Key result
In atherosclerosis-prone mice, the absence of AnxA1 aggravated neointima formation after wire injury due to increased macrophage accumulation and proliferation.
Why the study?
Does Annexin A1 protect against neointima formation after arterial wire injury in atherosclerosis-prone mice?
Does Annexin A1 protect against neointima formation after arterial wire injury in atherosclerosis-prone mice?
Annexin A1 plays a protective role in healing after arterial wire injury by limiting macrophage accumulation, highlighting it as a potential therapeutic target to prevent restenosis.
AnxA1 deficiency aggravates post-injury neointimal hyperplasia in hyperlipidemic mice; leaves open whether AnxA1 augmentation could reduce restenosis.
Objective— Restenosis as a consequence of arterial injury is aggravated by inflammatory pathways. Here, we investigate the role of the proresolving protein annexin A1 (AnxA1) in healing after wire injury. Approach and Results— Apoe −/− and Apoe −/− Anxa1 −/− mice were subjected to wire injury while fed a high-cholesterol diet. Subsequently, localization of AnxA1 and AnxA1 plasma levels were examined. AnxA1 was found to localize within endothelial cells and macrophages in the neointima. Levels of AnxA1 in the plasma and its lesional expression negatively correlated with neointima size, and in the absence of AnxA1, neointima formation was aggravated by the accumulation and proliferation of macrophages. In contrast, reendothelialization and smooth muscle cell infiltration were not affected in Apoe −/− Anxa1 −/− mice. Conclusions— AnxA1 is protective in healing after wire injury and could, therefore, be an attractive therapeutic compound to prevent from restenosis after vascular damage.
No takes yet. Share an insight, caveat, or question.
Jong et al. (2016) studied Restenosis after arterial injury. AnxA1 deficiency (Anxa1 -/-) vs. Apoe -/- mice (AnxA1 intact) was evaluated on Neointima formation and size. In atherosclerosis-prone mice, the absence of AnxA1 aggravated neointima formation after wire injury due to increased macrophage accumulation and proliferation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: