Abstract
Background: Intermittent hypoxia (IH) is a hallmark feature in obstructive sleep apnea (OSA), which is increasingly recognized as an independent risk factor of cardiovascular diseases. Different fatty acid binding proteins (FABPs), including adipocyte (A)-FABP (FABP4) and epidermal (E)-FABP (FABP5), are now widely accepted as biomarkers associated with increased cardio-metabolic risks and carotid atherosclerosis. We hypothesize that IH exposure may regulate the expression of FABPs in two major cell types involved in the development of atherosclerosis, namely adipocytes and macrophages.
Methods: Human preadipocytes and THP-1 cells were cultivated in the differentiation media until reaching final differentiation level of ∼80% before treatment. Differentiated cells were exposed to intermittent normoxia (IN as control) or IH [a 10-min hypoxia (5% O2) followed by a 5-min normoxia (21% O2) for 64 cycles using the BioSpherix OxyCycler C42 system (Redfield, NY)]. FABP4 and FABP5 mRNA expressions were measured by RT-PCR, and protein by Western blot.
Results: Adipocytes expressed very high levels of FABP4 and low levels of FABP5 while differentiated macrophages expressed high levels of both FABP4 and FABP5, consistent with previous reports. IH exposure resulted in an up-regulation of FABP5 but not FABP4 expression in adipocytes. Macrophage FABP4 and FABP5 levels remained unchanged following IH treatment, suggesting that the two cell types are likely to have distinct functions.
Conclusions: These data suggest that FABP5 may play a role in atherogenesis in OSA subjects.
Acknowledgement: This research is supported by Hong Kong Research Grant Council (RGC) Grant (HKU 7667/07M).
- © 2011 ERS
