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  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
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Protein and mRNA expression levels of VEGF-A and TGF-B1 in different types of human coronary atherosclerotic lesions

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Autor
Panutsopulos, D.; Papalambros, E.; Sigala, F.; Zafiropoulos, A.; Arvanitis, D. L.; Spandidos, D. A.
Datum
2005
Schlagwort
human coronary artery
coronary artery disease
growth factors
immunohistochemistry
GROWTH-FACTOR-BETA
SMOOTH-MUSCLE-CELLS
ENDOTHELIAL-CELLS
PLAQUE
PHENOTYPE
GENE-EXPRESSION
ARTERY-DISEASE
T-CELLS
MACROPHAGES
RECEPTOR
COLOCALIZATION
Medicine, Research & Experimental
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Zusammenfassung
It is well documented that inflammation plays a major role in the establishment and progression of atherosclerosis. Endothelial cells, vascular smooth muscle cells and m onocytes/macrophages are involved in this process by expressing inflammatory factors. The aim of the present study was to evaluate potential association and risk of VEGF-A and TGF-beta 1 in human coronary atherosclerotic lesions. Twenty-six fresh human coronary artery segments were collected at autopsy. Conventional histology was performed and samples were classified into: no lesion group (NL), fatty streak group (FS), plaque group (P) and complicated lesion group (CL) based on the atherosclerotic lesion type. RNA extraction-analysis with RT-PCR and immunohistochemistry was also performed. We observed that VEGF-A protein and mRNA expression increased during atherogenesis. The expression levels (protein and mRNA levels) of TGF-beta 1 were decreased from NL to the FS group while, strong protein-staining and signal of mRNA expression in P and CL groups were observed. Our findings suggest a crucial role of VEGF-A in the development of coronary artery disease. The high protein and mRNA expression levels of TGF-beta 1 in P and CL suggest that this factor may be implicated in the deposition of excessive extracellular matrix in the intima of the vessel wall, contributing to the expansion of the atheromatic plaque.
URI
http://hdl.handle.net/11615/31623
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