C1QL1/CTRP14 Is Largely Dispensable for Atherosclerosis Formation in Apolipoprotein-E-Deficient Mice

Area of Science:

• Cardiovascular Biology
• Molecular Biology
• Genomics

Background:

• Complement C1ql-like 1 (C1QL1), also known as CTRP14, is a protein primarily synthesized in the brain and adipose tissues.
• The functional roles of C1QL1/CTRP14 outside of these tissues, particularly in cardiovascular disease, are largely unknown.
• Atherosclerosis is a complex inflammatory disease characterized by plaque buildup in arteries.

Purpose of the Study:

• To investigate the influence of C1QL1 on atherosclerosis development.
• To analyze the transcriptomic alterations in the aorta associated with C1QL1 expression.
• To determine if C1QL1 plays a role in modulating atherosclerotic plaque formation.

Main Methods:

• Apolipoprotein E (ApoE) knockout mice were fed a Western diet to induce atherosclerosis.
• Adenovirus-mediated overexpression of C1QL1 (Ad-C1QL1) or a control (Ad-GFP) was administered via tail vein injection.
• Atherosclerotic plaque area was quantified, and aortic tissue underwent RNA sequencing for transcriptomic analysis.

Main Results:

• Overexpression of C1QL1 in ApoE knockout mice did not significantly alter the area of atherosclerotic plaques compared to controls.
• RNA sequencing identified only 111 differentially expressed genes (DEGs) in aortic lesions, enriched in 26 signaling pathways.
• DEGs included genes related to metabolism and human diseases like type II diabetes, but not directly linked to atherosclerosis formation in this context.

Conclusions:

• C1QL1 appears to be largely dispensable for the development of atherosclerosis in ApoE-deficient mice.
• C1QL1 does not significantly improve or inhibit atherosclerotic plaque formation in the aorta under the studied conditions.
• The transcriptomic changes observed suggest potential indirect associations with metabolic pathways rather than direct involvement in aortic atherosclerosis.