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Hydrogen sulphide facilitates exocytosis by regulating the handling of intracellular calcium by chromaffin cells

Overview of attention for article published in Pflügers Archiv - European Journal of Physiology, May 2018
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Title
Hydrogen sulphide facilitates exocytosis by regulating the handling of intracellular calcium by chromaffin cells
Published in
Pflügers Archiv - European Journal of Physiology, May 2018
DOI 10.1007/s00424-018-2147-7
Pubmed ID
Authors

Ricardo de Pascual, Andrés M. Baraibar, Iago Méndez-López, Martín Pérez-Ciria, Ignacio Polo-Vaquero, Luis Gandía, Sunny E. Ohia, Antonio G. García, Antonio M. G. de Diego

Abstract

Gasotransmitter hydrogen sulphide (H2S) has emerged as a regulator of multiple physiological and pathophysiological processes throughout. Here, we have investigated the effects of NaHS (fast donor of H2S) and GYY4137 (GYY, slow donor of H2S) on the exocytotic release of catecholamines from fast-perifused bovine adrenal chromaffin cells (BCCs) challenged with sequential intermittent pulses of a K+-depolarizing solution. Both donors caused a concentration-dependent facilitation of secretion. This was not due to an augmentation of Ca2+ entry through voltage-activated Ca2+ channels (VACCs) because, in fact, NaHS and GYY caused a mild inhibition of whole-cell Ca2+ currents. Rather, the facilitation of exocytosis seemed to be associated to an augmented basal [Ca2+]c and the K+-elicited [Ca2+]c transients; such effects of H2S donors are aborted by cyclopiazonic acid (CPA), that causes endoplasmic reticulum (ER) Ca2+ depletion through sarcoendoplasmic reticulum Ca2+ ATPase inhibition and by protonophore carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), that impedes the ability of mitochondria to sequester cytosolic Ca2+ during cell depolarization. Inasmuch as CPA and FCCP reversed the facilitation of secretion triggered by K+ in the presence of NaHS and GYY, is seems that such facilitation is tightly coupled to Ca2+ handling by the ER and mitochondria. On the basis of these results, we propose that H2S regulates catecholamine secretory responses triggered by K+ in BCCs by (i) mobilisation of ER Ca2+ and (ii) interference with mitochondrial Ca2+ circulation. In so doing, the clearance of the [Ca2+]c transient will be delayed and the Ca2+-dependent trafficking of secretory vesicles will be enhanced to overfill the secretory machinery with new vesicles to enhance exocytosis.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 3 18%
Student > Bachelor 3 18%
Student > Doctoral Student 2 12%
Professor 2 12%
Student > Ph. D. Student 2 12%
Other 2 12%
Unknown 3 18%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 4 24%
Agricultural and Biological Sciences 3 18%
Biochemistry, Genetics and Molecular Biology 2 12%
Environmental Science 1 6%
Nursing and Health Professions 1 6%
Other 3 18%
Unknown 3 18%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 May 2018.
All research outputs
#21,164,509
of 23,818,521 outputs
Outputs from Pflügers Archiv - European Journal of Physiology
#1,798
of 1,973 outputs
Outputs of similar age
#289,436
of 327,918 outputs
Outputs of similar age from Pflügers Archiv - European Journal of Physiology
#12
of 16 outputs
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