A comparison of PGC-1α mRNA and protein expression in response to 1-week endurance training on alternate days or 4 consecutive days

2015 ◽  
Vol 40 (11) ◽  
pp. 1210-1213 ◽  
Author(s):  
Li-Ping Huang ◽  
Min Yao ◽  
Ya-Li Wang ◽  
Allan Davie ◽  
Shi Zhou
Keyword(s):  
Protein Expression ◽  
Endurance Training ◽  
Messenger Rna ◽  
Gastrocnemius Muscle ◽  
Molecular Mechanisms ◽  
Treadmill Exercise ◽  
Cumulative Effect ◽  
Mrna And Protein Expression ◽  
Mechanisms Of Adaptation ◽  
Training Protocols

To understand the molecular mechanisms of adaptation to different training protocols, this study compared the effects of 4 sessions of 90 min treadmill exercise on alternate days or consecutive days in 1 week on messenger RNA (mRNA) and protein expression of proliferator-activated receptor-γ coactivator 1-α in rat gastrocnemius muscle. The mRNA significantly increased by 25.8-fold after alternate-day and 10.1-fold after consecutive-day training, while the protein showed no significant cumulative effect, 1.5–1.7-fold above baseline, in the 2 protocols.

scholarly journals Lycium barbarum Polysaccharides Promote Maturity of Murine Dendritic Cells through Toll-Like Receptor 4-Erk1/2-Blimp1 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xiangguo Duan ◽  
Yaru Lan ◽  
Xiaoyu Zhang ◽  
Shaozhang Hou ◽  
Jian Chen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Signal Molecules ◽  
Toll Like Receptor ◽  
Lycium Barbarum ◽  
Toll Like Receptor 4 ◽  
P38 Inhibitor ◽  
Mrna And Protein Expression ◽  
Lycium Barbarum Polysaccharides

In previous studies, Lycium barbarum polysaccharides (LBP), a traditional Chinese medicine, can promote immature dendritic cells (DCs) to mature. However, the molecular mechanisms by which LBP works are not yet elucidated. Here, we found that LBP can induce DCs maturation, which is mainly characterized by the upregulation of MHCII and costimulatory molecules (CD80, CD86), and increase the production of IL-6 and IL-4. Furthermore, we found that LBP could increase the mRNA and protein expression of TLR4, p38, Erk1/2, JNK, and Blimp1 signal molecules. More interestingly, after blocking by Toll-like receptor 4 inhibitor, Resatorvid (TAK 242), the mRNA and protein expression of TLR4, Erk1/2, and Blimp1 was significantly decreased while the expression of p38 and JNK has not changed. Then, we found that after blocking by p38 inhibitor (SB203580), Erk inhibitor (PD98059), and JNK inhibitor (SP603580) separately, Blimp1 protein expression was significantly reduced; after downregulating Blimp1 by Blimp1-siRNA, the production of IL-6 was reduced. In conclusion, our results indicate that LBP can induce maturation of DCs through the TLR4-Erk1/2-Blimp1 signal pathway instead of the JNK/p38-Blimp1 pathway. Our findings may provide a novel evidence for understanding the molecular mechanisms of LBP on activating murine DCs.

Induction of calcyclin after ischemic injury to rat kidney

1997 ◽  
Vol 273 (3) ◽  
pp. F380-F385 ◽  
Author(s):  
A. J. Lewington ◽  
B. J. Padanilam ◽  
M. R. Hammerman
Keyword(s):  
Protein Expression ◽  
Calcium Binding ◽  
Messenger Rna ◽  
Rat Kidney ◽  
Ischemic Injury ◽  
Recovery Process ◽  
Thick Ascending Limb ◽  
Mrna And Protein Expression ◽  
Polymerase Chain

Genes differentially expressed after acute renal ischemic injury were identified using differential display-polymerase chain reaction (DD-PCR). Messenger RNA for calcyclin, a member of the S100 family of calcium-binding proteins, is increased in kidneys by 6 h following ischemic injury to rats compared with sham surgery. The level of calcyclin mRNA is increased 10-fold by 1 day postinjury and declines thereafter. In situ hybridization demonstrates little calcyclin mRNA in kidneys of sham-operated rats. However, calcyclin protein is present in glomeruli and distal tubules (DT). Compared with kidneys from sham-operated controls, both calcyclin mRNA and protein expression are increased at 1-3 days following ischemic injury in the thick ascending limb of Henle, the DT, and in damaged regenerating segments of proximal tubules. By 7 days postischemia there is a reduction in mRNA and protein expression. Calcyclin could play a role in the regulation of renal cell proliferation and regeneration in the recovery process after acute ischemic injury.

scholarly journals Supervillin contributes to LPS-induced inflammatory response in THP-1 cell-derived macrophages

2021 ◽  
Author(s):  
Jun Zhou ◽  
Yuhui Que ◽  
Lihua Pan ◽  
Xu Li ◽  
Chao Zhu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Actin Binding ◽  
Tnf Α ◽  
Mrna And Protein Expression ◽  
Underlying Mechanisms

Abstract Supervillin (SVIL), the largest member of villin/gelsolin family, is an actin-binding and membrane-associated protein, that can also be localized to the nucleus. It has been reported that the mRNA expression of SVIL in neutrophils could be increased by lipopolysaccharide (LPS), but the underlying mechanisms remain unknown. Moreover, SVIL was also observed to be involved in the regulation of macrophages’ movement. However, it is not clear whether SVIL is involved in the LPS-induced inflammatory response in macrophages. This work was to investigate the underlying molecular mechanisms of LPS regulating SVIL expression in macrophages and hence the possible role of SVIL in LPS-induced inflammation. Our data showed that in THP-1-derived macrophages, LPS stimulation significantly increased SVIL mRNA and protein expression. Inhibition of TLR4 by Resatorvid (Res) completely reversed the expression of SVIL and inflammatory cytokines (IL-6, IL-1β and TNF-α) induced by LPS. Additionally, ERK1/2 and NF-κB inhibitors (U0126 and BAY) significantly reduced SVIL and IL-6, IL-1β & TNF-α expression. Furthermore, down-regulation of SVIL by SVIL-specific shRNA significantly attenuated the expression of IL-6, IL-1β & TNF-α induced by LPS. Taken together, as a downstream molecule of TLR4/NF-κB and ERK1/2, SVIL was involved in the inflammatory response of LPS-induced elevated IL-6, IL-1β and TNF-α in macrophages.

scholarly journals Serum from Chronic Hepatitis B Patients Promotes Growth and Proliferation via the IGF-II/IGF-IR/MEK/ERK Signaling Pathway in Hepatocellular Carcinoma Cells

2018 ◽  
Vol 47 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Yuanyuan Ji ◽  
Zhidong Wang ◽  
Haiyan Chen ◽  
Lei Zhang ◽  
Fei Zhuo ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Chronic Hepatitis ◽  
Cell Growth ◽  
Hepatitis B ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Erk Signaling ◽  
Mrna And Protein Expression ◽  
Hcc Cells

Background/Aims: Chronic hepatitis B virus (HBV) infection (CHB) plays a central role in the etiology of hepatocellular carcinoma (HCC). Emerging evidence implicates insulin-like growth factor (IGF)-II as a major risk factor for the growth and development of HCC. However, the relationship between HBV infection and IGF-II functions remains to be elucidated. Methods: Levels of circulating IGF-II and IGF-I receptor (IGF-IR) in healthy donors (HDs) and CHB patients were tested by ELISA. Human HCC cell lines (HepG-2, SMMC-7721, MHCC97-H) were incubated with serum from HDs and CHB patients at various concentrations for 24, 48, and 72 h. MTT and plate colony formation assays, BrdU ELISA, ELISA, small-interfering RNA (siRNA) transfection, quantitative real-time PCR, and western blot were applied to assess the functional and molecular mechanisms in HCC cell lines. Results: Serum levels of IGF-II and IGF-IR were significantly higher in CHB patients than in HDs. Additionally, serum from CHB patients directly induced cell growth, proliferation, IGF-II secretion, and HDGF-related protein-2 (HRP-2) and nuclear protein 1 (NUPR1) mRNA and protein expression in HCC cells. Moreover, serum from CHB patients increased IGF-II–induced cell growth, proliferation, and HRP-2 and NUPR1 mRNA and protein expression in HCC cells. Blockade of IGF-IR clearly inhibited the above effects. Most importantly, interference with IGF-II function markedly repressed the cell proliferation and HRP-2 and NUPR1 mRNA and protein expression induced by serum from CHB patients. Furthermore, serum from CHB patients induced ERK phosphorylation via IGF-IR, with the MEK inhibitor PD98059 significantly decreasing CHB patient serum-induced IGF-II secretion, cell proliferation, and HRP-2 and NUPR1 mRNA and protein expression. Conclusion: Serum from CHB patients increases cell growth and proliferation and enhances HRP-2 and NUPR1 expression in HCC cells via the IGF-II/IGF-IR/MEK/ERK signaling pathway. These findings help to explain the molecular mechanisms underlying HBV-related HCC and may lead to the development of effective therapies.

Upregulation and Overexpression of DVL1, the Human Counterpart of the Drosophila Dishevelled Gene, in Prostate Cancer

2005 ◽  
Vol 91 (6) ◽  
pp. 546-551 ◽  
Author(s):  
Kazunori Mizutani ◽  
Shizuyo Miyamoto ◽  
Takemitsu Nagahata ◽  
Noboru Konishi ◽  
Mitsuru Emi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Messenger Rna ◽  
Histological Grade ◽  
Immunohistochemical Analysis ◽  
Beta Catenin ◽  
Mrna And Protein Expression ◽  
Prostate Cancers

Aims and Background The Wnt/beta-catenin signaling pathway is one of the main carcinogenic mechanisms in human malignancies including prostate cancer. Recently, the DVL1 gene was identified as a middle molecule of the Wnt/beta-catenin signaling pathway. In addition, alterations of the DVL1 gene have been reported in breast and cervical cancer. The abnormality of beta-catenin in prostate cancer has been well studied, so the examination of the DVL1 gene in prostate cancer is appealing. Methods We investigated DVL1 messenger RNA alterations by semiquantitative PCR (SQ-PCR) in 20 primary prostate cancers and assessed the protein expression by immunohistochemical analysis in the same samples. In addition, DVL1 and beta-catenin protein expression was evaluated with a new validated set of 20 prostate cancers. Results SQ-PCR revealed significant overexpression of DVL1 in prostate cancer (65%). Upregulation of the DVL1 gene product in prostate cancer was confirmed by immunostaining. With SQ-PCR and immunostaining, none of the cases showed underexpression or downregulation of DVL1. In addition, the data showed correlations between DVL1 mRNA and protein expression. Interestingly, the expression level of DVL1 increased with worsening histological grade. In addition, a correlation between DVL1 expression and beta-catenin expression was confirmed. Conclusions DVL1 was overexpressed in prostate cancer and its overexpression might be related to prostate cancer progression through the Wnt/beta-catenin pathway.

scholarly journals Functionally enhanced placenta-derived mesenchymal stem cells inhibit adipogenesis in orbital fibroblasts with Graves’ ophthalmopathy

2020 ◽  
Author(s):  
Jae Yeon Kim ◽  
Sohae Park ◽  
Hyun-Jung Lee ◽  
Helen Lew ◽  
Gi Jin Kim
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Adipogenic Differentiation ◽  
Graves Ophthalmopathy ◽  
Mrna And Protein Expression ◽  
Tissue Specimens ◽  
Phosphatase Of Regenerating Liver

Abstract Background: Placenta-derived mesenchymal stem cells (PD-MSCs) have unique immunomodulatory properties, and phosphatase of regenerating liver-1 (PRL-1) regulates the self-renewal ability of stem cells and promotes proliferation. Graves’ ophthalmopathy (GO) is an autoimmune inflammatory disease of the orbit and is characterized by increased orbital levels of adipose tissue. Because the mechanism of inhibiting adipogenesis in orbital fibroblast (OF) with GO patients remains uncertain, the major objective of the present study is to investigate the mechanisms by which PRL-1-overexpressing PD-MSCs (PD-MSCsPRL-1, PRL-1+) alleviate adipogenesis in OFs derived from GO patients.Methods: Primary OFs were isolated from orbital adipose tissue specimens from GO patients. After maturation as adipogenic differentiation, normal and GO-derived OFs were cocultured with naïve PD-MSCs and PD-MSCsPRL-1. Western blotting was conducted to evaluate the molecular mechanisms associated with adipogenesis inhibition in GO.Results: The characteristics of PD-MSCsPRL-1 were similar to those of naïve cells. OFs from GO patients underwent stimulated adipocyte differentiation and had significantly decreased lipid accumulation after coculture with PD-MSCsPRL-1 compared with naïve cell coculture. The mRNA and protein expression of adipogenic markers was decreased in PD-MSCsPRL-1. The protein expression of phosphorylated PI3K/AKT/mTOR in OFs from GO patients was downregulated by coculture with PD-MSCsPRL-1, which secreted IGFBPs. Interestingly, IGFBP2, -4, and -7 expression in PD-MSCsPRL-1, which was mediated by integrin alpha 4 (ITGA4) and integrin beta 7 (ITGB7), was higher than that in naïve cells and upregulated phosphorylated focal adhesion kinase (pFAK) downstream factors.Conclusion: In summary, PD-MSCPRL-1-secreted IGFBPs inhibit adipogenesis in OFs from GO patients by upregulating FAK and blocking IGF, providing a novel therapeutic strategy using functionally enhanced MSCs to treat degenerative diseases.

Adipocyte aquaporin 7 (AQP7) expression in lean children and children with obesity. Possible involvement in molecular mechanisms of childhood obesity

2018 ◽  
Vol 31 (10) ◽  
pp. 1081-1089 ◽  
Author(s):  
Eleni Oikonomou ◽  
Eirini Kostopoulou ◽  
Andrea Paola Rojas-Gil ◽  
George Georgiou ◽  
Bessie E. Spiliotis
Keyword(s):  
Childhood Obesity ◽  
Protein Expression ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Obesity And Diabetes ◽  
Aquaporin 7 ◽  
Adipocyte Hypertrophy ◽  
Lean Children

Abstract Background Aquaporin 7 (AQP7), a water/glycerol transporting protein, regulates adipocyte glycerol efflux and influences lipid and glucose homeostasis. Altered AQP7 expression in adults leads to impaired glycerol dynamics, adipocyte hypertrophy and it predisposes them to obesity and diabetes. To assess its possible involvement in childhood obesity, this study investigated the expression of adipocyte AQP7 in cultured adipocytes of children. Methods Primary in vitro differentiated adipocyte cultures were developed from surgical biopsies of subcutaneous abdominal adipose tissue from 61 (46 prepubertal, 15 pubertal) lean children (body mass index [BMI] <85%) and 41 (22 prepubertal, 19 pubertal) children with obesity (BMI >95%). AQP7 expression was studied by reverse transcription polymerase chain reaction and Western immunoblotting and insulin by enzyme-linked immunosorbent assay. Results AQP7 messenger RNA (mRNA) was increased in the younger obese prepubertal (YOP) children but decreased in the obese adolescents (OA) (p=0.014) who also had increased insulin and homeostatic model assessment – insulin resistance (HOMA-IR). Lean pubertal (LP) children and YOP had increased 41 kDa AQP7 protein expression (p=0.001 and p=0.005, respectively). The OA who expressed 34 kDa AQP7 had lower triglyceride (TG) levels than those who did not express it (p=0.013). In the lean children, TG were negatively correlated with 34 kDa AQP7 (p=0.033). Conclusions The lower AQP7 mRNA expression in the OA may reflect a predisposition to adipocyte hypertrophy and metabolic dysfunction, as in the adults, whereas the YOP may be protected from this. The increased 41 kDa AQP7 protein expression in the LP may reflect the increased energy requirements of puberty for glycerol while in the YOP it may also be protective against the development of adipocyte hypertrophy.

scholarly journals BASP1 Suppresses Cell Growth and Metastasis through Inhibiting Wnt/β-Catenin Pathway in Gastric Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Li Li ◽  
Qinghua Meng ◽  
Guoying Li ◽  
Limei Zhao
Keyword(s):  
Gastric Cancer ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Wilms Tumor ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Protein Expressions ◽  
Mrna And Protein Expression ◽  
Polymerase Chain

Objective. Our research is designed to explore the function of brain acid soluble protein 1 (BASP1) in the progression of gastric cancer (GC) and its underlying molecular mechanisms. Methods. In this study, the expression of BASP1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in both GC tissue and GC cells. The cell cloning, proliferation, apoptosis, migration, and invasion potential of AGS and HGC-27 cells were, respectively, determined using colony formation assay, 5-ethynyl-20-deoxyuridine (EDU) assay, flow cytometry, and Transwell assay. The protein expressions of Bax, caspase-3, Bcl-2, matrix metalloproteinases 2 (MMP-2), MMP-9, Wilms tumor 1 (WT1), Wnt, and β-catenin in AGS and HGC-27 cells were measured by western blot. In addition, the mRNA expressions of WT1, Wnt, and β-catenin in AGS and HGC-27 cells were detected by qRT-PCR. Results. BASP1 expression was significantly downregulated in both GC tissue and GC cells. BASP1 overexpression markedly repressed proliferation, migration, and invasion and facilitated apoptosis in AGS and HGC-27 cells. In addition, BASP1 overexpression notably promoted the protein expression of Bax and caspase-3 in AGS and HGC-27 cells and inhibited the expression of Bcl-2, MMP-2, and MMP-9. Moreover, BASP1 overexpression significantly inhibited the mRNA and protein expression of WT1, Wnt, and β-catenin in AGS and HGC-27 cells. Conclusion. BASP1 could significantly suppress cell proliferation, migration, and invasion and promote apoptosis through inhibiting the activation of the Wnt/β-catenin pathway in GC.

Evaluation of carvacrol on pituitary and sexual hormones and their receptors in the testicle of male diabetic rats

2020 ◽  
Vol 39 (8) ◽  
pp. 1019-1030 ◽  
Author(s):  
H Shoorei ◽  
A Khaki ◽  
M Shokoohi ◽  
AA Khaki ◽  
A Alihemmati ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Protein Expression ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Messenger Rna ◽  
Follicle Stimulating Hormone ◽  
Diabetic Group ◽  
Control Group ◽  
Mrna And Protein Expression ◽  
Stimulating Hormone

Diabetes mellitus (DM) is a complex metabolic disease and it is also closely associated with a reduction in fertility in male patients. The purpose of the present study was to investigate the antidiabetic effect of carvacrol (CRV), as a potent antioxidant, on the numbers of germ cells and Sertoli cells in testicular tissue, and the messenger RNA (mRNA) and protein expression of some genes involved in spermatogenesis, including luteinizing hormone/choriogonadotropin receptor ( LHCGR), follicle-stimulating hormone receptor ( FSHR), and steroidogenic factor 1 ( SF-1), as well as hormones such as luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), and insulin. Adult male Wistar rats ( n = 32) were randomly divided into four groups (eight animals per group), including healthy control that received 0.2% Tween 80, diabetic control group, the diabetic group treated orally with CRV (75 mg/kg), and CRV group that received orally CRV (75 mg/kg). The duration of the treatment period lasted 8 weeks. In the diabetic group, the numbers of Sertoli cells and germ cells were significantly decreased, while the treatment with CRV prevented the degree of the damage to the cells mentioned earlier. CRV administration elevated the concentrations of insulin, T, FSH, and LH. Moreover, treatment with CRV significantly enhanced the levels of the mRNA and protein expression of SF-1, LHCGR, and FSHR. According to the obtained results, CRV administration could prevent the deleterious effects of DM on testicular germ cells, and it increases the levels of hormones and some essential genes, such as SF-1, LHCGR, and FSHR, involved in the process of spermatogenesis.

scholarly journals Novel Treatment of Hypertension by Specifically Targeting E2F for Restoration of Endothelial Dihydrofolate Reductase and eNOS Function Under Oxidative Stress

Hypertension ◽  
2019 ◽  
Vol 73 (1) ◽  
pp. 179-189 ◽  
Author(s):  
Hong Li ◽  
Qiang Li ◽  
Yixuan Zhang ◽  
Wenting Liu ◽  
Bo Gu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Cells ◽  
Protein Expression ◽  
Dihydrofolate Reductase ◽  
Promoter Activity ◽  
Molecular Mechanisms ◽  
Therapeutic Option ◽  
Protein Levels ◽  
Treatment Of Hypertension ◽  
Mrna And Protein Expression

We have shown that hydrogen peroxide (H 2 O 2 ) downregulates tetrahydrobiopterin salvage enzyme DHFR (dihydrofolate reductase) to result in eNOS (endothelial NO synthase) uncoupling and elevated blood pressure. Here, we aimed to delineate molecular mechanisms underlying H 2 O 2 downregulation of endothelial DHFR by examining transcriptional pathways hypothesized to modulate DHFR expression and effects on blood pressure regulation of targeting these novel mechanisms. H 2 O 2 dose and time dependently attenuated DHFR mRNA and protein expression and enzymatic activity in endothelial cells. Deletion of E2F-binding sites, but not those of Sp1 (specificity protein 1), abolished H 2 O 2 attenuation of DHFR promoter activity. Overexpression of E2F1/2/3a activated DHFR promoter at baseline and alleviated the inhibitory effect of H 2 O 2 on DHFR promoter activity. H 2 O 2 treatment diminished mRNA and protein expression of E2F1/2/3a, whereas overexpression of E2F isoforms increased DHFR protein levels. Chromatin immunoprecipitation assay indicated direct binding of E2F1/2/3a to the DHFR promoter, which was weakened by H 2 O 2 . E2F1 RNA interference attenuated DHFR protein levels, whereas its overexpression elevated tetrahydrobiopterin levels and tetrahydrobiopterin/dihydrobiopterin ratios in vitro and in vivo. In Ang II (angiotensin II)–infused mice, adenovirus-mediated overexpression of E2F1 markedly abrogated blood pressure to control levels, by restoring endothelial DHFR function to improve NO bioavailability and vasorelaxation. Bioinformatic analyses confirmed a positive correlation between E2F1 and DHFR in human endothelial cells and arteries, and downregulation of both by oxidized phospholipids. In summary, endothelial DHFR is downregulated by H 2 O 2 transcriptionally via an E2F-dependent mechanism, and that specifically targeting E2F1/2/3a to restore DHFR and eNOS function may serve as a novel therapeutic option for the treatment of hypertension.

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