Effect of nitric oxide deficiency on the pulmonary PTHrP system
  • Metaadatok
Tartalom: http://real.mtak.hu/40238/
Archívum: MTA Könyvtár
Gyűjtemény: Status = Published
Type = Article
Cím:
Effect of nitric oxide deficiency on the pulmonary PTHrP system
Létrehozó:
Brockhoff, Bastian
Schreckenberg, Rolf
Forst, Svenja
Heger, Jacqueline
Bencsik, PĂ©ter
Kiss, Krisztina
Ferdinandy, PĂ©ter
Schulz, Rainer
SchlĂĽter, Klaus-Dieter
Kiadó:
Wiley-Blackwell Publishing Ltd.
Dátum:
2016-08-31
Téma:
R850-854 Experimental medicine / kisérleti orvostudomány
Tartalmi leírás:
Nitric oxide (NO) deficiency is common in pulmonary diseases, but its effect on pulmonary remodelling is still controversial. As pulmonary
parathyroid hormone-related protein (PTHrP) expression is a key regulator of pulmonary fibrosis and development, the effect of chronic NO
deficiency on the pulmonary PTHrP system and its relationship with oxidative stress was addressed. NO bioavailability in adult rats was reduced
by systemic administration of L-NAME via tap water. To clarify the role of NO synthase (NOS)-3-derived NO on pulmonary expression of PTHrP,
NOS-3-deficient mice were used. Captopril and hydralazine were used to reduce the hypertensive effect of L-NAME treatment and to interfere
with the pulmonary renin-angiotensin system (RAS). Quantitative RT-PCR and immunoblot techniques were used to characterize the expression
of key proteins involved in pulmonary remodelling. L-NAME administration significantly reduced pulmonary NO concentration and caused
oxidative stress as characterized by increased pulmonary nitrite concentration and increased expression of NOX2, p47phox and p67phox. Furthermore,
L-NAME induced the pulmonary expression of PTHrP and of its corresponding receptor, PTH-1R. Expression of PTHrP and PTH-1R
correlated with the expression of two well-established PTHrP downstream targets, ADRP and PPARc, suggesting an activation of the pulmonary
PTHrP system by NO deficiency. Captopril reduced the expression of PTHrP, profibrotic markers and ornithine decarboxylase, but neither that
of PTH-1R nor that of ADRP and PPARc. All transcriptional changes were confirmed in NOS-3-deficient mice. In conclusion, NOS-3-derived NO
suppresses pulmonary PTHrP and PTH-1R expression, thereby modifying pulmonary remodelling.
Nyelv:
magyar
Típus:
Article
PeerReviewed
info:eu-repo/semantics/article
Formátum:
text
Azonosító:
Brockhoff, Bastian and Schreckenberg, Rolf and Forst, Svenja and Heger, Jacqueline and Bencsik, PĂ©ter and Kiss, Krisztina and Ferdinandy, PĂ©ter and Schulz, Rainer and SchlĂĽter, Klaus-Dieter (2016) Effect of nitric oxide deficiency on the pulmonary PTHrP system. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 20 (10). pp. 1-11. ISSN 1582-1838
Kapcsolat:
http://dx.doi.org/ 10.1111/jcmm.12942