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PKC and MAPK signalling pathways regulate vascular endothelin receptor expression.

David Nilsson¹, Angelica Wackenfors, Lotta Gustafsson

¹Department of Medicine, Lund University Hospital, Lund, Sweden.

European Journal of Pharmacology

|November 23, 2007

Summary

This summary is machine-generated.

Protein kinase C (PKC) and mitogen-activated kinases (MAPK) regulate vascular endothelin receptors in porcine coronary arteries. Inhibiting these pathways may offer therapeutic targets for cardiovascular disease.

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Area of Science:

Cardiovascular Biology
Molecular Pharmacology
Cell Signaling

Background:

Vascular endothelin receptors (ET(A) and ET(B)) are implicated in cardiovascular disease pathogenesis.
Arterial culture models exhibit receptor alterations, making them suitable for studying endothelin receptor regulation.

Purpose of the Study:

To investigate the involvement of protein kinase C (PKC) and mitogen-activated kinases (MAPK) in regulating endothelin receptors in porcine coronary arteries.
To determine if inhibiting PKC and MAPK can modulate endothelin receptor expression and function in cultured arteries.

Main Methods:

Porcine coronary arteries were cultured for 24 hours and analyzed using in vitro pharmacology, real-time PCR, and immunofluorescence.
Receptor function was assessed using sarafotoxin 6c and endothelin-1.
PKC and MAPK involvement was studied using specific inhibitors (bisindolylmaleimide I, Ro-32-0432, PD98059, SP600125, SB203580).

Main Results:

Organ culture increased ET(A) and ET(B) receptor protein expression and ET(B) receptor mRNA levels.
PKC inhibitors blocked these culture-induced changes.
MAPK inhibitors targeting ERK1/2 and JNK, but not p38 MAPK, also inhibited the receptor alterations.

Conclusions:

PKC and MAPK signaling pathways are involved in the regulation of endothelin receptor expression in porcine coronary arteries.
Targeting these intracellular pathways presents a potential therapeutic strategy to prevent vascular endothelin receptor dysregulation in cardiovascular disease.