About: 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     Goto   Sponge   Distinct   Permalink

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  • 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. (en)
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 (en)
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 (en)
skos:notation
  • RIV/00216208:11120/07:43906709!RIV13-MSM-11120___
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • I
http://linked.open...iv/cisloPeriodika
  • 2
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
http://linked.open.../riv/druhVysledku
http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
http://linked.open...dnocenehoVysledku
  • 446278
http://linked.open...ai/riv/idVysledku
  • RIV/00216208:11120/07:43906709
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • ACE inhibitor; radiation injury; TGF-beta I; PAR-1 (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • DE - Spolková republika Německo
http://linked.open...ontrolniKodProRIV
  • [9B98F65DA571]
http://linked.open...i/riv/nazevZdroje
  • Pathology Research and Practice
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 203
http://linked.open...iv/tvurceVysledku
  • Matěj, Radoslav
  • Housa, Daniel
http://linked.open...ain/vavai/riv/wos
  • 000244679600007
issn
  • 0344-0338
number of pages
http://bibframe.org/vocab/doi
  • 10.1016/j.prp.2006.10.006
http://localhost/t...ganizacniJednotka
  • 11120
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