syedzayyan/paper_mill_benchmark huggingface dataset:
Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

This study aimed to explore the effect of micro rna-592-5p (mi r-592-5p) on hypoxic-ischemic brain damage (hibd)-induced hippocampal neuronal injury in a neonatal mouse model relative to the involvement of one target gene, ptgdr, and the pgd2/ dp signaling pathway.Methods: a total of 30 neonatal mice aged 7 days were randomly selected to establish an hibd mouse model.Hippocampal neuronal cells were transfected into a control group, a blank group, a negative control (nc) group, an mi r-592-5p mimics group, an mi r-592-5p inhibitors group, an si rna-ptgdr group and an mi r-592-5p inhibitors + si rna-ptgdr group.Reverse transcription-quantitative polymerase chain reaction (rt-q pcr) and western blot analyses were performed to detect the expression levels of mi r-592-5p, ptgdr, dp2, bcl-2 and bax in tissues and cells.Cell proliferation, cell cycle and apoptosis were detected by mtt assay and flow cytometry, respectively.Results: the expression levels of mi r-592-5p and bcl-2 decreased, while the expression levels of ptgdr, dp2 and bax increased in the hibd group.Ptgdr is a target gene of mi r-592-2p.Compared with the nc and blank groups, the expression levels of ptgdr, dp2 and bax decreased, while the expression levels of mi r-592-5p and bcl-2 increased in the mi r-592-5p mimics group.The si rna-ptgdr group showed the same trend as that observed in the mi r-592-5p mimics group, except with no difference in mi r-592-5p expression.The mi r-592-5p inhibitors group showed an opposite gene expression trend compared to that in the mi r-592-5p mimics group.The s phase of the cell cycle was prolonged, the g1 phase was reduced, proliferation was increased, and the apoptosis rate was decreased in the si rna-ptgdr and mi r-592-5p mimics groups.Opposite trends for cell cycle, proliferation and apoptosis were observed in the mi r-592-5p inhibitors group.Conclusions: our study suggests that mi r-592-5p upregulation protects against hippocampal neuronal injury caused by hibd by targeting ptgdr and inhibiting the pgd2/dp signaling pathway.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MicroRNA-374 Exerts Protective Effects by Inhibiting SP1 Through Activating the PI3K/ Akt Pathway in Rat Models of Myocardial Ischemia-Reperfusion After Sevoflurane Preconditioning

Ischemic heart disease is a leading cause of death in cardiovascular diseases, and micro rnas (mi rs) have been reported to be potential therapeutic targets in heart disease.Herein, this study aims to investigate the effects of micro rna (mi r)-374 on myocardial ischemia-reperfusion (i/r) injury in rat models pretreated with sevoflurane by targeting sp1 through the pi3k/akt pathway.Methods: sd rats were grouped into sham, i/r and sevoflurane + i/r (sevoflurane preconditioning and i/r) groups.The biochemical indicators, pathological changes, positive expression of sp1 protein, and apoptosis rates were measured using biochemical detection, evans blue-ttc staining, immunohistochemistry and tunel staining.Rt-q pcr and western blotting were used to investigate the expression of mi r-374 m rna and the protein expression of sp1, pi3k, ho-1, p53, i nos, c-fos, akt/p-akt, and gsk-3β/p-gsk-3β.Cardiomyocytes were treated with mi r-374 mimics, mi r-374 inhibitors, or si rna-sp1.Cardiomyocyte proliferation and cycle distribution and apoptosis were studied by mtt and flow cytometry.Results: compared with the i/r group, in the sevoflurane + i/r group, serum sod and il-10 increased, while mda, ldh, ck, tnf-α, il-6 and il-10 decreased, as did the percentage of infarct area, the positive rate of sp1 and the apoptosis index.The expression of sp1, p53, i nos and c-fos decreased, and the mi r-374 expression of pi3k, ho-1, akt/p-akt, gsk-3β/p-gsk-3β increased.With the upregulation of mi r-374 and the downregulation of sp1, the expression of sp1, p53, i nos and c-fos decreased, as did the proportion of cells in g1 phase and the apoptosis rate; the expression of pi3k, ho-1, akt/p-akt, gsk-3β/p-gsk-3β increased.The results in the mi r-374 inhibitor group contrasted with the above results.Conclusion: the results indicated that mi r-374 could alleviate myocardial i/r damage in rat models pretreated with sevoflurane by targeting sp1 by activating the pi3k/akt pathway.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

Long non-coding rna (lnc rna) and glucagon-like peptide 1 receptor (glp-1r) are crucial for heart development and for adult heart structural maintenance and function.Herein, we performed a study to explore the effect of lnc rna linc00652 (linc00652) on myocardial ischemia-reperfusion (i/r) injury by targeting glp-1r through the cyclic adenosine monophosphate-protein kinase a (c amp/pka) pathway.Methods: bioinformatics software was used to screen the long-chain non-coding rnas associated with myocardial ischemia-reperfusion and to predict target genes.The m rna and protein levels of linc00652, glp-1r and creb were detected by rt-q pcr and western blotting.In order to identify the interaction between linc00652 and myocardial i/r injury, the cardiac function, the hemodynamic changes, the pathological changes of the myocardial tissues, the myocardial infarct size, and the apoptosis of myocardial cells of mice were measured.Meanwhile, the levels of serum il-1β and tnf-α were detected.Results: linc00652 was overexpressed in the myocardial cells of mice with myocardial i/r injury.Glp-1r is the target gene of linc00652.We also determined higher levels of linc00652 and glp-1r in the i/r modeled mice.Additionally, si-linc00652 decreased cardiac pathology, infarct size, apoptosis rates of myocardial cells, and levels of il-1β and tnf-α, and increased glp-1r expression cardiac function, normal hemodynamic index, and the expression and phosphorylation of glp-1r and creb proteins.Conclusion: taken together, our key findings of the present highlight linc00652 inhibits the activation of the c amp/pka pathway by targeting glp-1r to reduce the protective effect of sevoflurane on myocardial i/r injury in mice.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Long Noncoding RNA FER1L4 Suppresses Tumorigenesis by Regulating the Expression of PTEN Targeting miR-18a-5p in Osteosarcoma

Novel long non-coding rna fer-1-like protein 4 (fer1l4) has been reported to play crucial regulatory roles in tumor progression.However, its clinical significance and biological role in osteosarcoma (os) is completely unknown.The aim of the present study was to investigate the role of fer1l4 in os progression and the underlying mechanism.Methods: we analyzed the expression levels of fer1l4 in tissues of os patients and cell lines via quantitative rt-pcr (q rt-pcr).The effect of fer1l4 on cell proliferation, colony formation, migration and invasion was analyzed by cell counting kit-8 (cck-8), colony formation, wound healing and transwell invasion assay, respectively.Novel targets of fer1l4 were selected through a bioinformatics soft and confirmed using a dual-luciferase reporter system and q rt-pcr.To detect the role of fer1l4 in vivo tumorigenesis, tumor xenografts were created.Results: we found that the expression of fer1l4 was significantly downregulated in os tissues and cell lines; moreover, low expression of fer1l4 was associated with advanced tumor-nude-metastasis (tnm) stage, lymph node metastases, and poor overall survival.Functional assays showed that upregulation of fer1l4 significantly inhibited os cell proliferation, colony formation, migration, and invasion in vitro, as well as suppressed tumor growth in vivo.Assays performed to determine the underlying mechanism, indicated that fer1l4 interacted directly with mi r-18a-5p.Subsequently, we found that fer1l4 significantly increased pten expression, a known target of mi r-18a-5p, in os cells.Furthermore, pten was found to be down-regulated, and positively correlated with fer1l4 in os tissues.Conclusion: these findings suggest that fer1l4, acting as a competing endogenous rna (ce rna) of mi r-18a-5p, exerts its anti-cancer role by modulating the expression of pten.Thus, fer1l4 may be a novel target for the prevention and treatment of os.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MiR-1-3p Suppresses the Proliferation, Invasion and Migration of Bladder Cancer Cells by Up-Regulating SFRP1 Expression

Bladder cancer is of compelling morbidity and mortality due to its high recurrence rate.Little development has been made in the last decades in the therapy methods.Thus, the mechanism of its growth and invasiveness involving novel molecular targets are needed.Objective: our research objective is to confirm the hypothesis that mi r-1-3p suppresses the proliferation, invasion and migration of bladder cancer cells.Methods: the expression levels of mi r-1-3p and sfrp1 were evaluated using rt-q pcr in bladder cancer tissues and cells as well as in normal tissues and cells.J82 cell lines were selected as experiment subjects due to their low expression levels of mi r-1-3p.Plasmids carrying mi r-1-3p mimics, mi r-1-3p inhibitors and sfrp1 were transfected into the j82 cell lines.Subsequently, the protein expression of sfrp1 was detected using western blot analysis, and cell proliferation, apoptosis, invasion and migration ability was measured using mtt, the flow cytometry, the transwell test and wound healing assays, respectively results: bladder cancer tissues and cells exhibited significant decrease in the expression of mi r-1-3p and sfrp1 compared to normal tissues and cells, and human bladder cancer cell line j82 exhibited the most significant decrease in these expressions (p &lt; 0.05).Mi r-1-3p up-regulates sfrp1 expression in bladder cancer cells, and the over-expression of mi r-1-3p can suppress the proliferation, invasion and migration ability of bladder cancer cells.This mechanism is similar to the effect of sfrp1 over-expression on bladder cancer cells.Conclusion: mi r-1-3p suppresses the proliferation, invasion and migration of bladder cancer cells by up-regulating sfrp1 expression.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
Effects of PKM2 Gene Silencing on the Proliferation and Apoptosis of Colorectal Cancer LS-147T and SW620 Cells

This paper aims to explore the effects of pyruvate kinase (pk) m2 gene silencing on the proliferation and apoptosis of colorectal cancer (crc) ls-147t and sw620 cells.Methods: crc ls-147t and sw620 cells highly expressing pkm2 were randomly selected by quantitative real-time polymerase chain reaction (q rt-pcr) and then assigned into the blank (no transfection), pkm2-sh rna (transfection with sh rna) and empty plasmid (transfection with empty plasmid) groups.Immunofluorescence was applied to detect pkm2 protein expression.Q rt-pcr and western blotting were conducted to assess m rna and protein expression of pkm2, p53 and p21.The cell counting kit-8 (cck-8) assay was used to assess cell proliferation.Flow cytometry was used to assess the cell cycle and apoptosis rate, and a senescence-associated β-galactosidase staining kit was used to assess cell senescence.Results: pkm2 exhibited high m rna expression among crc ls-147t and sw620 cells with remarkable protein expression noted in the cytoplasm and nucleus.The pkm2-sh rna group exhibited reduced pkm2 m rna and protein expression, whereas p53 and p21 expression was increased compared with the blank and empty plasmid groups.Cell proliferation in pkm2-sh rna cells decreased significantly compared with the blank group and empty plasmid groups.The pkm2-sh rna group exhibited more cells in the g1 phase and fewer cells in the g2/m phase compared with the blank and empty plasmid groups.In addition, the pkm2-sh rna group exhibited significantly increased apoptosis rates and β-galactosidase activity compared with the blank and empty plasmid groups.Conclusion: our study demonstrates that pkm2 gene silencing suppresses proliferation and promotes apoptosis in ls-147t and sw620 cells.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Chronic respiratory conditions continue to plague millions of people worldwide.We aimed to elucidate the detailed mechanisms of micro rna-485 (mi r-485) in airway smooth muscle cell (asmc) proliferation and apoptosis in chronic asthmatic mice.Methods: a mouse model of chronic asthma was established.Ovalbumin was used to induce chronic asthma in the mice.The levels of transforming growth factor β (tgf-β), interleukin (il)-4, il-5, il-13 and il-17 in bronchoalveolar lavage fluid in mice were measured by enzyme-linked immunoassays (elisas).Asmcs were transfected with mi r-485 mimic, mi r-485 inhibitor and si rna-smurf2.The reverse transcription quantitative polymerase chain reaction (rt-q pcr) and western blot analyses were applied to detect the m rna and protein levels of smurf2, α-sma, tgf-β1 and decapentaplegic homolog (smads).The mtt assay was utilized for cell proliferation, while flow cytometry was conducted to assess cell cycle distribution and apoptosis.Results: lower expression of mi r-485 and higher expression levels of tgf-β1, il-4, il-5, il-13 and il-17 were detected in mice with chronic asthma.Smurf2 was identified as the target gene of mi r-485.Upregulation of mi r-485 mimic and downregulation of smurf2 decreased expression levels of smurf2, α-sma, tgf-β1 and smad3, inhibited cell proliferation and increased apoptosis, while contrary results were observed in asmcs transfected with mi r-485 inhibitor.Conclusion: overexpressed mi r-485 inhibits cell proliferation and promotes apoptosis of asmcs through the smurf2-mediated tgf-β/smads signaling pathway in mice with chronic asthma.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
MicroRNA-142 Inhibits Proliferation and Promotes Apoptosis in Airway Smooth Muscle Cells During Airway Remodeling in Asthmatic Rats via the Inhibition of TGF-β -Dependent EGFR Signaling Pathway

Asthma is a heterogeneous disease characterized by chronic airway inflammation resulting from airway hyper-responsiveness to diverse stimuli.In this study, we investigated whether micro rna-142 (mi r-142) expression affects proliferation and apoptosis in airway smooth muscle cells (asmcs) during airway remodeling in asthmatic rats.Methods: thirty six wistar rats were randomly classified into a control group and an model group.Mi r-142 mimics and inhibitors were constructed, and asmcs were transfected using liposomes according to the following groups: blank, negative control (nc), mi r-142 mimics, mi r-142 inhibitors, si-tgf-β and mi r-142 inhibitors + si-tgf-β.We verified that mi r-142 targets tgf-β using a dual-luciferase reporter assay.The expression levels of mi r-142, tgf-β, egfr and apoptosis signaling pathway-related genes were determined using rt-q pcr and western blotting.Changes in cell proliferation, cell cycle progression and apoptosis were analyzed using mtt assays and flow cytometry.Results: rats with asthma had higher expression levels of egfr and akt and lower mi r-142 levels.Mi r-142 was negatively correlated with tgf-β expression.In asmcs, the expression of tgf-β, egfr, akt, phosphorylated-akt (p-akt), bcl-2 and bcl-xl and the rate of early apoptosis were decreased while expression of bax and p21 and the proliferation rate were elevated with the upregulation of mi r-142.The opposite results were observed with the downregulation of mi r-142.Finally, the proliferative rate was decreased while the apoptosis rate was increased and expression levels of egfr, akt, p-akt, bcl-2 and bcl-xl were reduced while bax and p21 were elevated in the asmcs transfected with mi r-142 inhibitors and si-tgf-β.Conclusion: the results of our study suggest that mi r-142 inhibits proliferation and promotes apoptosis in asmcs during airway remodeling in asthmatic rats by inhibiting tgf-β expression via a mechanism involving the egfr signaling pathway.

Journal: Cellular Physiology and Biochemistry (2018)
Publication types: Research Article;
Protective Effects of Microrna-22 Against Endothelial Cell Injury by Targeting NLRP3 Through Suppression of the Inflammasome Signaling Pathway in a Rat Model of Coronary Heart Disease

This study aimed to identify the role of micro rna-22 (mi r-22) in endothelial cell (ec) injury in coronary heart disease (chd) by targeting nlrp3 through the inflammasome signaling pathway.Methods: a total of 24 healthy male sprague-dawley (sd) rats were divided into normal and atherosclerosis groups.The atherosclerosis rats were assigned into blank, negative control (nc), mi r-22 mimic, mi r-22 inhibitor and mi r-22 inhibitor + si nlrp3 groups.A luciferase reporter gene assay was used to detect the relationship between mi r-22 and nlrp3.Mi r-22 expression as well as nlrp3 and caspase-1 m rna and protein expression were measured using quantitative real-time polymerase chain reaction (q rt-pcr) and western blotting.The activity and apoptosis of coronary arterial endothelial cells (caecs) were determined by mtt and hoechst 33258.Caec lumen formation was detected by a lumen formation assay.An enzyme-linked immunosorbent assay (elisa) was used to detect il-1β, il-6, il-10 and il-18 levels.Results: the results indicated that the atherosclerosis group significantly decreased mi r-22 expression but increased nlrp3 and caspase-1 m rna and protein expression.The cell survival rate was significantly increased in the mi r-22 mimic group and significantly reduced in the mi r-22 inhibitor group.The mi r-22 mimic group displayed a lower apoptosis rate and more cells with obvious lumen walls and numerous tubular structures, while cells in the mi r-22 inhibitor group were unable to form lumen walls and had a scattered distribution compared to the blank group.The elisa showed that il-1β, il-6 and il-18 levels were markedly decreased, while il-10 was clearly increased in the mi r-22 mimic group.In contrast, in the mi r-22 inhibitor group, il-1β, il-6 and il-18 levels were significantly increased, and il-10 levels were decreased.Conclusion: our findings indicated that mi r-22 could lower the levels of pro-inflammatory cytokines by inhibiting the nlrp3 inflammasome pathway, which suppresses caec apoptosis and protects caecs in rats with chd.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;
In Vitro Effects of HAS-2 Gene Silencing on the Proliferation and Apoptosis of the MCF-7 Human Breast Cancer Cell Line

Breast cancer is characterized by a distinct metastatic pattern involving the regional lymph nodes, bone marrow, lung and liver.This study is aimed to investigate the effects of silencing the has-2 gene on the proliferation and apoptosis of human breast cancer cells.Methods: mcf-7 cells were collected and assigned into control, scrambled si rna and has-2- si rna groups.After transfection, the morphological changes in the mcf-7 cells were observed using phase contrast microscopy.Q rt-pcr and western blot assays were used to detect the m rna and protein expression of apoptosis-related proteins.Cck-8 and flow cytometry were performed to evaluate cell proliferation, the cell cycle and apoptosis.Results: in the control and the scrambled si rna groups, cells grew adhered to the wall and mainly showed a spindle shape with a clear nucleolus.Compared with the control and scrambled si rna groups, increases in the number of cells in early apoptosis and metaphase cells in apoptosis were observed in the has-2-si rna group.The has-2-si rna group showed decreased expression of has-2 relative to that in the control and scrambled si rna groups.No significant differences in cell proliferation, cell cycle distribution or apoptosis were noted between the control and scrambled si rna groups.In the has-2-si rna group, the cell proliferation ability decreased significantly, but the number of cells in the g0/g1 stage, the number of apoptotic cells and the expression of caspase-3 and caspase-9 increased significantly.Conclusion: our findings indicate that has-2 gene silencing may inhibit proliferation and promote apoptosis in the mcf-7 human breast cancer cell line.

Journal: Cellular Physiology and Biochemistry (2016)
Publication types: Research Article;
Mechanism of MicroRNA-146a/Notch2 Signaling Regulating IL-6 in Graves Ophthalmopathy

We intended to investigate the significance of micro rna-146a, notch2 and il-6 on graves ophthalmopathy (go) and the relationships among them.Methods: about 27 go patients were incorporated in this study, including 13 patients with inactive go and14 patients with active go.Another 15 patients who had previously received strabismus orthopedics or ophthalmectomy due to trauma were selected as the control population.Qrt-pcr assay was used to detect micro rna-146a and notch2 expression levels in plasma.Mtt assay and flow cytometry were respectively used to assess the viability and mitosis of the fibroblasts isolated from orbital connective tissue.Double antibody sandwich enzyme-linked immunosorbent assay (elisa) was employed to detect serum il-6 levels.The dual luciferase reporter gene assay was used to verify the targeting relationship between micro rna-146a and notch2.Results: compared with the control group, the relative expression of mi r-146a was significantly increased whereas the relative expression of notch2 was significantly decreased (all p &lt; 0.05) in go patients compare with the control.Notch2 can be directly targeted by micro rna-146a.The over-expression of mi r-146a markedly facilitated orbital fibroblasts (ofs) viability and mitosis whereas markedly suppressed cell apoptosis (all p &lt; 0.05).Exogenous micro rna-146a mimics could down-regulat the expression of notch2 and up-regulate il-6 (p &lt; 0.05).The inhibition of micro rna-146 resulted in the elevated expression of notch2 and decreased expression of il-6 (p &lt; 0.05).Conclusion: micro rna-146a may increase the il-6 levels and exacerbate go by directly targeting notch2.

Journal: Cellular Physiology and Biochemistry (2017)
Publication types: Research Article;