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Updated: May 29, 2025

Measurement of Pulse Propagation Velocity, Distensibility and Strain in an Abdominal Aortic Aneurysm Mouse Model
Published on: February 23, 2020
Prenyl diphosphate synthase subunit 2 is downregulated in abdominal aortic aneurysm and retards the progression of
Jun Yong1, Shanshan Tang2, Lin Yu2
1Department of Vascular Surgery, Yantai Yuhuangding Hospital, Yantai, China.
Objective:
Abdominal aortic aneurysm (AAA) is a complex and fatal vascular disease for which specific treatments are still lacking. This study explored the effect and possible mechanisms of prenyl diphosphate synthase subunit 2 (PDSS2) on angiotensin II (Ang II)-induced AAA in human vascular smooth muscle cells (VSMCs).
Material And Methods:
The AAA cell model was established by treating VSMCs with 1 μM Ang II for 24 h. The effect of Ang II on VSMC viability was detected by cell counting kit-8 assay. The role of PDSS2 on VSMC proliferation was examined using the 5-ethynyl-2'-deoxyuridine method. The influence of Ang II and PDSS2 on VSMC apoptosis was analyzed by flow cytometry. The expression changes of PDSS2, apoptosis-related proteins, and phosphatidylinositol 3 kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway-related proteins were detected by Western blot analysis.
Results:
After treatment with Ang II, the VSMCs showed decreased viability and increased apoptosis (P < 0.01). PDSS2 expression was low in the AAA tissues and Ang II-treated VSMCs (P < 0.01). PDSS2 promoted the proliferation and blocked the apoptosis of Ang II-treated VSMCs, and si-PDSS2 showed the opposite effect (P < 0.01). PDSS2 also decreased the levels of p-mTOR, p-AKT, and p-PI3K, which, in turn, were increased by si-PDSS2 (P < 0.01).
Conclusion:
PDSS2 was downregulated in AAA and retarded the progression of VSMCs partially through the PI3K/AKT/mTOR pathway. This work explored the molecular mechanism of PDSS2 in the prevention, diagnosis, and treatment of AAA.
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