Gewählte Publikation:
SHR
Neuro
Krebs
Kardio
Lipid
Stoffw
Microb
Kockskamper, A; von Lewinski, D; Zhu, D; Kockskamper, J; Khafaga, M; Schmidt, AG; Post, H; Pieske, B.
Relevance of stretch-induced phosphorylation of MAPK and p90rsk in human myocardium.
Front Biosci (Elite Ed). 2013; 5(6):883-892
Doi: 10.2741/E667
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
-
Kockskämper Anke
-
von Lewinski Dirk
- Co-Autor*innen der Med Uni Graz
-
Khafaga Mounir
-
Kockskämper Jens
-
Pieske Burkert Mathias
-
Post Heiner
-
Schmidt Albrecht
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
-
Stretch activates various signal transduction pathways including mitogen-activated protein kinases (MAPK). Stretch-induced phosphorylation of MAPK-contribution to contractility in human myocardium is unknown. We tested the effects of stretch on p44/42-, p38-MAPK and p90rsk phosphorylation and the functional relevance for force development in failing (F) and non-failing (NF) human myocardium. Trabeculae were stretched to a diastolic tension of 12mN/mm2 for 2.5 to 30 minutes and frozen for Western Blot analysis. Stretch induced a time-dependent increase in phosphorylation of p44/42-, p38-MAPK and p90rsk. For functional analysis, trabeculae from F myocardium were stretched and the immediate (Frank-Starling mechanism; FSM) and delayed (slow force response; SFR) increase in twitch force was assessed before and after blocking the activation of p44/42-MAPK (30 micromol/L U0126) and p38-MAPK (10 micromol/L SB203580). Inhibition of p44/42-MAPK almost completely blocked the SFR (106.7 3.7% vs. 125.4 2.9%), while p38-MAPK-blockade significantly increased the SFR (124.6 1.9% vs. 121.2 2.2%). Stretch induced a time-dependent increase in p44/42-, p38-MAPK and p90rsk phosphorylation in F and NF myocardium. While p44/42-MAPK phosphorylation contributed to the SFR, p38-MAPK activation antagonized the stretch-induced SFR.
- Find related publications in this database (using NLM MeSH Indexing)
-
Heart Failure - enzymology
-
Humans -
-
Mitogen-Activated Protein Kinases - metabolism
-
Myocardium - enzymology
-
Phosphorylation -
-
Ribosomal Protein S6 Kinases, 90-kDa - metabolism
-
Stress, Mechanical -