Heat shock augments myosin phosphatase target-subunit phosphorylation

Area of Science:

• Physiology
• Molecular Biology
• Cardiovascular Research

Background:

• Previous studies indicated heat shock augments vascular contraction.
• The precise molecular mechanisms underlying heat shock-induced vascular contraction require further elucidation.

Purpose of the Study:

• To investigate the role of myosin phosphatase target-subunit (MYPT1) phosphorylation in heat shock-induced vascular contraction.
• To determine if Rho-kinase mediates the augmented vascular contraction following heat shock.

Main Methods:

• Endothelium-denuded rat aortic rings were subjected to heat shock (42°C for 45 min).
• Vascular contraction was measured 4 hours post-heat shock.
• Western blot analysis was performed to assess phosphorylation levels of MYPT1 and MLC(20).
• The effect of Y27632, a Rho-kinase inhibitor, was evaluated.

Main Results:

• Heat shock significantly increased phosphorylation of MYPT1 at Thr855 and MLC(20) in rat aorta.
• These phosphorylation increases were associated with augmented vascular contraction.
• Y27632 inhibited both MYPT1 and MLC(20) phosphorylation, as well as vascular contraction, in heat shock-treated aorta.

Conclusions:

• Heat shock augments vascular contraction through enhanced MYPT1 phosphorylation.
• Rho-kinase plays a critical role in mediating heat shock-induced increases in MYPT1 phosphorylation and vascular contraction.