Effect of chronic hypoxia and role of stearoyl-CoA desaturase 1 (SCD1) on the inflammatory response of human primary macrophages
A hypoxic microenvironment in solid tumors frequently is associated with poor outcome due to metabolic adaptation of cells in the tumor microenvironment that supports tumor cells survival and proliferation. However, little is known about how macrophages (M?) metabolically and phenotypically adapt to chronic hypoxia (CH) and how this in turn affects tumor-associated inflammation. Here, we subjected M?s to CH to compare their inflammatory phenotype with normoxic M?s. In addition, we transfected SCD1, the rate-limiting enzyme of fatty acid desaturation, to investigate its role in M? adaptation to oxygen shortage and its contribution to the inflammatory function. Overall design: Human primary macrophages under chronic hypoxia (1% oxygen for 5 days) and normoxia (21% oxygen) with and without stearoyl-CoA desaturase (SCD1) or control and harvested 5 days after transfection (n = 6).