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Hypoxia induced cholecystokinin gene expression in 3D engineered muscle.

ABSTRACT: At high altitude, hypoxic atmosphere decreases the oxygen partial pressure (pO2) in the body, inducing several metabolic changes in tissues and cells. Furthermore, it exerts potent anorectic effects, thus causing energy deficit. Two decades ago, a marked increase in the level of resting plasma cholecystokinin (CCK) was observed at Mt. Kanchenjunga basecamp (BC) located at 5,100 m above the sea level, compared to sea-level control values. Interestingly, acute exercise also raises plasma CCK and exerts potent anorectic effects under normoxic conditions. However, the molecular mechanism underlying these effects has not yet been established. We employed acute electrical pulse stimulation (EPS), followed by a microarray analysis, to discover novel myokines in 3D engineered muscle. Acute EPS efficiently affects the contractile function, inducing a decline of the contractile force. Surprisingly, microarray analysis revealed an EPS-induced activation of the cholecystokinin receptor (CCKR)-mediated signaling. Furthermore, Cck was constitutively expressed in 3D engineered muscle, and was upregulated by hypoxic conditions. Notably, a hypoxia responsive element (HRE) was detected in the Cck promoter of mice and humans. Our results suggested that, under hypoxic conditions, Hif-1a binding to HRE transactivated Cck expression in mice and humans. Furthermore, the plasma CCK elevation after acute exercise or at high altitude might be partly attributed to myogenic cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE135373 | GEO | 2021/04/13

REPOSITORIES: GEO

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