Analysis of porcine peripheral blood mononuclear cells proteome by 2-DE and MS: Analytical and biological variability in the protein expression level and protein identification

PROTEOMICS ◽  
2006 ◽  
Vol 6 (S1) ◽  
pp. S215-S225 ◽  
Author(s):  
María Ramirez-Boo ◽  
Juan J. Garrido ◽  
Samuel Ogueta ◽  
Juan J. Calvete ◽  
Consuelo Gómez-Díaz ◽  
...  
Intervirology ◽  
2018 ◽  
Vol 61 (5) ◽  
pp. 237-246
Author(s):  
Yuyuan Ma ◽  
Xiong Zhao ◽  
Junting Jia ◽  
Yongxian Yang ◽  
Rui Fan ◽  
...  

2019 ◽  
Vol 16 (3) ◽  
pp. 265-271 ◽  
Author(s):  
Mahsa Taeb ◽  
Abdollah Jafarzadeh ◽  
Seyed Shahabeddin Mortazavi-Jahromi ◽  
Nahid Zainodini ◽  
Mohammad Reza Mirzaei ◽  
...  

Objective: This research aimed to study the anti-aging and anti-inflammatory effects of low and high doses of the β-D-mannuronic (M2000) on gene expression of enzymes involved in oxidative stress (including SOD2, GST, GPX1, CAT, iNOS, and MPO) in peripheral blood mononuclear cells (PBMCs) of healthy donors under in vitro conditions. Methods: The PBMCs were separated and the RNAs were then extracted and the cDNAs synthesized, and expression levels of the mentioned genes were detected by qRT-PCR. Results: Our results indicated that the high dose of this drug could significantly reduce the expression level of the SOD2 gene compared to the lipopolysaccharide (LPS) group (p < 0.0001). Moreover, it was found that the high dose of this drug could significantly decrease the expression level of the GST gene compared to the LPS group (p < 0.0001). However, no significant reductions were observed in expression levels of the CAT and GPX1 genes compared to the LPS group. Furthermore, our data revealed that the level of iNOS and MPO gene expression was significantly reduced, in both doses of M2000, respectively, compared to the LPS group (p < 0.0001). Conclusion: This research showed that M2000 as a novel NSAID with immunosuppressive properties could modify oxidative stress through lowering expression levels of the SOD2, GST, iNOS, and MPO genes compared to the healthy expression levels, with a probable reduction of the risk of developing inflammatory diseases related to age and aging.


2020 ◽  
Author(s):  
Jyoti Kundu ◽  
Shikha Bakshi ◽  
Himanshu Joshi ◽  
Sanjay K Bhadada ◽  
Indu Verma ◽  
...  

AbstractBackgroundDiabetes is an important risk factor for developing tuberculosis. This association leads to exacerbation of tuberculosis symptoms and delayed treatment of both the diseases. Molecular mechanism and biomarkers/drug targets related to copathogenesis of tuberculosis and diabetes, however, still remains to be poorly understood. In this study, proteomics based 2D-MALDI/MS approach was employed to identify host signature proteins which are altered during copathogenesis of tuberculosis and diabetes.MethodsComparative proteome of human peripheral blood mononuclear cells (PBMCs) from healthy controls, tuberculosis and diabetes patients in comparison to comorbid diabetes and tuberculosis patients was analyzed. Gel based proteomics approach followed by in gel trypsin digestion and peptide identification by mass spectrometry was used for signature protein identification.ResultsTotal of 18 protein spots with differential expression in TBDM patients in comparison to other groups were identified. These include Vimentin, tubulin beta chain protein, superoxide dismutase, Actin related protein 2/3 complex subunit 2, PDZ LIM domain protein, Rho-GDP dissociation inhibitor, Ras related protein Rab, dCTPpyrophosphatase 1, Transcription initiation factor TFIID subunit 12, coffilin 1, three isoforms of Peptidylprolylcis-trans isomerase A, three isoforms of Protein S100A9, Protein S100A8 and SH3 domain containing protein. These proteins belonged to four functional categories i.e. structural, cell cycle/growth regulation, signaling and intermediary metabolism.ConclusionProteins identified to be differentially expressed in TBDM patient can act as potent biomarkers and as predictors for copathogenesis of tuberculosis and diabetes.


2018 ◽  
Vol 105 (3) ◽  
pp. 247-256 ◽  
Author(s):  
JJ McCormick ◽  
TA VanDusseldorp ◽  
CG Ulrich ◽  
RL Lanphere ◽  
K Dokladny ◽  
...  

Autophagy is a lysosome degradation pathway through which damaged organelles and macromolecules are degraded within the cell. A decrease in activity of the autophagic process has been linked to several age-associated pathologies, including triglyceride accumulation, mitochondrial dysfunction, muscle degeneration, and cardiac malfunction. Here, we examined the differences in the autophagic response using autophagy-inducer rapamycin (Rapa) in peripheral blood mononuclear cells (PBMCs) from young (21.8 ± 1.9 years) and old (64.0 ± 3.7 years) individuals. Furthermore, we tested the interplay between the heat shock response and autophagy systems. Our results showed a significant increase in LC3-II protein expression in response to Rapa treatment in young but not in old individuals. This was associated with a decreased response in MAP1LC3B mRNA levels, but not SQSTM1/p62. Furthermore, HSPA1A mRNA was upregulated only in young individuals, despite no differences in HSP70 protein expression. The combined findings suggest a suppressed autophagic response following Rapa treatment in older individuals.


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