Effects of Abnormal Savda Munzip on the Proliferation Activity and Migration Ability of Fibroblasts Derived from Hypertrophic Scar In Vitro

Background. To explore the effect of ASMq on proliferation and migration ability of the fibroblast derived from HS of donor (HSFbs) in vitro.Methods. The HSFbs were cultured from tissue specimens and passaged to the 3~4 generation, which were treated with the different concentrations of ASMq and 5-Fu from 1 to 11 days. The difference of HSFbs proliferation activity was analyzed by the CCK-8 method. The HSFbs migration ability in ASMq (0.4 mg/mL) was analyzed by the Cell Scratch method.Results. Transmission electron microscope result shows ASMq concentration significantly increases and fibroblast cell structure markedly change in the experimental group. The proliferation activity of the HSFbs was obviously weakened in ASMq groups than those of the group A (P<0.05) at seven days. The group C (0.4 mg/mL) is better suitable than other three ASMq treatment groups. Cell Migration Assay shows that the migration ability HSFbs was significantly reduced in ASMq (0.4 mg/mL) treatment group compared with those of blank control group at both 24 h and 48 h (P<0.05).Conclusions. These results suggest that ASMq effectively restrains the proliferation and migration ability of the HTSFbs in vitro, which can be one of the mechanisms for the prevention and treatment of HS.

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Based on the Effect of Huazhengsanji Prescription and Cisplatin on Hypoxia-Induced HepG2 Hepatoma Cells HIF-1α and VEGF

10.21203/rs.3.rs-117504/v1 ◽

2020 ◽

Author(s):

Shanshan Wang ◽

Liu Yangyang ◽

Xu Xiaohao ◽

Liu Tiejun ◽

Shu Zunhua ◽

...

Keyword(s):

Hepg2 Cells ◽

Hepatoma Cells ◽

Combination Group ◽

Control Group ◽

High Dose ◽

Model Group ◽

Blank Control Group ◽

Migration Ability ◽

And Migration ◽

Proliferation And Migration

Abstract BackgroundHepatoma is one of the most common malignant tumors in my country, and its occurrence and development play an important role in the molecular mechanism of hypoxia microenvironment and angiogenesis. Huazhengsanji prescription(HZSJ) is an empirical prescription for the treatment of liver cancer, but its specific anti-tumor molecular mechanism is still unclear, and whether it has a synergistic effect with cisplatin(DDP), a chemotherapy drug for liver cancer, has not been reported yet. This article discusses the inhibition of the proliferation and migration of HepG2 hepatocarcinoma cells and the difference in the expression of HIF-1α and VEGF when the HZSJ, DDP and the two are used in combination, and compares and analyzes the mechanism of the HZSJ in enhancing the anticancer sensitivity of chemotherapeutics.MethodsHepG2 Hepatoma cells were divided into blank control group, hypoxia model group, DDP group, HZSJ group, HZSJ+DDP group, and the hypoxia environment was induced by the CoCl2 method. MTT method detects cell proliferation ability, scratch test detects cell migration ability, immunofluorescence method and western blot detect HIF-1α and VEGF protein expression.ResultsHZSJ has the effect of inhibiting the proliferation and migration of HepG2 cells, and has obvious concentration-dependent; The combined application of HZSJ and DDP has significantly stronger inhibitory effect on cell proliferation than the HZSJ group (P<0.01) and the DDP group (P<0.01, P<0.001). High-dose HZSJ can inhibit the migration ability of HepG2 cells (P<0.01); the combination of HZSJ and DDP can significantly reduce the migration rate of HepG2 cells after induction (P<0.01, P<0.01, P <0.01). The results of immunofluorescence and western blot showed that: compared with the blank control group, the expression levels of HIF-1α and VEGF protein in the model group were significantly increased (P<0.05, P<0.01, P<0.001); compared with the model group and DDP The expression of HIF-1α protein in the high-dose HZSJ group (200μg/mL) and the combination group decreased (P<0.05, P<0.01, P<0.001), but there was no difference between the groups. Compared with the model group, the high-dose HZSJ group (200μg/mL) can reduce the expression of VEGF (P<0.05); compared with the model group and the DDP group, the combination group can reduce the expression of VEGF (P< 0.01, P<0.001), and has obvious concentration dependence.ConclusionsHZSJ can inhibit the proliferation and migration of HepG2 hepatoma cells under hypoxia, which may be related to the reduction of HIF-1α and VEGF expression, and its increase in the anticancer sensitivity of the chemotherapy drug DDP may be related to both The synergistic inhibition of VEGF expression is related.

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miR-208a-3p promotes NSCLC proliferation and migration by suppressing lncRNA-MEG3 expression

10.21203/rs.3.rs-877755/v1 ◽

2021 ◽

Author(s):

Linfei Yang ◽

Qian Li ◽

Hai Zhong ◽

Liang Ye ◽

Surong Fang ◽

...

Keyword(s):

Protein Extraction ◽

Underlying Mechanism ◽

In Vitro Assays ◽

Cell Viability Assay ◽

Migration Assay ◽

Normal Tissues ◽

Viability Assay ◽

And Migration ◽

Proliferation And Migration

Abstract Background The disordered expression of maternally expressed gene 3 (MEG3) has been observed in non-small-cell lung cancer (NSCLC). However, the molecular mechanism accounting for this abnormal expression is not fully understood. Methods MEG3 expression was detected by qRT-PCR in 51 cases of NSCLC and adjacent normal tissues. Then, the relationship between MEG3 and miR-208a-3p was assessed in vitro by cell viability assay, cell migration assay, protein extraction and western blot analysis. Resoults We observed that MEG3 expression was decreased in NSCLC tissues. And MEG3 expression was negatively related to lymph node metastasis and differentiation. Moreover, MEG3 expression is regulated by miR-208a-3p expression by overexpression and knockout experiments. Furthermore, we focused on the underlying mechanism of MEG3 downregulation. We found that the overexpression of miR-208a-3p reduced the level of MEG3 expression based on computational predictions and in vitro assays. Using CCK-8 and transwell migration assays, we found that the overexpression of miR-208a-3p can increased proliferation and apoptosis in NSCLC cells. Moreover, the depletion of MEG3 rescued the proliferation and migration induced by miR-208a-3p knockdown. Conclusion Taken together, the results of this study reveal that miR-208a-3p promotes NSCLC tumorigenesis by negatively regulating MEG3 expression and functions as an oncogenic miRNA in NSCLC.

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The Potential Role of Cycloastragenol in Promoting Diabetic Wound Repair In Vitro

BioMed Research International ◽

10.1155/2019/7023950 ◽

2019 ◽

Vol 2019 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Yi Cao ◽

Li Xu ◽

Xiaohong Yang ◽

Yuan Dong ◽

Hongbin Luo ◽

...

Keyword(s):

Wound Healing ◽

Wound Repair ◽

Cell Counting ◽

Migration Ability ◽

Cell Growth And Migration ◽

Cell Based Therapy ◽

And Migration ◽

Proliferation And Migration

Background. Refractory wound healing is a severe complication of diabetes with a significant socioeconomic burden. Whereas current therapies are insufficient to accelerate repair, stem cell-based therapy is increasingly recognized as an alternative that improves healing outcomes. The aim of the present study is to explore the role of cycloastragenol (CAG), a naturally occurring compound in Astragali Radix, in ameliorating refractory cutaneous wound healing in vitro, which may provide a new insight into therapeutic strategy for diabetic wounds. Methods. Human epidermal stem cells (EpSCs) obtained from nine patients were exposed to CAG, with or without DKK1 (a Wnt signaling inhibitor). A lentiviral short hairpin RNA (shRNA) system was used to establish the telomerase reverse transcriptase (TERT) and β-catenin knockdown cell line. Cell counting kit-8, scratch wound healing, and transwell migration assay were used to determine the effects of CAG in cell growth and migration. The activation of TERT, β-catenin, and c-Myc was determined using real-time qPCR and western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate the associations among CAG, TERT, and Wnt/β-catenin signals. Results. CAG not only promoted the proliferation and migration ability of EpSCs but also increased the expression levels of TERT, β-catenin, c-Myc. These effects of CAG were most pronounced at a dose of 0.3 μM. Notably, the CAG-promoted proliferative and migratory abilities of EpSCs were abrogated in TERT and β-catenin-silenced cells. In addition, the ChIP results strongly suggested that CAG-modulated TERT was closely associated with the activation of Wnt/β-catenin signaling. Conclusion. Our data indicate that CAG is a TERT activator of EpSCs and is associated with their proliferation and migration, a role it may play through the activation of Wnt/β-catenin signaling.

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Comparing effects and action mechanisms of BPA and BPS on HTR-8/SVneo placental cells

Biology of Reproduction ◽

10.1093/biolre/ioab139 ◽

2021 ◽

Author(s):

Marilin Profita ◽

Elena Fabbri ◽

Enzo Spisni ◽

Paola Valbonesi

Keyword(s):

Large Population ◽

First Trimester ◽

Maternal Serum ◽

Extravillous Trophoblast ◽

Bisphenol S ◽

Migration Ability ◽

Cord Serum ◽

And Migration ◽

Proliferation And Migration

Abstract Bisphenol A (BPA) is one of the most investigated compound as a suspected endocrine disrupting chemical. It has been found at nM concentrations in the maternal serum, cord serum, and amniotic fluid and also permeates placental tissues. Attempts are being made to replace BPA with the analog Bisphenol S (BPS). Also BPS was found in maternal and umbilical cord serum, and urine samples from a large population of pregnant women. A few studies investigated BPA impact on the placentation process, and even less are available for BPS. This work aimed to elucidate and compare the effects of BPA and BPS on physiological functions of HTR-8/SVneo cells, derived from extravillous trophoblast of first-trimester pregnancy. Proliferation and migration ability of trophoblast cells were assessed in vitro after exposure to BPA or BPS (10−13 - 10−3 M). Further, induction of the inflammatory response by the bisphenols was studied. To provide insight into the molecular pathways implicated in the responses, experiments were carried out in the presence or absence of tamoxifen as estrogen receptors (ERs) blocker, and U0126 as ERK1/2 phosphorylation inhibitor. Data indicate that BPA significantly affects both proliferation and migration of HTR-8/SVneo cells, through ER and ERK1/2 mediated processes. Differently, BPS only acts on proliferation, again through ER and ERK1/2 mediated processes. BPS, but not BPA, induces secretion of interleukins 6 and 8. Such effect is inhibited by blocking ERK1/2 phosphorylation. To the best of our knowledge, these are the first data showing that BPS affects trophoblast functions through ER/MAPK modulation.

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The Mechanism of Human Umbilical Mesenchymal Stem Cells (HUMSC) on Biological Behavior of Human Papillomavirus (HPV) Cells Through Restraining the Programmed Cell Death Protein 1/Programmed Cell Death Ligand 1 (PD-1/PD-L1) Signal Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2022.2884 ◽

2022 ◽

Vol 12 (2) ◽

pp. 265-272

Author(s):

Min Wang ◽

Yanong Zhu ◽

Tongmin Li ◽

Chaofeng Xia

Keyword(s):

Cell Death ◽

Test Group ◽

Signal Pathway ◽

Biological Behavior ◽

Control Group ◽

Migration Ability ◽

Blank Group ◽

Invasion And Migration ◽

And Migration

Biological behavior of HPV cell was observed by HUMSC through restraining PD-1/PD-L1 signal pathway. And HUMSC was adopted as target cell for the treatment on HPV. The rat HPV model was established and divided into three groups including blank group, control group and test group according to different reagents being injected into rats. Use HE staining method to observe the cancerous transformation of tumor tissue sections. The gene presentation of PD-1/PD-L1 and lymphocyte was detected with Western blot. The invasion and migration condition of cancer cells was observed from experiment in vitro. The quantity of cancer cells in test group was the least. And invasion and migration ability in test group was the weakest. The control group was the second. The number of tumor cells in the blank group was the largest. Strongest ability to invade and migrate. The presentation of PD-L1 was restrained partly by HUMSC. The increasing of immune-associated cells could be prompted by HUMSC. The quantity of CD3+, CD4+ and CD8+ in PB was the most in test group. The expression of blank groups is the lowest than others restrained by HUMSC. And quantity of abundant immune cells including CD3+, CD4+ and CD8+ could be activated partly through activating immune action of body. And monitoring function of immune system on HPV cells could be increased effectively. The invasion and migration ability in vitro of HPV could be reduced partly.

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The Expression and Significance of mTORC1 in Diabetic Retinopathy

10.21203/rs.2.18087/v1 ◽

2019 ◽

Author(s):

Yanli Liu ◽

Yarong Zheng ◽

Yekai Zhou ◽

Yi Liu ◽

Mengjuan Xie ◽

...

Keyword(s):

Cell Proliferation ◽

Diabetic Retinopathy ◽

Western Blotting ◽

Rat Model ◽

High Glucose ◽

Control Group ◽

Diabetes Group ◽

And Migration ◽

Proliferation And Migration

Abstract Background: To investigate the expression and significance of mechanistic target of rapamycin complex 1(mTORC1) in diabetic retinopathy(DR), and to find new targets and new methods for the treatment of DR.Methods: A DR rat model was prepared by general feeding combined with intraperitoneal injection of 10% streptozotocin (60 mg/kg). The rats were randomly divided into a control group (NDM group) and diabetes group (DM group).Three months later,the degrees of retinopathy were determined using hematoxylin and eosin staining,and the levels of p-S6, VEGF, and PEDF proteins were detected by immunohistochemistry and western blotting. Human retinal capillary endothelial cells (HRCECs) were cultured in high glucose conditions,then treated with rapamycin or transfected with siTSC1.The protein levels of p-S6 were assessed by western blotting. The 5-ethynyl-2´-deoxyuridine assay was used to detect cell proliferation, and the Transwell assay was used to detect cell migration.Results: A DM rat model was successfully developed. The expressions of p-S6 and VEGF proteins were significantly increased in the DM group (p < 0.05), and the expression of PEDF protein was significantly decreased compared with the control group (p < 0.05). In vitro,the p-S6 protein in high glucose(HG) induced HRCECs was increased compared with the normal control (p < 0.05), and cell proliferation and migration were increased compared with the normal glucose(NG) group (p < 0.05). After transfection with siTSC1 to activate mTORC1,the expression of p-S6 was increased,as well as cell proliferation and migration.In contrast rapamycin decreased p-S6 expression in HG induced HRCECs, as well as decrased proliferation and migration (p < 0.05).Conclusion: The mTORC1 played an important role in DR. After activation, mTORC1 induced expression of the p-S6 protein, regulated the expressions of VEGF and PEDF proteins, and changed the proliferation and migration of endothelial cells.The mTORC1 can therefore be used as a new target,as well as in the treatment of DR.

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Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway

Journal of Ophthalmology ◽

10.1155/2018/5708537 ◽

2018 ◽

Vol 2018 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

He Hu ◽

Shanshan Li ◽

Jianqiao Li ◽

Chao Huang ◽

Fang Zhou ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Retinal Pigment ◽

Cell Counting ◽

Control Group ◽

Vegf Receptor ◽

Phosphorylated Akt ◽

And Migration ◽

Proliferation And Migration

Purpose. Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial (RPE) cell, which plays an essential role in the progression of PVR, and the possible mechanisms. Methods. Small interfering (si) RNA-based gene transfer technology was used to decrease FMOD expression and to study its effects on RPEs in vitro. Cell Counting Kit-8 assays, transwells, and flow cytometry analysis were used to measure cell proliferation, migration, cell cycle, and apoptosis. Western blot was used to measure expression of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), extracellular signal-related kinase 1/2 (ERK1/2), and phosphoinositide 3 kinase (PI3K/AKT). Results. After transfection of RPEs with a FMOD-specific siRNA, cell proliferation and migration were inhibited to the percentage of 65% ± 5% and 39% ± 10%, respectively, compared to the control group. Depletion of FMOD induced cell cycle arrest and apoptosis in RPE cells. Downregulation of VEGF, VEGFR2, and phosphorylated AKT (p-AKT) were detected in transfected RPEs. Conclusion. Depletion of FMOD selectively downregulated the expression of VEGF and VEGFR2 and inhibited the signaling pathway of AKT phosphorylation, which consequently inhibited the proliferation and migration of RPE Cell.

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Ginkgolic Acid (GA) Inhibits the Growth of OCa by Inhibiting lncRNA MALAT1/JAK2 Axis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/5481271 ◽

2021 ◽

Vol 2021 ◽

pp. 1-7

Author(s):

Zhiyi Fei ◽

Yi Yu ◽

Mi Xiang ◽

Fang Luo

Keyword(s):

Nude Mice ◽

Acid Group ◽

Control Group ◽

Inhibitory Influence ◽

Migration Ability ◽

Ginkgolic Acid ◽

Lncrna Malat1 ◽

And Migration ◽

The Impact

Objective. We aimed to observe the impact of ginkgolic acid (GA) on the proliferation and metastasis ability of ovarian cancer (OCa) cells and to further explore whether GA affects the malignant progress of OCa via regulating the lncRNA MALAT1/JAK2 axis. Methods. OCa cells SKOV3 and CAOV3 were administered with 1 ng/ml GA, 5 ng/ml GA, 10 ng/ml GA, 20 ng/ml GA, and DSMO as control, respectively. The cell proliferation and migration ability of the abovementioned cells in each group were measured by CCK-8 test and Transwell experiments. The expression levels of lncRNA MALAT1 and JAK2 protein were examined by qRT-PCR and western blot, respectively. Subsequently, in OCa cells treated with GA, lncRNA MALAT1 overexpression vector was transfected to continue to detect the proliferation activity and migration ability of each treatment group. Finally, the regulation of GA on activity of lncRNA MALAT1/JAK2 axis in OCa cells was further explored in nude mice. Results. Our data showed that the proliferation inhibition rate of cells at each ginkgolic acid concentration was higher than that of the control group ( P < 0.05 ), suggesting that GA has an inhibitory influence on the proliferation of OCa cells, in a dose-dependent way. GA was able to inhibit the proliferation rate and migration ability of OCa cells. Administration of ginkgolic acid downregulated the levels of lncRNA MALAT1 and JAK2 protein. Overexpression of lncRNA MALAT1 partially reversed the inhibited OCa proliferative capacity caused by GA treatment. Consistent with the results observed in vitro, we also found that the OCa tumor weight and volume of nude mice injected with lncRNA MALAT1 overexpression vector were enhanced and JAK2 protein level increased remarkably in comparison to the ginkgolic acid group. Conclusions. In summary, GA may exert its inhibitory effect on the proliferative and migratory capacities of OCa cells through suppressing the activity of lncRNA MALAT1/JAK2 axis.

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Hair Growth Promotion Effect of Nelumbinis Semen Extract with High Antioxidant Activity

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/6661373 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Hyeon Ju Park ◽

Guang-Ri Jin ◽

Jae Hyun Jung ◽

Su Bin Hwang ◽

Su Hyun Lee ◽

...

Keyword(s):

Antioxidant Activity ◽

Hair Loss ◽

Hair Growth ◽

Growth Patterns ◽

Control Group ◽

And Migration ◽

Tgf Β1 ◽

Proliferation And Migration ◽

Nelumbinis Semen

This study investigated the hair regeneration promotion and hair loss prevention properties of Nelumbinis Semen (NS) extract in vitro and in vivo. The effect of NS on the proliferation and migration of human dermal papilla cells (hDPCs) was measured in vitro via CCK-8 and scratch migration assays, after which the antioxidant activity of NS was also quantified. NS extracts were then applied to the back of 7-week-old C57BL/6 mice for 3 weeks to monitor hair growth patterns and hair follicle (HF) histology. The mice were divided into three groups: negative control group (NC; DMSO), positive control group (PC; 3% minoxidil), and experimental group (NS extract 1,000 ppm). Moreover, to study the molecular mechanisms by which NS extract regenerates hair growth, real-time PCR was used to analyze factors related to the hair growth cycle. The NS extracts were found to possess high antioxidant properties due to their high flavonoid contents and electron-donating ability. Moreover, NS extracts enhanced hDPC proliferation and migration in a concentration-dependent manner (15.63–125 ppm). The hair growth index and growth area of the NS group (2.81 score, 81%) on day 14 were higher than those of the PC group (2.65 score, 68%) ( p < 0.05 ). Additionally, the HFs of the NS group were located deep in the subcutis, similar to the PC group with developed hair roots. Moreover, the mRNA expression of VEGF and IGF-1 was higher in the NS group compared to the PC group, whereas TGF-β1 expression was lower ( p < 0.05 ). Our findings indicate that NS modulates hair growth by increasing IGF-1 and VEGF expression while inhibiting that of TGF-β1. Therefore, our findings suggest that NS extract is a promising new hair loss treatment derived from a natural substance that helps promote hair growth and prevent hair loss.

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Autophagy-Sirtuin1(SIRT1) Modulated The Endothelial Progenitor Cells (EPCs) Proliferation and Migration Via wnt/β-Catenin/GSK3β Signaling Pathway and Alleviated The Coronary Atherosclerosis (CAS) in Mice

10.21203/rs.3.rs-203648/v1 ◽

2021 ◽

Author(s):

Yanwei Li ◽

Wei Cui ◽

Bing Song ◽

Xuying Ye ◽

Zhuqing Li ◽

...

Keyword(s):

Bone Marrow ◽

Cell Proliferation ◽

Coronary Artery ◽

Signaling Pathway ◽

Pathological Condition ◽

Control Group ◽

And Migration ◽

Sirt1 Activator ◽

Proliferation And Migration

Abstract Background and purpose: SIRT1 exerted its link to CAS risk in humans and EPCs presented its reparative role in CAS. In this study, we explored the role of SIRT1 in CAS mice and also its modulation in EPCs.Methods and materials: ApoE-/- mice were fed with high-fat and high-glucose food to establish the CAS animal model with the normally-raised C57BL/6 mice as a healthy control group. 5 ApoE mice were intravenously injected with SIRT1 activator, SRT 2104 and another 5 were injected with inhibitor Nicotinamide in tail. Weight changes were recorded per week. Blood samples were taken from posterior orbital venous plexus and detected by automatic biochemical analyzer for lipid concentrations. Coronary artery tissues were observed. HE staining displayed the pathological condition while Immunohistochemistry (IHC) evaluated the CD34+/VEGFR2+ relative density. In vitro, EPCs were isolated from bone marrow each group and then purified, cultured and verified using immunofluorescence staining (IFS). Thereafter, we examined the modulatory mechanism of SIRT1 in EPCs by RT-PCR, MTT, Western Blot (WB) and colony formation, scratch methods, connecting the wnt/β-catenin/GSK3β signaling pathway.Results：SIRT1 activation negatively regulated the weight and TC, TG and LDL. SIRT1 activator alleviated the lesion area and decreased the CD34+/VEGFR2+ density which was higher in coronary artery tissues in CAS and SIRT1 inhibitor groups. In vitro, SIRT1 activator promoted the bone marrow-derived EPCs proliferation, migration and activated wnt/β-catenin/GSK3β signaling pathway while inhibited the autophagy biomarkers ATG1 and LC3II. Furthermore, inhibition of autophagy led to the upregulation of SIRT1 and increase in cell proliferation, migration and wnt/β-catenin/GSK3β activity. The suppression of the pathway in turn lowered SIRT1 expression in EPCs, attenuated the cell proliferation and migration and promoted autophagy. Conclusion: Taken all the findings together, this research disclosed that SIRT1 activator might perform its protective role in CAS through autophagy inhibition via wnt/β-catenin/GSK3β signaling pathway in EPCs.

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