Hydrogen sulfide, oxygen, and calcium regulation in developing
human airway smooth muscle

J 2020

Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle

BARTMAN, Colleen M., Marta SCHILIRO, Martin HELÁN, Y. S. PRAKASH, David LINDEN et. al.

Základní údaje

Originální název

Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle

Autoři

BARTMAN, Colleen M. (840 Spojené státy), Marta SCHILIRO (840 Spojené státy), Martin HELÁN (203 Česká republika, domácí), Y. S. PRAKASH (840 Spojené státy), David LINDEN (840 Spojené státy) a Christina PABELICK (840 Spojené státy, garant)

Vydání

Faseb Journal, BETHESDA, FEDERATION AMER SOC EXP BIOL, 2020, 0892-6638

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10601 Cell biology

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 5.191

Kód RIV

RIV/00216224:14110/20:00116373

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.1096/fj.202001180R

UT WoS

000558418100001

Klíčová slova anglicky

calcium; contractility; fetal airway; oxygen; prematurity

Štítky

14110122, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 29. 10. 2020 13:18, Mgr. Tereza Miškechová

Anotace

V originále

Preterm infants can develop airway hyperreactivity and impaired bronchodilation following supplemental O-2(hyperoxia) in early life, making it important to understand mechanisms of hyperoxia effects. Endogenous hydrogen sulfide (H2S) has anti-inflammatory and vasodilatory effects with oxidative stress. There is little understanding of H2S signaling in developing airways. We hypothesized that the endogenous H2S system is detrimentally influenced by O(2)and conversely H2S signaling pathways can be leveraged to attenuate deleterious effects of O-2. Using human fetal airway smooth muscle (fASM) cells, we investigated baseline expression of endogenous H2S machinery, and effects of exogenous H2S donors NaHS and GYY4137 in the context of moderate hyperoxia, with intracellular calcium regulation as a readout of contractility. Biochemical pathways for endogenous H2S generation and catabolism are present in fASM, and are differentially sensitive to O(2)toward overall reduction in H2S levels. H2S donors have downstream effects of reducing [Ca2+](i)responses to bronchoconstrictor agonist via blunted plasma membrane Ca(2+)influx: effects blocked by O-2. However, such detrimental O(2)effects are targetable by exogenous H2S donors such as NaHS and GYY4137. These data provide novel information regarding the potential for H2S to act as a bronchodilator in developing airways in the context of oxygen exposure.

Citovat

BARTMAN, Colleen M., Marta SCHILIRO, Martin HELÁN, Y. S. PRAKASH, David LINDEN a Christina PABELICK. Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle. Faseb Journal. BETHESDA: FEDERATION AMER SOC EXP BIOL, 2020, roč. 34, č. 9, s. 12991-13004. ISSN 0892-6638. Dostupné z: https://dx.doi.org/10.1096/fj.202001180R.

@article{1677978,
   author = {Bartman, Colleen M. and Schiliro, Marta and Helán, Martin and Prakash, Y. S. and Linden, David and Pabelick, Christina},
   article_location = {BETHESDA},
   article_number = {9},
   doi = {http://dx.doi.org/10.1096/fj.202001180R},
   keywords = {calcium; contractility; fetal airway; oxygen; prematurity},
   language = {eng},
   issn = {0892-6638},
   journal = {Faseb Journal},
   title = {Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle},
   url = {https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fj.202001180R},
   volume = {34},
   year = {2020}
}

TY  - JOUR
ID  - 1677978
AU  - Bartman, Colleen M. - Schiliro, Marta - Helán, Martin - Prakash, Y. S. - Linden, David - Pabelick, Christina
PY  - 2020
TI  - Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle
JF  - Faseb Journal
VL  - 34
IS  - 9
SP  - 12991-13004
EP  - 12991-13004
PB  - FEDERATION AMER SOC EXP BIOL
SN  - 08926638
KW  - calcium
KW  - contractility
KW  - fetal airway
KW  - oxygen
KW  - prematurity
UR  - https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fj.202001180R
L2  - https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fj.202001180R
N2  - Preterm infants can develop airway hyperreactivity and impaired bronchodilation following supplemental O-2(hyperoxia) in early life, making it important to understand mechanisms of hyperoxia effects. Endogenous hydrogen sulfide (H2S) has anti-inflammatory and vasodilatory effects with oxidative stress. There is little understanding of H2S signaling in developing airways. We hypothesized that the endogenous H2S system is detrimentally influenced by O(2)and conversely H2S signaling pathways can be leveraged to attenuate deleterious effects of O-2. Using human fetal airway smooth muscle (fASM) cells, we investigated baseline expression of endogenous H2S machinery, and effects of exogenous H2S donors NaHS and GYY4137 in the context of moderate hyperoxia, with intracellular calcium regulation as a readout of contractility. Biochemical pathways for endogenous H2S generation and catabolism are present in fASM, and are differentially sensitive to O(2)toward overall reduction in H2S levels. H2S donors have downstream effects of reducing [Ca2+](i)responses to bronchoconstrictor agonist via blunted plasma membrane Ca(2+)influx: effects blocked by O-2. However, such detrimental O(2)effects are targetable by exogenous H2S donors such as NaHS and GYY4137. These data provide novel information regarding the potential for H2S to act as a bronchodilator in developing airways in the context of oxygen exposure.
ER  -

BARTMAN, Colleen M., Marta SCHILIRO, Martin HELÁN, Y. S. PRAKASH, David LINDEN a Christina PABELICK. Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle. \textit{Faseb Journal}. BETHESDA: FEDERATION AMER SOC EXP BIOL, 2020, roč.~34, č.~9, s.~12991-13004. ISSN~0892-6638. Dostupné z: https://dx.doi.org/10.1096/fj.202001180R.

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