◽  
Author(s):  
Jian Wang ◽  
Xiaobo Qiu ◽  
Tianhua Xu ◽  
Zitong Sheng ◽  
Li Yao
Keyword(s):  
Smooth Muscle ◽  
Western Blot ◽  
Ginkgo Biloba ◽  
Real Time Pcr ◽  
Negative Control Group ◽  
Ginkgo Biloba Extract ◽  
Negative Control ◽  
Control Group ◽  
Related Protein ◽  
Alizarin Red

Background: Abnormal mineral metabolism in patients with chronic kidney disease (CKD) may lead to vascular calcification, which is markedly associated with adverse events, including ischemic cardiac diseases and all-cause cardiovascular mortality. Thus, preventing and treating vascular calcification play an important role in improving the prognosis of CKD patients. Objectives: To investigate the potential functions of sclerostin and low-density lipoprotein receptor-related protein 4 (Lrp4) in alleviating the β-glycerophosphate (β-GP)-induced vascular smooth muscle cell (VSMC) calcification, and the protective effect of Ginkgo biloba extract (GBE). Methods: VSMC were extracted from Sprague-Dawley rat aorta and cultured in medium. The VSMCs were divided into 3 groups: (1) Negative control group, (2) β-GP group, in which the VSMCs were treated with β-GP, and (3) GBE and β-GP group, where the VSMCs were treated with both β-GP and GBE. The calcium nodules within the cells were examined by using Alizarin red S staining. The mRNA expression levels of β-catenin and bone gamma-carboxyglutamic-acid-containing proteins (BGP) were detected by real-time PCR. The protein levels of sclerostin and Lrp4 were determined by Western blot. Results: Alizarin red S staining showed that the VSMCs in β-GP group had a distinct orange-red precipitate when compared with VSMCs in the negative control group, while the orange-red precipitate of the GBE and β-GP group was significantly reduced compared to the β-GP group. Real-time PCR showed that the mRNA levels of β-catenin and BGP in VSMCs of β-GP group were significantly higher than those of the negative control group (p < 0.05); while they were significantly reduced in VSMCs of the GBE and β-GP group (p < 0.05). Western blot results showed that the expression of sclerostin in the β-GP group was significantly higher than that in the control group (p < 0.05), whereas Lrp4 was significantly lower than in control group (p < 0.05). Sclerostin in GBE and β-GP group was significantly reduced (p < 0.05), but Lrp4 was significantly elevated when compared with that of the β-GP group (p < 0.05). Conclusion: β-GP induced VSMC calcification by activating the Wnt/β-catenin signaling pathway. Sclerostin and Lrp4 were involved in β-GP-induced VSMC calcification and play an important role. GBE could alleviate VSMC calcification induced by β-GP through inhibiting the Wnt/β-catenin signaling pathway.

scholarly journals High Glucose Enhances the Odonto/Osteogenic Differentiation of Stem Cells from Apical Papilla via NF-KappaB Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Yanping Wang ◽  
Yanqiu Wang ◽  
Yadie Lu ◽  
Jinhua Yu
Keyword(s):  
Stem Cells ◽  
Western Blot ◽  
Osteogenic Differentiation ◽  
Real Time ◽  
Signaling Pathway ◽  
Mtt Assay ◽  
High Glucose ◽  
Rt Pcr ◽  
Alizarin Red ◽  
Apical Papilla

Objective. The transport and metabolism of glucose are important during mammalian development. High glucose can mediate the biological characteristics of mesenchymal stem cells (MSCs). However, the role of high glucose in the odonto/osteogenic differentiation of stem cells from apical papilla (SCAPs) is unclear. Materials and Methods. SCAPs were isolated and identified in vitro. Then, SCAPs were cultured in normal α-MEM and high glucose α-MEM separately. MTT assay was applied to observe the proliferation of SCAPs. ALP activity, alizarin red staining, real-time RT-PCR, and western blot were used to detect the odonto/osteogenic capacity of SCAPs as well as the participation of NF-κB pathway. Results. SCAPs in 25mmol/L glucose group expressed the maximum proteins of RUNX2 and ALP as compared with those in 5, 10, and 15 mmol/L groups. MTT assay showed that 25 mmol/L glucose suppressed the proliferation of SCAPs. ALP assay, alizarin red staining, real-time RT-PCR, and western blot showed 25 mmol/L high glucose can obviously enhance the odonto/osteogenic capacity of SCAPs. Moreover, the NF-κB pathway was activated in 25mmol/L glucose-treated SCAPs and the odonto/osteogenic differentiation was inhibited following the inhibition of NF-κB signaling pathway. Conclusions. High glucose can enhance the odonto/osteogenic capacity of SCAPs via NF-κB pathway.

scholarly journals Nonmuscle myosin II shRNA inhibit migration and contraction in rat hepatic stellate cells through regulating AKT/mTOR/S6K/4EBP1 signaling pathway

2018 ◽  
Author(s):  
Zhenghong Li ◽  
Yun Feng ◽  
Ruling Zhang ◽  
Peiwen Wang ◽  
Lungen Lu ◽  
...  
Keyword(s):  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Hepatic Stellate Cells ◽  
Real Time Pcr ◽  
Stellate Cell ◽  
Myosin Ii ◽  
Stellate Cells ◽  
Nonmuscle Myosin ◽  
Nonmuscle Myosin Ii

AbstractMigration and contraction of activated hepatic stellate cell (HSC) are essential factors for cirrhosis formation and development. It has been demonstrated that blebbistatin, a nonmuscle myosin II (NMMII) inhibitor, can inhibit the migration and contraction of HSC, whereas the main cell signaling pathway is still unknown. Mammalian target of rapamycin (mTOR) signaling pathway may be involved in many cells migration and contraction, whether NMMII and mTOR have any crosslinks draw our attention. In the currently study, we used LV-RNAi to specifically attenuate mTOR and NMMII in rat HSC. We aimed to examine the effect of mTOR LV-RNAi on the migration and contraction of HSC and explore the crosslink between mTOR cell signal and NMMII. Using real-time PCR and western blot, we found that mTOR and the downstream factors including S6K and 4EBP1 all up-regulated with the activation of HSC, mTOR and NMMII LV-RNAi was transfected into activated HSC using lipofectamine 2000. The levels of mRNA and proteins were also examined using real-time PCR and western blot respectively. The expression of mTOR can be down-regulated by NMMII LV-RNAi significantly, as well as the expression of S6K, 4EBP1, α-SMA and collagen I, but the level of AKT was up-regulated. Then we used Transwell system and collagen lattices to examine the NMMII and mTOR LV-RNAi efficiency on HSC migration and contraction, as we hypothesized, both of the LV-RNAi could inhibit HSC migration and contraction significantly. These results indicated that nonmuscle myosin II shRNA inhibit migration and contraction in rat hepatic stellate cells through the regulation of mTOR/S6K/4EBP1 signaling pathway

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.

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