Kiss1 receptor knockout exacerbates airway hyperresponsiveness and remodeling in a mouse model of allergic asthma.

ABSTRACT:

Background

In asthma, sex-steroids signaling is recognized as a critical regulator of disease pathophysiology. However, the paradoxical role of sex-steroids, especially estrogen, suggests that an upstream mechanism or even independent of estrogen plays an important role in regulating asthma pathophysiology. In this context, in our previous studies, we explored kisspeptin (Kp) and its receptor Kiss1R's signaling in regulating human airway smooth muscle cell remodeling in vitro and airway hyperresponsiveness (AHR) in vivo in a mouse (wild-type, WT) model of asthma. In this study, we evaluated the effect of endogenous Kp in regulating AHR and remodeling using Kiss1R knockout (Kiss1R^-/-) mice.

Methods

C57BL/6J WT (Kiss1R^+/+) and Kiss1R^-/- mice, b

SUBMITTER: Ambhore NS 

PROVIDER: S-EPMC11520794 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature