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1

Characterization of proteins associating with 5' terminus of PGHS-1 mRNA

100%
Bunimov N., Laneuville O.
Cellular and Molecular Biology Letters
|
2010
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tom 15
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nr 2
Induction of Prostaglandin Endoperoxide H Synthase-1 (PGHS-1) gene has been previously documented in a few studies during events such as development and cellular differentiation. However, molecular mechanisms governing the regulation of PGHS-1 gene expression and contributing to changes in protein levels are poorly understood. Using the MEG-01 cell model of PGHS-1 gene induction, our laboratory has previously demonstrated that the 5’UTR and the first two exons of PGHS-1 mRNA had a significant impact on decreasing the translational efficiency of a reporter gene and suggested that the presence of a secondary structure is required for conservation of this activity. This 5’end of PGHS-1 mRNA sequence has also been shown to associate with nucleolin protein. In the current study, we set to investigate the protein composition of the mRNP (messenger ribonucleoprotein) associating with the 5’end of PGHS-1 mRNA and to identify its protein members. RNA/protein binding assays coupled with LC-MS analysis identified serpin B1 and NF45 (nuclear factor 45) proteins as potential members of PGHS-1 mRNP complex. Immunoprecipitation experiments using MEG-01 protein extracts validated mass spectrometry data and confirmed binding of nucleolin, serpin B1, NF45 and NF90. The RNA fraction was extracted from immunoprecipitated mRNP complexes and association of RNA binding proteins, serpin B1, NF45 and NF90, to PGHS-1 mRNA target sequence was confirmed by RT-PCR. Together these data suggest that serpin B1, NF45 and NF90 associate with PGHS-1 mRNA and can potentially participate in the formation a single or a number of PGHS-1 ribonucleoprotein complexes, through nucleolin that possibly serves as a docking base for other protein complex members.
2

The role of nuclear and cytoplasmic factors in the regulation of the interautogamous interval [IAI] in the Paramecium aurelia species complex

100%
Prajer M., Kosciuszko H.
Folia Biologica
|
1998
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tom 46
|
nr 1-2
3

The mitochondrial localization of RelB and NFATx in immature T cells

84%
Stasik I., Rapak A., Ziolo E., Strzadala L.
Cellular and Molecular Biology Letters
|
2008
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tom 13
|
nr 4
493-501
In order to exert their activity, transcription factors must be transported to the nucleus. Certain transcription factors have also been found on mitochondria. Here, the localization of RelB and NFATx in the mitochondrial fractions of normal thymocytes and thymic lymphoma cells is shown for the first time. CREB was only found in the nucleus, while p50 (NFκB) was found in both the nucleus and the cytoplasm, but outside the mitochondria. The translocation of transcription factors to the mitochondria is differentially regulated. Unlike RelB, which is always present in the mitochondrial fraction, NFATx appeared on the mitochondria in cells treated with ionomycin together with an immunosuppressant and inhibitor of calcineurin (FK506). This data reveals that the mitochondrial localization of some transcription factors is precisely controlled by a calcium signal sensitive to FK506 in T cells.
4
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The effect of salvianolate on cardiomyocyte remodeling improvement after myocardial infarction through calcineurin/nuclear factor C3 of the activated T cell/β-myosin heavy chain pathway regulation

84%
Chen C., Zhu P., Yu H., Liu L., Lin X., Bai Y., Yang Y.
Journal of Physiology and Pharmacology
|
2022
|
tom 73
|
nr 3
Enormous evidences in clinic and experimental studies have demonstrated that salvianolate (Sal) could treat cardiovascular diseases such as myocardial infarction (MI), but the underlying mechanism was still needed to be explored. This study aims to investigate the effect of Sal on cardiomyocyte remodeling after MI in rats and explore whether the possible mechanism was related to decreasing the β-myosin heavy chain (β-MHC) expression in cardiomyocytes via the calcineurin (CaN)/nuclear factor C3 of the activated T cell (NFATc3) pathway. Both MI model and angiotensin II induced primary myocardial cells obtained from rats were used in this study. After treatment with Sal, the cardiac function was assessed by color Doppler echocardiography, while MI area, myocardial cell area and heart mass index (HMI) were analyzed via Masson and hematoxylin and eosin staining (HE) stain, respectively. Additionally, CaN activity, and CaN, NFATc3, β-MHC mRNA and protein expressions in myocardial tissue and myocardial cells were tested via corresponding methods, mainly including real-time fluorescence-based quantitative polymerase chain reaction (RT-qPCR), Western blot (WB), immunohistochemistry and fluorescence staining analysis. As a result we obtained the high dose of Sal in vivo could perform beneficial effects on cardiomyocyte remodeling of MI rats, mainly manifesting as improving fractional shortening and ejection fraction rates, reducing the MI area, myocardial cross-sectional area and HMI (P<0.05, 0.01), inhibiting the activity of CaN in myocardial tissue, down-regulating β-MHC mRNA and protein expressions, and decreasing the nuclear translocation of NFATc3 (P<0.05). In the in vitro experiments, 10 µmol/L of Sal could inhibit the increase of the myocardial cell area and CaN activity, down-regulate the mRNA and protein of CaN A subunit, β-MHC; and inhibit the nuclear translocation of NFATc3 (P<0.05, 0.01). In conclusion: use of Sal can improve cardiomyocyte remodeling and down-regulate the expression of β-MHC in cardiomyocytes, of which the mechanism might be related to the reduction of the nuclear translocation of NFATc3 as well as the down-regulation of CaNA subunit expression and/or the inhibition of CaN activity. The results will provide a laboratory basis for the clinical application of Sal.
5
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Ghrelin ameliorated inflammation and oxidative stress in isoproterenol induced myocardial infarction through the endothelial nitric oxide synthase (eNOS)/nuclear factor erythroid 2-related factor-2 (NRF2)/heme oxygenase-1 (HO-1) signaling pathway

84%
El-Shaer N. O., El Gazzar W. B., Allam M. M., Anwer H. M.
Journal of Physiology and Pharmacology
|
2021
|
tom 72
|
nr 2
Although there is accumulating evidence which suggests that the administration of ghrelin could be used to preserve cardiac function, delay the progression of heart failure post-myocardial infarction, and attenuate ventricular remodeling, there is still no definitive data that clearly highlights the mechanisms by which ghrelin exerts cardioprotective effects. The present study aimed to investigate whether ghrelin could affect nuclear factor erythroid 2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and endothelial nitric oxide synthase (eNOS) expression and exert anti-inflammatory as well as antioxidant-like actions through this signaling pathway. Rats were assorted into four groups with 10 in each: Group I (Control), Group II (received ghrelin only), Group III (MI was induced by isoproterenol (ISO)), Group IV (MI was induced by isoproterenol and within 30 min of each ISO dose, rats received ghrelin; 100 µg /kg subcutaneously two times per day). We assessed the effects of acylated ghrelin on the biochemical changes, ECG parameters, heart rate, histopathological scoring and the mRNA expression of eNOS, Nrf2 (confirmed immunohistochemically) as well as HO 1 genes in the cardiac tissues. Nuclear factor-κB, tumor necrosis factor-α, interleukin-6, and inducible nitric oxide synthase were assessed as inflammatory markers. Ghrelin markedly improved the oxidative stress injury and inflammation, showed histological preservation of the cardiac muscle fibers morphology, ameliorated the ISO-induced ECG changes and caused a significant elevation in eNOS, HO-1, and Nrf2 expression. In conclusion, ghrelin exerts cardioprotective effect in ISO-induced myocardial infarction by promoting the eNOS/Nrf2/HO-1 pathway.
6
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Kaempferol protects against streptozotocin-induced diabetic cardiomyopathy in rats by a hypoglycemic effect and upregulating SIRT1

84%
Alshehri A. S., El-Kott A. F., Eleawa S. M., El-Gerbed M. S. A., Khalifa H. S., El-Kenawy A. E., Albadrani G. M., Abdel-Daim M. M.
Journal of Physiology and Pharmacology
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2021
|
tom 72
|
nr 3
This study investigated if kaempferol could attenuate the oxidative, inflammatory, and fibrotic damage of the left ventricles (LVs) in streptozotocin (STZ)-diabetic rats by modulating silent mating type information regulation 2 homolog 1 (SIRT1) signaling. Adult male rats were divided into 5 groups (n = 12/each) as control, control + kaempferol, STZ-induced diabetes mellitus (STZ-DM), STZ-DM + kaempferol, and STZ-DM + kaempferol + EX-527, a sirtuin 1 (SIRT1) inhibitor. Administration of kaempferol to diabetic rats significantly preserved the systolic and diastolic functions of the LVs that was associated with a significant reduction in ventricular collagen deposition, infiltration of inflammatory cells, and protein expression of Bcl2-associated X protein (Bax), cleaved caspase-3, and cytochrome-C. In both the control and diabetic rats, kaempferol attenuated the loss in body weights, reduced fasting glucose levels, and increased fasting insulin levels and HOMA-β. Besides, kaempferol lowered the levels of reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), downregulated the transforming growth factor-β1 (TGF-β1) and reduced the nuclear levels of NF-κB p65. In concomitant, kaempferol increased the LV levels of manganese superoxide dismutase (MnSOD) and glutathione (GSH) and stimulated the total protein levels of Bcl2, the nuclear activity of SIRT1, and nuclear levels of nuclear factor erythroid 2-related factor 2 (Nrf2). These events were associated with increased deacetylase activity and total levels of SIRT1 and a parallel decrease in the acetylation of Nrf2, NF-κB, smad2, and FOXO1. In conclusion: kaempferol attenuate diabetic cardiomyopathy in STZ-treated rats through its hypoglycaemic and insulin-releasing effects, as well as a cardiac independent mechanism that involves activation of SIRT1.
7
Content available remote

Comparison of acetaminophen toxicity in primary hepatocytes isolated from transgenic mice with different apolipoprotein E alleles

67%
Mezera V., Kucera O., Moravcova A., Peterova E., Rousar T., Rychtrmoc D., Sobotka O., Cervinkova Z.
Journal of Physiology and Pharmacology
|
2015
|
tom 66
|
nr 6
8
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Ellagic acid prevents streptozotocin-induced hippocampal damage and memory loss in rats by stimulating Nrf2 and nuclear factor-κB, and activating insulin receptor substrate/PI3K/Akt axis

67%
Alfaris N. A., Alshammari G. M., Altamimi J. Z., Aljabryn D. H., Alagal R. I., Aldera H., Alkhateeb M. A., Yahya M. A.
Journal of Physiology and Pharmacology
|
2021
|
tom 72
|
nr 4
This study examined the protective effect of ellagic acid (EA) against streptozotocin (STZ)-induced hippocampal damage and memory loss and investigated some mechanisms of action. Adult male rats were divided into 4 groups (n = 12) as control, control + EA (50 mg/kg), STZ-DM, and STZ-DM + EA. Treatments were given orally and daily for 8 weeks. Memory function was assessed by the Morris water maze (MWM) and passive learning avoidance test. In addition, blood samples were used to measure glucose and insulin levels. Also, the hippocampus was used to measure markers of oxidative stress, inflammation, and insulin signaling. Associated with the improved memory, EA preserved the structure of the CA1 area of rats’ hippocampus and suppressed the hippocampal expression of Bax and cleaved caspase 3. Concomitantly, EA increased rats’ weekly weights gain and fasting plasma insulin levels and reduced the hippocampal levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and plasma glucose levels in diabetic rats. In both the control and STZ-DM rats, EA significantly lowered the hippocampal levels of reactive oxygen species (ROS) and malondialdehyde (MDA) but significantly increased the hippocampal levels of glutathione (GSH) and manganese superoxide dismutase (MnSOD), as well as the nuclear levels of NF-κB and nuclear factor-erythroid 2-related factor (Nrf-2). Besides, and in the hippocampus of both groups, EA increased the phosphorylation of insulin receptor substrate (IRS), PI3K, Akt, GS3Kβ, and CREB, and increased levels of BDNF and Bcl-2. In conclusion, these data suggest that the neuroprotective effect of EA on rats’ hippocampus and memory function is associated with upregulation of Nrf2 and Bcl-2, suppression of NF-κB, and activation of CREB and IRS/PI3K/Akt/ GS3Kβ axis.
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