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2016-06-29 - Colloque/Article dans les actes avec comité de lecture - Anglais - 1 page(s)

Pierard Mélany, Delpierre Antoine, Conotte Stéphanie, Tassin Alexandra , Zouaoui Boudjeltia Karim , Legrand Alexandre , "Modulations of adiponectin pathway induced by hypoxia in murin and cellular models" in Federation of European Physiological Societies, Paris, France, 2016

  • Codes CREF : Physiologie générale [animale] (DI3228)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)

Abstract(s) :

(Anglais) Hypoxaemia is a component of respiratory diseases frequently observed in severe COPD patients (Chronic Obstructive Pulmonary Diseases). It initiates compensatory mechanisms mainly mediated by a family of transcription factors (Hypoxia Inducible Factors HIFs). Hypoxemia was suggested to modulate Adiponectin (Ad) pathway. Due to its anti-diabetic, anti-inflammatory and anti-atherosclerotic properties, we postulate that alteration of Ad pathway could participate to metabolic troubles and cardiovascular co-morbidities in COPD patients. To better understand the specific impact of hypoxaemia on Ad pathway, we studied Ad plasmatic level, Ad multimeric forms and AdipoR1/AdipoR2 receptor abundance in a mouse model of chronic hypoxemia (FiO2 10%, 8h/day). After 35 days, hypoxaemia induced a decreased level of low molecular weight (MW) forms in favour of higher MW multimers as well as a tissue-specific modulation of AdipoR abundance. As these alterations could impact the atherogenic risk, we evaluated AdipoR abundance in RAW murine macrophages exposed to low oxygen level (1%, 24h). We first verified the induction of HIF 1α on nuclear protein extracts. We then demonstrated that exposure to hypoxia induced a reduced AdipoR2 level. Such deregulation could modify intra-cellular lipid accumulation and pro-inflammatory cytokine production. Investigations on these two hallmarks of cardiovascular risk are ongoing. Therefore, we demonstrate that hypoxaemia modifies the distribution of Ad forms and causes AdipoR modulation both in vivo and in vitro. These troubles could participate to pathophysiological mechanisms linked to COPD co-morbidities.