Corrigendum to: “The Rho kinase (ROCK) inhibitor Y-27632 reduces the β 2-adrenoceptor density but enhance cAMP formation in primary equine bronchial epithelial cells” [Eur. J. Pharmacol. 2021 Sep 15; 907:174323].

This research paper investigates the influence of the Rho kinase (ROCK) inhibitor Y-27632 on β2-adrenoceptor density and the generation of a cellular messenger called cAMP in horse bronchial cells. The drug appears to reduce β2-adrenoceptor density but amplifies the production of cAMP.

Explanation of the Study

The paper explores an experiment utilizing primary equine bronchial epithelial cells (EBEC), which are cells from the bronchi of a horse’s lung. The experiment uses Y-27632, a Rho-kinase (ROCK) inhibitor, to determine its effects on:

• The density of β2-adrenoceptors in the cells, which are a subtype of adrenoceptors involved in various body responses such as lung bronchodilation.
• The formation of cAMP, a cellular messenger that is vital in various biological responses, typically following β-agonist stimulation.

Results of the Study

Following are the major results of the study:

• Y-27632 was found to decrease the number of β2-adrenoceptors in EBEC considerably, with no significant effect on the receptor’s affinity for the radioligand [125I]-iodocyanopindolol (ICYP), a tracer molecule used in experiments.
• Contrastingly, the production of intracellular cAMP (formed following β-agonist stimulation) was elevated in the presence of Y-27632. This increase was especially pronounced for three specific β-agonists: isoproterenol, epinephrine, and norepinephrine.
• The alteration in cAMP production did not cause the concentration-effect curves of the β-agonists to shift leftwards.
• Further, two antagonists, ICI 118.551 and propranolol, reversed the cAMP production instigated by isoproterenol in both Y-27632-treated and control cells, hinting that the cAMP formation was related merely to the β2-adrenoceptor subtype.

Conclusion and Implications of the Study

The study concluded that the ROCK inhibitor Y-27632 influences the density and function of β2-adrenoceptors differentially – it reduces the receptor number but heightens cAMP formation. This indicates a functional interaction between β2-adrenoceptors and ROCK pathways. Furthermore, the study suggests reconsidering this differential regulation in relation to the beneficial effects of Y-27632 in asthma therapy.