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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F07%3A43906709%21RIV13-MSM-11120___
rdf:type
skos:Concept n17:Vysledek
dcterms:description
Transforming growth factor beta 1 (TGF-beta 1) plays an important role in the development of radiation- and drug-induced organ diseases. Proteinases-activated receptor I (PAR-1) is involved in many pathophysiologic processes after its activation by serine proteases. The aim of the present study was to determine messenger RNA (mRNA) production of TGF-beta 1 and PAR-1 in the lungs after local irradiation. Mice of C5713L/6 and C3H/J strains with different susceptibility to fibrosis development were exposed to a of 15 Gy. Non-irradiated mice of both strains were used as negative controls. Control (irradiated) and irradiated angiotensin-converting enzyme (ACE) inhibitor-treated animals were examined simultaneously. The ACE inhibitor group was given butylaminiperindopril for 9 days after irradiation (15 Gy) at a daily dose of 0.1 or 0.2 mg/kg per rectum. On day 9, all mice were sacrificed, and the production of mRNA TGF-beta 1 and PAR-1 in lung tissue was determined semiquantitatively using reverse transcriptase polymerase chain reaction, and immunohistochemical analysis of PAR-1 expression in pulmonary tissue was performed. In the fibrosing murine strain C57B1/6, there was an increase in the mRNA TGF-beta 1 and PAR-1 levels in lungs 9 days after irradiation as compared with non-irradiated controls and non-fibrosing murine strain C3H/J. In butylaminiperindopril-treated mice, a decrease in transcript of TGF-beta 1 and PAR-1 was observed. Thus, PAR-1 is involved in radiation-induced lung fibrosis in correlation with TGF-beta 1 production. Administration of ACET influences PAR-1 and TGF-beta 1 expression. Transforming growth factor beta 1 (TGF-beta 1) plays an important role in the development of radiation- and drug-induced organ diseases. Proteinases-activated receptor I (PAR-1) is involved in many pathophysiologic processes after its activation by serine proteases. The aim of the present study was to determine messenger RNA (mRNA) production of TGF-beta 1 and PAR-1 in the lungs after local irradiation. Mice of C5713L/6 and C3H/J strains with different susceptibility to fibrosis development were exposed to a of 15 Gy. Non-irradiated mice of both strains were used as negative controls. Control (irradiated) and irradiated angiotensin-converting enzyme (ACE) inhibitor-treated animals were examined simultaneously. The ACE inhibitor group was given butylaminiperindopril for 9 days after irradiation (15 Gy) at a daily dose of 0.1 or 0.2 mg/kg per rectum. On day 9, all mice were sacrificed, and the production of mRNA TGF-beta 1 and PAR-1 in lung tissue was determined semiquantitatively using reverse transcriptase polymerase chain reaction, and immunohistochemical analysis of PAR-1 expression in pulmonary tissue was performed. In the fibrosing murine strain C57B1/6, there was an increase in the mRNA TGF-beta 1 and PAR-1 levels in lungs 9 days after irradiation as compared with non-irradiated controls and non-fibrosing murine strain C3H/J. In butylaminiperindopril-treated mice, a decrease in transcript of TGF-beta 1 and PAR-1 was observed. Thus, PAR-1 is involved in radiation-induced lung fibrosis in correlation with TGF-beta 1 production. Administration of ACET influences PAR-1 and TGF-beta 1 expression.
dcterms:title
Radiation-induced production of PAR-1 and TGF-beta 1 mRNA in lung of C57BI6 and C3H murine strains and influence of pharmacoprophylaxis by ACE inhibitors Radiation-induced production of PAR-1 and TGF-beta 1 mRNA in lung of C57BI6 and C3H murine strains and influence of pharmacoprophylaxis by ACE inhibitors
skos:prefLabel
Radiation-induced production of PAR-1 and TGF-beta 1 mRNA in lung of C57BI6 and C3H murine strains and influence of pharmacoprophylaxis by ACE inhibitors Radiation-induced production of PAR-1 and TGF-beta 1 mRNA in lung of C57BI6 and C3H murine strains and influence of pharmacoprophylaxis by ACE inhibitors
skos:notation
RIV/00216208:11120/07:43906709!RIV13-MSM-11120___
n3:aktivita
n10:I
n3:aktivity
I
n3:cisloPeriodika
2
n3:dodaniDat
n6:2013
n3:domaciTvurceVysledku
n5:4091507 n5:2483327
n3:druhVysledku
n15:J
n3:duvernostUdaju
n16:S
n3:entitaPredkladatele
n8:predkladatel
n3:idSjednocenehoVysledku
446278
n3:idVysledku
RIV/00216208:11120/07:43906709
n3:jazykVysledku
n4:eng
n3:klicovaSlova
ACE inhibitor; radiation injury; TGF-beta I; PAR-1
n3:klicoveSlovo
n11:TGF-beta%20I n11:radiation%20injury n11:PAR-1 n11:ACE%20inhibitor
n3:kodStatuVydavatele
DE - Spolková republika Německo
n3:kontrolniKodProRIV
[9B98F65DA571]
n3:nazevZdroje
Pathology Research and Practice
n3:obor
n13:FD
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
5
n3:rokUplatneniVysledku
n6:2007
n3:svazekPeriodika
203
n3:tvurceVysledku
Housa, Daniel Matěj, Radoslav
n3:wos
000244679600007
s:issn
0344-0338
s:numberOfPages
8
n9:doi
10.1016/j.prp.2006.10.006
n18:organizacniJednotka
11120