scholarly journals The influence of malachite green on the level of transcriptional expression of the laccase and DyP-peroxidase genes of the Azospirillum brasilense

2020 ◽  
Author(s):  
M. A. Kupryashina ◽  
T. E. Pylaev ◽  
V. E. Nikitina
Keyword(s):  
Malachite Green ◽  
Azospirillum Brasilense ◽  
Expression Level ◽  
Synthetic Dyes ◽  
Transcriptional Expression ◽  
Bacterial Enzymes ◽  
Genes Expression

Malachite green (MG), a widely-used and recalcitrant dye, has been confirmed to be carcinogenic and mutagenic against many organisms. Herein, we were aimed at the investigation of the hypothetic role of ligninolytic bacterial enzymes similar to fungal ones in the degradation of synthetic dyes. A multiple increase in the laccases and DyP-peroxidases genes expression level was recorded by RT-qPCR for bacteria of the genus Azospirillum in the presence of MG.

MicroRNA-520c-3p Modulates Doxorubicin-Chemosensitivity in HepG2 Cells

2020 ◽  
Vol 21 (2) ◽  
pp. 237-245 ◽  
Author(s):  
Mohamed A. Ragheb ◽  
Marwa H. Soliman ◽  
Emad M. Elzayat ◽  
Mervat S. Mohamed ◽  
Nada El-Ekiaby ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Therapeutic Strategy ◽  
Suppressive Effect ◽  
Expression Level ◽  
Tumor Suppressor Function ◽  
Protein Expression Level ◽  
Blot Technique ◽  
Induction Of Apoptosis ◽  
The Impact

Background: Doxorubicin (DOX) is the most common drugs used in cancer therapy, including Hepatocellular Carcinoma (HCC). Drug resistance, is one of chemotherapy’s significant problems. Emerging studies have shown that microRNAs (miRNAs) could participate in regulating this mechanism. Nevertheless, the impact of miRNAs on HCC chemoresistance is still enigmatic. Objective: Investigating the role of miR-520c-3p in enhancement of anti-tumor effect of DOX against HepG2 cells. Methods: Expression profile for liver related miRNAs (384 miRNAs) has been analyzed on HepG2 cells treated with DOX using qRT-PCR. miR-520c-3p, the most deregulated miRNA, was selected for combination treatment with DOX. Expression level for LEF1, CDK2, CDH1, VIM, Mcl-1 and TP53 was evaluated in miR-520c-3p transfected cells. Cell viability, colony formation, wound healing as well as apoptosis assays have been demonstrated. Furthermore, Mcl-1 protein level was measured using western blot technique. Results: The present data indicated that miR-520c-3p overexpression could render HepG2 cells chemo-sensitive to DOX through enhancing its suppressive effects on proliferation, migration, and induction of apoptosis. The suppressive effect of miR-520c-3p involved altering the expression levels of some key regulators of cell cycle, proliferation, migration and apoptosis including LEF1, CDK2, CDH1, VIM, Mcl-1 and TP53. Interestingly, Mcl-1 was found to be one of the potential targets of miR-520c-3p, and its protein expression level was down-regulated upon miR-520c-3p overexpression. Conclusion: Our data referred to the tumor suppressor function of miR-520c-3p that could modulate chemosensitivity of HepG2 cells toward DOX treatment, providing a promising therapeutic strategy in HCC.

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

GLUTAMATE SYNTHASE FROM AZOSPIRILLUM BRASILENSE: ROLE OF FLAVINS AND IRON SULFUR CENTERS

1991 ◽  
pp. 749-754
Author(s):  
Maria A. Vanoni ◽  
Giuliana Zanetti ◽  
Bruno Curti ◽  
Dale E. Edmondson
Keyword(s):  
Azospirillum Brasilense ◽  
Glutamate Synthase ◽  
Iron Sulfur

Role of a Fasciclin domain protein in photooxidative stress and flocculation in Azospirillum brasilense Sp7

2021 ◽  
pp. 103875
Author(s):  
Ashutosh Prakash Dubey ◽  
Parul Pandey ◽  
Shivangi Mishra ◽  
Parikshit Gupta ◽  
Anil Kumar Tripathi
Keyword(s):  
Azospirillum Brasilense ◽  
Photooxidative Stress ◽  
Azospirillum Brasilense Sp7 ◽  
Domain Protein

JAK2/STAT3 in role of arsenic-induced cell proliferation: a systematic review and meta-analysis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Shugang Li ◽  
Shanshan Ran ◽  
Qingxin Ren
Keyword(s):  
Cell Proliferation ◽  
Meta Analysis ◽  
Arsenic Concentration ◽  
Arsenic Exposure ◽  
Malignant Cell ◽  
Dose Effect ◽  
Expression Level ◽  
Exposure Concentration ◽  
Effect Relationship

Abstract Objectives Malignant cell proliferation is one of the important mechanisms of arsenic poisoning. A large number of studies have shown that STAT3 plays an important role in cell malignant proliferation, but there are still many contradictions in the effect of arsenic on JAK2/STAT3. This study aims to explore the role of JAK2/STAT3 in arsenic-induced cell proliferation. Methods By taking normal cells as the research object and using Standard Mean Difference (SMD) as the effect size, meta-analysis was used to explore the effect of arsenic on JAK2/STAT3. Then, the dose-effect Meta was used to further clarify the dose-effect relationship of arsenic on JAK2/STAT3. Results Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI [1.05, 7.37]), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation. In addition, this study also found that arsenic exposure dose (<5 μmol m−3), time(<24 h) and cell type were important sources of heterogeneity in the process of exploring the effects of arsenic on p-STAT3, IL-6 and p-JAK2. Dose-effect relationship meta-analysis results showed that arsenic exposure significantly increased the expression level of IL-6. When the arsenic exposure concentration was less than 7 μmol m−3, the expression level of p-JAK2 upregulated significantly as the arsenic exposure concentration gradually increasing. Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 μmol m−3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 μmol m−3. Conclusions Exposure to low dose of arsenic could promote the expression of JAK2/STAT3 and induce the malignant proliferation of cells through upregulating IL-6, and there was dose-effect relationship among them.

THE ROLE OF CIRCADIAN REGULATION OF GHRELIN LEVELS IN PARKINSON’S DISEASE (LITERATURE REVIEW)

2021 ◽  
Vol 74 (7) ◽  
pp. 1750-1753
Author(s):  
Kateryna A. Tarianyk ◽  
Nataliya V. Lytvynenko ◽  
Anastasiia D. Shkodina ◽  
Igor P. Kaidashev
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clock Genes ◽  
Biological Rhythms ◽  
Circadian Regulation ◽  
Diurnal Changes ◽  
Dopaminergic Therapy ◽  
Peripheral Oscillators ◽  
Genes Expression

The paper is aimed at the analysis of the role of the circadian regulation of ghrelin levels in patients with Parkinson’s disease. Based on the literature data, patients with Parkinson’s disease have clinical fluctuations in the symptoms of the disease, manifested by the diurnal changes in motor activity, autonomic functions, sleep-wake cycle, visual function, and the efficacy of dopaminergic therapy. Biological rhythms are controlled by central and peripheral oscillators which links with dopaminergic neurotransmission – core of the pathogenesis of Parkinson`s disease. Circadian system is altered in Parkinson`s disease due to that ghrelin fluctuations may be changed. Ghrelin is potential food-entrainable oscillator because it is linked with clock genes expression. In Parkinson`s disease this hormone may induce eating behavior changing and as a result metabolic disorder. The “hunger hormone” ghrelin can be a biomarker of the Parkinson’s disease, and the study of its role in the pathogenesis, as well as its dependence on the period of the day, intake of levodopa medications to improve the effectiveness of treatment is promising.

Green Cardamom Plus Low Calorie Diet Can Decrease Inflammatory Genes Expression Among Obese Women With Poly Cystic Ovarian Syndrome, A Double Blind Randomized Clinical Trial

2021 ◽  
Author(s):  
Sahar Cheshmeh ◽  
Maysa Ghayyem ◽  
Firoozeh Khamooshi ◽  
Neda Heydarzadeh ◽  
Niloofar Hojati ◽  
...  
Keyword(s):  
Expression Level ◽  
Low Grade ◽  
Obese Women ◽  
Double Blind ◽  
Low Calorie ◽  
Low Calorie Diet ◽  
Genes Expression ◽  
Tnf Α ◽  
Calorie Diet ◽  
Green Cardamom

Abstract PurposePolycystic ovary syndrome (PCOS) is a common cause of endocrine disorder and infertility among womenin which is related with low grade inflammation. Therefore, this current randomized, double-blind, placebo-controlledclinical trial assessed the effects of green cardamom supplementation on inflammatory markers and gene expressionamong obese women with PCOS.MethodsWe included 194 obese PCOS women that gave all of them low calorie diet. These subjects were randomlydivided in two studied groups including intervention with 3 g/day green cardamom (n=99) and placebo groups (n=95).Anthropometric indices, androgen hormones, and inflammatory factors (tumor necrosis factor-a (TNF-α), Interleukin6 (IL-6), and C- reactive protein (CRP)) were assessed before and after four months intervention. Their TNF-α, IL-6,and CRP genes expression level were measured using reverse transcription-polymerase chain reaction (RT-PCR)method.ResultsAnthropometric indices were improved in both two studied groups (P<0.001). Among androgen hormonesluteinizing hormone, androstenedione, and dehydroepiandrosterone were significantly decreased (P<0.001), as wellas, follicle-stimulating hormone was significantly increased (P<0.001) in the green cardamom group. Our findingsshowed that TNF-α, IL-6, and CRP serum were significantly decreased after the intervention with green cardamomplus low calorie diet (P<0.001). In addition, the expression level of TNF-α and CRP genes were significantly decreasedin intervention groups (P<0.001).ConclusionsThis present study support the beneficial anti-inflammatory effect of green cardamom on theinflammatory status in the PCOS women.Level of evidenceLevel I, randomized clinical trialTrial registrationThis trial was registered with the Iranian Clinical Trials Registry (registration number:IRCT20200608047697N1). 1 August, 2020; https://www.irct.ir/trial/48748

scholarly journals P01.01 The role of exosome miRNA between tumor cells and microglias during the progression of medulloblastoma

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii24-iii24
Author(s):  
Q Chang ◽  
L Zhu ◽  
N Li
Keyword(s):  
Tumor Cells ◽  
Critical Role ◽  
Expression Level ◽  
Migration And Invasion ◽  
Specific Marker ◽  
Migration Ability ◽  
Daoy Cell ◽  
Bv2 Cells ◽  
Close Relationship

Abstract BACKGROUND Medulloblastoma (MB) is the most common malignant paediatric brain tumor. Recent studies show that M2 cells were relative more abundant in Shh subtype of MBs compared with other three subtypes. It’s known that M2 cells have close relationship with many tumors’ progression. But if they play any role in the progression of Shh subtype of MB is not yet clear. Many studies demonstrate that exosomes carring miRNAs have close relationship with tumor invasion. The aim of present study is to clarify the role of exosome miRNA between tumor cells and microglias during the progression of Shh subtype of medulloblastoma. MATERIAL AND METHODS Immunofluerescence staining using iNOS and Arg1, which is M1 and M2 specific marker, respectively, was performed in four subtypes of MBs. After coculture of exosomes extracted from Shh subtype of MB cell (DAOY) with microglia cell (BV2), Q-PCR and ELISA assay were done to evaluate the polarization status of the microglia. Transwell and scratch assay were then performed to detect the migration ability of DAOY cell after treatment of exosomes from polirized M2 cells. MiRNA sequencing by Ion Proton technology was then done to analyze the miRNAs expression level between Shh subtype and other subtype of MBs. Transformation assay was used to overexpress and inhibit the expression of these miRNAs respectively to further clarify the role of exosome miRNA in the polarization of BV2 cells. RESULTS M2 cells were observed more abundant than other three subtypes of tumors, supporting that M2 cells play some role in this subtype of MBs. Exosomes of DAOY cells can induce the polarization of M2 cells. The polarized M2 cells can improved the migration and invasion ability of DAOY cell. Dozens of miRNAs were identified with different expression level between Shh subtype of MBs and other subtype of MB cells. Among them, 4 miRNAs were reported to be related with polariztion of M2 in many other lesions. Three of the 4 miRNAs can induce the polarization of M2 in present study. CONCLUSION Our study demonstrated exosome miRNA play a critical role between tumor cells and microglias during the progression of Shh subtype of medulloblastoma.

scholarly journals Role of Renocortical Cyclooxygenase-2 for Renal Vascular Resistance and Macula Densa Control of Renin Secretion

2001 ◽  
Vol 12 (5) ◽  
pp. 867-874
Author(s):  
HAYO CASTROP ◽  
FRANK SCHWEDA ◽  
KARL SCHUMACHER ◽  
KONRAD WOLF ◽  
ARMIN KURTZ
Keyword(s):  
Vascular Resistance ◽  
Macula Densa ◽  
Renal Vascular Resistance ◽  
Renin Secretion ◽  
Expression Level ◽  
Flow Rates ◽  
Low Salt ◽  
Cox 2 ◽  
Renal Vascular

Abstract. This study aimed to assess the role of cyclooxygenase-2 (COX-2)-derived prostanoids for the macula densa control of renal afferent arteriolar resistance and for renin secretion. For this purpose, studied were the effects of blocking macula densa salt transport by the loop diuretic bumetanide (100 μM) on renal perfusate flow and on renin secretion in isolated perfused rats, in which renocortical COX-2 expression was prestimulated in vivo by treatment with the angiotensin-converting enzyme inhibitor ramipril, with low-salt diet, or with a combination of both. These maneuvers stimulated COX-2 expression in an order of ramipril + low salt ≫ low salt > ramipril > controls. Flow rates through isolated kidneys at a constant pressure of 100 mmHg were dependent on the pretreatment regimen, in the way that they went in parallel with COX-2 expression. The COX-2 inhibitor NS-398 (10 μM) lowered flow rates depending on the COX-2 expression level and was most pronounced therefore after pretreatment with low salt + ramipril. NS-398 did not change the increase of flow in response to bumetanide but attenuated the stimulation of renin secretion in response to bumetanide in a manner depending on the expression level of COX-2. These findings suggest that in states of increased renocortical expression of COX-2, overall renal vascular resistance and the macula densa control of renin secretion become dependent on COX-2—derived prostanoids.

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