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Status: Bibliographieeintrag

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Verfasst von:Blackwood, Erik A. [VerfasserIn]   i
 Thuerauf, Donna J. [VerfasserIn]   i
 Stastna, Miroslava [VerfasserIn]   i
 Stephens, Haley [VerfasserIn]   i
 Sand, Zoe [VerfasserIn]   i
 Pentoney, Amber [VerfasserIn]   i
 Azizi, Khalid [VerfasserIn]   i
 Jakobi, Tobias [VerfasserIn]   i
 Van Eyk, Jennifer E. [VerfasserIn]   i
 Katus, Hugo [VerfasserIn]   i
 Glembotski, Christopher C. [VerfasserIn]   i
 Doroudgar, Shirin [VerfasserIn]   i
Titel:Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response
Verf.angabe:Erik A. Blackwood, Donna J. Thuerauf, Miroslava Stastna, Haley Stephens, Zoe Sand, Amber Pentoney, Khalid Azizi, Tobias Jakobi, Jennifer E. Van Eyk, Hugo A. Katus, Christopher C. Glembotski, Shirin Doroudgar
E-Jahr:2020
Jahr:25 April 2020
Umfang:13 S.
Fussnoten:Gesehen am 10.12.2020
Titel Quelle:Enthalten in: Journal of molecular and cellular cardiology
Ort Quelle:New York, NY [u.a.] : Elsevier, 1970
Jahr Quelle:2020
Band/Heft Quelle:143(2020), Seite 132-144
ISSN Quelle:1095-8584
Abstract:The effects of ER stress on protein secretion by cardiac myocytes are not well understood. In this study, the ER stressor thapsigargin (TG), which depletes ER calcium, induced death of cultured neonatal rat ventricular myocytes (NRVMs) in high media volume but fostered protection in low media volume. In contrast, another ER stressor, tunicamycin (TM), a protein glycosylation inhibitor, induced NRVM death in all media volumes, suggesting that protective proteins were secreted in response to TG but not TM. Proteomic analyses of TG- and TM-conditioned media showed that the secretion of most proteins was inhibited by TG and TM; however, secretion of several ER-resident proteins, including GRP78 was increased by TG but not TM. Simulated ischemia, which decreases ER/SR calcium also increased secretion of these proteins. Mechanistically, secreted GRP78 was shown to enhance survival of NRVMs by collaborating with a cell-surface protein, CRIPTO, to activate protective AKT signaling and to inhibit death-promoting SMAD2 signaling. Thus, proteins secreted during ER stress mediated by ER calcium depletion can enhance cardiac myocyte viability.
DOI:doi:10.1016/j.yjmcc.2020.04.012
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1016/j.yjmcc.2020.04.012
 Volltext: http://www.sciencedirect.com/science/article/pii/S0022282820300948
 DOI: https://doi.org/10.1016/j.yjmcc.2020.04.012
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Cardiac myocyte death
 Cardiokine
 Cardioprotection
 ER stress
 Heart failure
 Proteostasis
K10plus-PPN:1742419623
Verknüpfungen:→ Zeitschrift

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