BARTMAN, Colleen M., Marta SCHILIRO, Martin HELÁN, Y. S. PRAKASH, David LINDEN and Christina PABELICK. Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle. Faseb Journal. BETHESDA: FEDERATION AMER SOC EXP BIOL, 2020, vol. 34, No 9, p. 12991-13004. ISSN 0892-6638. Available from: https://dx.doi.org/10.1096/fj.202001180R.
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Basic information
Original name Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle
Authors BARTMAN, Colleen M. (840 United States of America), Marta SCHILIRO (840 United States of America), Martin HELÁN (203 Czech Republic, belonging to the institution), Y. S. PRAKASH (840 United States of America), David LINDEN (840 United States of America) and Christina PABELICK (840 United States of America, guarantor).
Edition Faseb Journal, BETHESDA, FEDERATION AMER SOC EXP BIOL, 2020, 0892-6638.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 5.191
RIV identification code RIV/00216224:14110/20:00116373
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1096/fj.202001180R
UT WoS 000558418100001
Keywords in English calcium; contractility; fetal airway; oxygen; prematurity
Tags 14110122, rivok
Tags International impact, Reviewed
Changed by Changed by: Mgr. Tereza Miškechová, učo 341652. Changed: 29/10/2020 13:18.
Abstract
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.
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