Authors
ShengYu Mu, Tatsuo Shimosawa, and Toshiro Fujita
Summary
In the current study, we found that β2 adrenergic receptor (β2AR) stimulation induced histone acetylation through HDAC8 inhibition, and then decreased transcription of the WNK4 gene by enhancing the binding of glucocorticoid receptor (GR) and negative-GR-responsive-element (nGRE) in WNK4 promoter region. Infusion of isoproterenol decreased WNK4 expression and activated the Na+-Cl- co-transporter in mice, which developed salt-induced hypertension. In rodent models of salt-sensitive hypertension and sympathetic over-activity, salt-loading suppressed renal WNK4 compared to controls, thus inducing salt-dependent hypertension. Our protocol covers the entire procedure for evaluating cAMP-induced histone acetylation in the transcriptional regulation of WNK4. Further more our work also clarifies the involvement of aberrant renal β2AR-WNK4 pathway in salt-induced hypertension.Further details
The protocol was published on Protocol Exchange on 16 May 2011. To see the entire protocol, click on the source link.Advertisement
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