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Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response
EA. Blackwood, DJ. Thuerauf, M. Stastna, H. Stephens, Z. Sand, A. Pentoney, K. Azizi, T. Jakobi, JE. Van Eyk, HA. Katus, CC. Glembotski, S. Doroudgar
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R01 HL149931
NHLBI NIH HHS - United States
R01 HL135893
NHLBI NIH HHS - United States
R01 HL132075
NHLBI NIH HHS - United States
P01 HL112730
NHLBI NIH HHS - United States
P01 HL085577
NHLBI NIH HHS - United States
R01 HL141463
NHLBI NIH HHS - United States
- MeSH
- apoptóza MeSH
- autokrinní signalizace MeSH
- biologické markery MeSH
- epidermální růstový faktor metabolismus MeSH
- kardiomyocyty účinky léků metabolismus MeSH
- krysa rodu rattus MeSH
- kultivované buňky MeSH
- membránové glykoproteiny metabolismus MeSH
- myši MeSH
- náchylnost k nemoci MeSH
- nádorové proteiny metabolismus MeSH
- parakrinní signalizace MeSH
- proteom * MeSH
- proteomika * metody MeSH
- sarkoplazmatické retikulum metabolismus MeSH
- signální transdukce účinky léků MeSH
- stres endoplazmatického retikula * účinky léků MeSH
- thapsigargin farmakologie MeSH
- vápník metabolismus MeSH
- vápníková signalizace účinky léků MeSH
- viabilita buněk MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
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.
Department of Internal Medicine 3 Heidelberg University Hospital Heidelberg Germany
DZHK Partner Site Heidelberg Mannheim Germany
Institute of Analytical Chemistry of the Czech Academy of Sciences Brno Czech Republic
Citace poskytuje Crossref.org
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- $a 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.
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