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Showing 3 results for Adenosine
M Bonyadi , A Mohammadi , M Khalajkondori, S Taghavi ,
Volume 15, Issue 2 (7-2015)
Abstract
Background & objectives: Recurrent spontaneous abortion (RSA) is defined by two or more consecutive miscarriages before 20 weeks of gestation. Adenosine deaminase (ADA) is an enzyme of purine salvage pathway and has two important isoenzymes ADA1 and ADA2. The adenosine deaminase G22A polymorphism (ADA*2) increases the level of adenosine. Adenosine may play a protective role against recurrent spontaneous abortions, since it regulates blood flow into the uterus and placenta. In consideration of the effect of decreased enzymatic activity of adenosine deaminase G22A polymorphism on adenosine levels we evaluated the protective effect of ADA*2 allele against recurrent spontaneous abortions in north-west of Iran.
Methods: A total of 100 women were recruited to form two groups. First one, with a history of recurrent spontaneous abortions (N=50), and the second one, without a history of abortions (N=50). Genomic DNA was extracted from peripheral blood with a commercial kit and PCR-RFLP analysis was used to identify the G22A genetic polymorphism. Fisher's exact test and odds ratio values were used to compare the proportions of adenosine deaminase genotypes and alleles between women with and without a history of recurrent spontaneous abortion (p<0.05).
Results: The frequency of homozygotes (AA) was 2% in control group, whereas no homozygote (AA) was found in the case group. The frequency of heterozygotes (AG) was 20% in control group and 8% in the case group (p<0.05). The frequency of homozygotes (GG) was 78% in control group and 92% in the case group (p<0. 05). A significant increase in the frequency of AG genotype in controls (p=0.014, OR=0.348) relative to women with the history of RSA demonstrates the protective effect of AG genotype in controls.
Conclusion: The data suggest that women carrying the G22A polymorphism (ADA*2 allele) and AG genotype which is associated with the lower enzymatic activity are better protected against recurrent spontaneous abortions.
Maryam Rahimzadeh , Leila Pirdel,
Volume 18, Issue 1 (4-2018)
Abstract
Background & objectives: Mesenchymal stem cells have been known as hypo-immunogenic and immunosuppressive cells. Exposure of mesenchymal stem cells to interferon γ (IFN-γ) may influence their immunomodulatory properties. In the present study, the expression level of adenosine producing CD39 and CD73 ectonucleotides as an immunosuppressant were evaluated in Wharton’s Jelly- derived Mesenchymal Stem Cells (WJ-MSCs) in the presence and absence of IFN-g.
Methods: In this experimental study, MSCs were isolated, cultured, and propagated from Wharton's jelly obtained from human umbilical cord. The phenotypic characterization of these cells was performed via analysis of their surface markers using flow cytometry. Then, the cultured mesenchymal stem cells were treated with IFN-g. After 24 hours, the expression levels of CD39 and CD73 genes were analyzed using qPCR in control and IFN-g-treated cells.
Results: Flow cytometric analysis of stem cells revealed morphological similarity to fibroblastic cells and expression of CD105 and CD73 markers in these cells. The results of qPCR showed that the expression level of CD39 was significantly increased in IFN-g-treated cells compared to non-treated cells, while there was no significant difference in CD73 expression level between control and IFN-g - treated cells.
Conclusion: The results indicated the possible role of IFN-g in development of the immunoregulatory capacity of mesenchymal stem cells through expression of target genes. However this should be studied precisely.
Miss Neda Omidian, Houshang Najafi,
Volume 20, Issue 4 (1-2021)
Abstract
Background & objectives: One of the most important causes of acute kidney injury is ischemia-reperfusion (IR). Some studies have shown that adenosine A1 receptor inhibition have protective effects against Ischemia–reperfusion induced renal injuries, while other studies have demonstrated the opposite. The aim of the present study was to review the methodology of these studies to reach a final conclusion about the effects of adenosine A1 receptor on ischemia-reperfusion-induced renal injuries.
Methods: Data base motors including Scopus, PubMed, Google Scholar, Science Direct and Embase were searched. The terms and keywords used included ischemia-reperfusion, acute kidney injury, acute renal failure, A1 adenosine receptor and their combination.
Results: Increased adenosine levels following renal Ischemia-reperfusion cause vasoconstriction in afferent arteriole and vasodilatation in efferent arteriole through A1 adenosine receptor activation, which in turn reduces glomerular filtration rate (GFR). Inhibition of A1 adenosine receptor leads to short-term correction of renal functional parameters following renal Ischemia-reperfusion, by increasing renal blood flow and thus improving GFR. But this increase in GFR exacerbates kidney damages through the kidneys workload enhancement, which will show up in the next few hours.
Conclusions: Although selective inhibition of A1 adenosine receptor in the short term improves renal function parameters, but exacerbates renal damages in the following hours. Therefore, adenosine A1 receptor stimulation has protective effects against IR-induced kidney injury.
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