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Signalling pathways involved in urotensin II induced ventricular myocyte hypertrophy
Hadeel S Al Ali1,2, Glenn C Rodrigo1, David G Lambert3
1Department of Cardiovascular Sciences, Clinical Sciences Wing, Glenfield Hospital, University of Leicester, Leicester, United Kingdom.
Plos One
|January 17, 2025
Summary
Urotensin II (UII) peptide contributes to cardiac hypertrophy by activating ERK1/2, p38, and CaMKII pathways. Inhibiting the UII/UT receptor system may help treat heart disease and reduce adverse remodeling.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Pathologic myocardial hypertrophy is a major cause of heart failure (HF).
- Elevated circulating urotensin II (UII) levels are observed in HF, but its role in hypertrophy development is unclear.
- Urotensin II (UII) is a peptide hormone implicated in cardiovascular function.
Purpose of the Study:
- To investigate the role of UII and its receptor UT in cardiac hypertrophy development.
- To identify signaling molecules involved in UII-induced cardiac hypertrophy.
Main Methods:
- Isolated adult rat ventricular myocytes were treated with UII.
- Hypertrophy was quantified using length/width ratio measurements.
- Signaling pathway activation (ERK1/2, p38, CaMKII, JNK) was assessed via Western blotting.
- Sarcoplasmic reticulum (SR) Ca2+-leak was measured.
Main Results:
- UII treatment significantly increased myocyte hypertrophy (reduced L/W ratio).
- The UT-antagonist SB657510 reversed UII-induced hypertrophy.
- UII activated ERK1/2, p38, and CaMKII signaling pathways, which were essential for hypertrophy.
- No significant increase in SR Ca2+-leak was observed.
Conclusions:
- Urotensin II (UII) promotes cardiac hypertrophy through MAPK and CaMKII signaling.
- Increased circulating UII may contribute to left ventricular hypertrophy.
- Inhibiting the UII/UT receptor system could be a therapeutic strategy for heart disease.
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