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Updated: Aug 6, 2026
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Myeloid-Specific Pck1 Deficiency Does Not Alter Aortic Root Atherosclerosis in Mice
Juying Han1, Emmanuel Opoku1, Jonathan D Smith1,2
1Department of Heart, Blood, and Kidney Research, Cleveland Clinic, Cleveland, OH, USA, 44195.
Background:
We previously performed a strain intercross between atherosclerosis resistant AKR Apoe -/- mice and atherosclerosis sensitive DBA/2 Apoe -/- mice and identified the Ath28 quantitative trait locus (QTL) on the distal end of chromosome 2. Congenic strain fine mapping identified the Ath28.1 QTL atherosclerosis modifying subregion, encompassing 217 Kb, containing for only three protein-coding genes, Zbp1, Pck1, and Pmepa1, encoding respectively, Z-DNA binding protein 1, phosphoenolpyruvate carboxykinase 1, and prostate transmembrane protein androgen induced 1.
Methods:
The effect of macrophage-specific knockout of Pck1 (KO) was tested using the AAV2 transduced proprotein convertase subtilisin kexin type 9 (PCSK9) overexpression mouse model of hyperlipidemia and atherosclerosis.
Results:
Unexpectedly, macrophage Pck1 deficiency lowered body weight, liver weight, and HDL-cholesterol levels in both sexes, while total and non-HDL cholesterol levels were only decreased in male mice. Aortic root lesion area and necrotic lesion area were unchanged in KO mice of both sexes.
Conclusion:
Pck1 was not confirmed as an atherosclerosis modifier gene.
