Background:
The vessel restenosis is related to the inflammatory events in subendothelial space.
It is proposed that the inflammatory agents affect the prostaglandin synthesis pathway. In this
study, we investigated the COX-1, COX-2, PTGDS and miRNA-520a-5p expression levels and
the serum 15-Deoxy-∆
12,14
–PGJ2 metabolite values in patients with the stenosed and re-stenosed
vessels. Furthermore, the associations between genes and miR-520 were evaluated in the monocyte
transfection studies.
Methods:
The subjects (n=60) were included three groups; healthy subjects (control (stenosis <
5%), stent no restenosis (SNR, restenosis < 5%) and in-stent restenosis (ISR, restenosis > 70%)).
The miRNA and gene expression levels were measured by RT-qPCR technique. 15-Deoxy-∆
12,14
–PGJ2 values were measured by the ELISA technique. The miR-520 was transfected into
myocytes using PEI polymer.
Results:
The monocyte COX-1, COX-2 and PTGDS gene expression levels and the serum 15-
Deoxy-∆
12,14
–PGJ2 values increased significantly in the patients. Furthermore, the miR-520
correlated conversely with the COX-1, and PTGDS gene expression levels.
Conclusion:
The results showed that the PGD2 synthesis pathway is active in the patients and,
miR-520 may be involved in the function of this pathway.
Background:The integrin family receptors stimulate the cellular proliferation and migration through
the focal adhesion pathway by the activation of PTK2, VASP and TSP1 proteins. The purpose of this study was
to investigate the integrin-ligated motifs through the activation of focal adhesion pathway.Methods:A chimeric peptide was predicted from the integrin-mediated ligands by bioinformatics tools. The
VSMCs were treated with the chimeric peptide and simvastatin. The PTK2, VASP and TSP1 protein and gene
expression levels were measured by RT-qPCR and Western Blotting techniques, respectively. AutoDock Tools
were used for the docking technique.Results:The PTK2, VASP and TSP1 protein expression levels increased significantly in the VSMCs treated with
chimeric peptide in conversely with the effects of simvastatin. The docking results suggested two motifs in the
chimeric peptide.Conclusion:In conclusion, the chimeric peptide activated the focal adhesion pathway. The motifs 1 and 2 may be
directly involved in the transduction of signal by integrin family receptors.
Background:
The Matrix Metalloproteinase (MMPs) secreted from macrophages can affect the extracellular
matrix remodeling process and improve varicose veins.
Aim:
The aim of this study was to investigate the MMP-2 and MMP-9 gene expression and activity levels in the
differentiated macrophages M2 of subjects with varicose veins, and to evaluate a peptide construct on their catalytic
functions.
Methods:
The macrophages were differentiated from the monocytes using M-CSF. The MMP-2 and MMP-9 gene
expression and activity levels were measured by RT-qPCR and Zymography techniques, respectively. A peptide
construct (ESLCG) was predicted with bioinformatics tools, and was prepared for the study of enzyme functions
as compared to Batimastat. Furthermore, the docking studies were obtained for the evaluation of interactions
between peptide construct, Batimastat and enzyme 3D structures.
Results:
The results showed significant increases in MMP2 and MMP9 gene expression levels (P <0.001 and
P <0.004, respectively) and gelatinolytic activities (P <0.001 and P <0.0001, respectively) in the macrophages. In
agreement with the inhibitory effects of Batimastat, the peptide construct inhibited the MMP-2 and MMP-9 gelatinolytic
activities up to 6.8 and 6.5 folds in the concentration of 150 µM. The docking analyses showed that the
Lys187, Arg98, Leu49, Gly189, Leu190, Met97, Tyr53 and Phe57 residues of MMP-2 and the Leu187, His190,
Glu402, His401, His405 and His411 residues of MMP-9 are interacted with the atoms of Batimastat and ESLCG
peptide.
Conclusion:
The ESLCG peptide may be applied as an inhibitor of MMP-2 and MMP-9 enzymes in the subjects
with varicose veins.
Background &Aims:
It is well-known that the coronary artery stenosis is related to lipid
profile. This is a descriptive cross-sectional study to investigate the relationship between the serum
fat-soluble vitamins (A, E and D), circulating proprotein convertase subtilisin/kexin type 9
(PCSK9), and lipid profile in the study population.
Methods:
A total of 120 overweight subjects were participated in this study. The circulating
PCSK9 and vitamin D were measured by ELISA technique. The serum vitamin A and vitamin E
amounts were simultaneously measured by the HPLC method. The Serum Small Dense LDLCholesterol
(sdLDL-C) values were evaluated using heparin-Mg2+ precipitation technique. The lipid
profile was measured by routine laboratory techniques.
Results:
The serum vitamin E values correlated significantly to vitamin A (r= 0.47, P= 0.0001),
VLDL-C (r= 0.30, P= 0.002), total cholesterol (r= 0.309, P= 0.001), PCSK9 (r= 0.233, P= 0.01)
and total triglyceride (r= 0.61, P= 0.0001) values. The circulating PCSK9 values correlated significantly
to LDL-C (r= 0.17, P= 0.05) and total cholesterol (r= 0.23, P= 0.009) values. However, there
were not correlations between the levels of serum D and A vitamins, the serum LDL-C, sdLDL-C
and total cholesterol values.
Conclusion:
The data showed the correlations between serum vitamin E and PCSK9-related LDLC
values lower than the normal range. Furthermore, the results suggested a nutritional need on the
patents considering supplementation or fortification of vitamin E for the overweight subjects with
higher LDL-C levels.
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