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Wyświetlanie 1-2 z 2
Tytuł:
The influence of elastin degradation products, glucose and atorvastatin on metalloproteinase-1, -2, -9 and tissue inhibitor of metalloproteinases-1, -2, -3 expression in human retinal pigment epithelial cells
Autorzy:
Dorecka, Mariola
Francuz, Tomasz
Garczorz, Wojciech
Siemianowicz, Krzysztof
Romaniuk, Wanda
Powiązania:
https://bibliotekanauki.pl/articles/1039285.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
metalloproteinase
TIMP
atorvastatin
HRPE
Opis:
Purpose: Hyperglycemia and increased concentrations of elastin degradation products (EDPs) are common findings in patients with diabetes, atherosclerosis and hypertension. The aim of this study was to assess the influence of high glucose, EDPs and atorvastatin on MMP-1, MMP-2, MMP-9 and TIMP1-3 gene expression in human retinal pigment epithelial cells (HRPE) in vitro. Method: HRPE were cultured for 24 hours with the substances being tested (glucose, EDPs), alone or in combination. Additionally, the cells were treated with atorvastatin in two different concentrations (1 or 10 μM). After incubation, total cellular RNA was extracted and used for gene expression evaluation. Gene expression was measured using the real-time RT-PCR technique. Results: Glucose, EDPs and atorvastatin had no impact on TIMP-1 and TIMP-3 expression. HRPE cells treated with glucose or EDPs with the addition of atorvastatin had a statistically significant decrease of TIMP-2 expression; glucose alone decreased MMP-1 expression. Atorvastatin decreased expression of all assessed genes, except TIMP-1 and TIMP-3 in a dose-dependent manner. Conclusions: Our results confirm the importance of MMPs and TIMPs in retinal vascular biology. Atorvastatin-induced MMPs gene expression can deeply affect extracellular matrix turnover, which may play an important role in the progression of ocular diseases.
Źródło:
Acta Biochimica Polonica; 2014, 61, 2; 265-270
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Influence of elastin-derived peptides, glucose, LDL and oxLDL on nitric oxide synthase expression in human umbilical artery endothelial cells
Autorzy:
Garczorz, Wojciech
Francuz, Tomasz
Gmiński, Jan
Likus, Wirginia
Siemianowicz, Krzysztof
Jurczak, Teresa
Strzałka-Mrozik, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1039891.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nitric oxide synthase
oxidized LDL
LDL
EDP
atherosclerosis
hyperglycemia
endothelium
elastin-derived peptides
eNOS
Opis:
Endothelial dysfunction plays an important role in the development of atherosclerosis. Elastin-derived peptides (EDP), hyperglycemia, hypercholesterolemia and oxidized LDL have a proven proatherosclerotic potential. Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant. Here we studied the influence of those proatherosclerotic factors on eNOS gene and protein expression in artery-derived endothelial cells. Human umbilical artery endothelial cells (HUAEC) were incubated with or without: glucose (270 mg/dl), LDL (200 mg/dl), oxidized LDL (oxLDL 25 mg/dl) or κ-elastin (0.5 and 2.5 µg/ml). Gene expression was assessed by real time RT-PCR, whilst the eNOS protein by ELISA. In cells incubated with 2.5 µg/ml of κ-elastin, a 31 % increase of eNOS mRNA expression was observed, but the protein level remained unchanged. OxLDL, LDL and glucose decreased the eNOS protein level by 74 %, 37 % and 29 %, respectively. OxLDL decreased eNOS mRNA by 42 %. LDL non-significantly decreased eNOS mRNA expression. An elevated glucose level did not affect the eNOS mRNA expression. Hyperglycemia and an elevated level of LDL, particularly oxLDL, decreased the level of eNOS protein in endothelial cells. As κ-elastin did not decrease the expression of eNOS gene in HUAEC, the proatherogenic properties of elastin-derived peptides are unlikely to be due to their influence on eNOS.
Źródło:
Acta Biochimica Polonica; 2011, 58, 3; 375-379
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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