NR4A2 and NR4A3 selectively modulate elements of the monocyte response to buffered hypercapnia

In wild type, NR4A2-deficient, and NR4A3-deficient monocytes we used RNA-sequencing to investigate the effect of 4hrs of exposure to buffered hypercapnia (10% CO2) compared to normocapnia (5% CO2) with and without the pro-inflammatory stimulus LPS (2.5ug/ml) for the final 2hrs. Buffered hypercapnia causes transcriptional changes associated with altered metabolic function in both the basal and stimulated states. To investigate the effect of NR4A2 ot NR4A3 depletion on the hypercapnic response in monocytes, we exposed NR4A2-deficient and NR4A3-deficient monocytes to 10% CO2 or 5% CO2 for 4 hours in the presence or absence of LPS (2.5ug/ml) for the final 2 hours.