BDNF secretion by human pulmonary artery endothelial cells in response to hypoxia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F14%3A00077285" target="_blank" >RIV/00216224:14110/14:00077285 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/14:00061000

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.yjmcc.2014.01.006" target="_blank" >http://dx.doi.org/10.1016/j.yjmcc.2014.01.006</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.yjmcc.2014.01.006" target="_blank" >10.1016/j.yjmcc.2014.01.006</a>

Jazyk výsledku

angličtina

Název v původním jazyce

BDNF secretion by human pulmonary artery endothelial cells in response to hypoxia

Popis výsledku v původním jazyce

Within human pulmonary artery, neurotrophin growth factors [NTs; e.g. brain-derived neurotrophic factor (BDNF)] and their high-affinity receptors (tropomyosin-related kinase; Trk) and low-affinity receptors p75 neurotrophin receptor (p75NTR) have been reported, but their functional role is incompletely understood. We tested the hypothesis that BDNF is produced by human pulmonary artery endothelial cells (PAECs). In the context of hypoxia as a risk factor for pulmonary hypertension, we examined the effect of hypoxia on BDNF secretion and consequent autocrine effects on pulmonary endothelium. Initial ELISA analysis of circulating BDNF in 30 healthy human volunteers showed that 72 h exposure to high altitude (similar to 11,000 ft, alveolar PO2 = 100 mm Hg) results in higher BDNF compared to samples taken at sea level. Separately, in human PAECs exposed for 24 h to normoxia vs. hypoxia (1-3% O-2), ELISA of extracellular media showed increased BDNF levels.

Název v anglickém jazyce

BDNF secretion by human pulmonary artery endothelial cells in response to hypoxia

Popis výsledku anglicky

Within human pulmonary artery, neurotrophin growth factors [NTs; e.g. brain-derived neurotrophic factor (BDNF)] and their high-affinity receptors (tropomyosin-related kinase; Trk) and low-affinity receptors p75 neurotrophin receptor (p75NTR) have been reported, but their functional role is incompletely understood. We tested the hypothesis that BDNF is produced by human pulmonary artery endothelial cells (PAECs). In the context of hypoxia as a risk factor for pulmonary hypertension, we examined the effect of hypoxia on BDNF secretion and consequent autocrine effects on pulmonary endothelium. Initial ELISA analysis of circulating BDNF in 30 healthy human volunteers showed that 72 h exposure to high altitude (similar to 11,000 ft, alveolar PO2 = 100 mm Hg) results in higher BDNF compared to samples taken at sea level. Separately, in human PAECs exposed for 24 h to normoxia vs. hypoxia (1-3% O-2), ELISA of extracellular media showed increased BDNF levels.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

<a href="/cs/project/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: Fakultní nemocnice u sv. Anny v Brně - Mezinárodní centrum klinického výzkumu (FNUSA - ICRC)</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Molecular and Cellular Cardiology

ISSN

0022-2828

e-ISSN

—

Svazek periodika

68

Číslo periodika v rámci svazku

March 2014

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

89-97

Kód UT WoS článku

000334653200011

EID výsledku v databázi Scopus

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