Galectin-3 is dispensable for thoracic aortic aneurysmal formation and rupture in mice

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Thoracic aortic aneurysm (TAA) development involves disruption of extracellular matrix structural proteins such as collagen and elastin. An increased level of Galectin-3 (Gal-3), a β-galactoside-binding lectin, was reported in ascending aortic aneurysmal patients. To examine the role of Gal-3 on TAA formation in mice, two models were used: administration of lysyl oxidase inhibitor, β-aminopropionitrile (BAPN 0.5%, 0.3%, and 0.1% wt/vol) to 3- to 4 -week-old male and female Gal-3 wild-type (WT) or deficient knockout (KO) mice for 4 weeks in drinking water; and 8- to 10-week-old Gal-3 WT or KO mice were infused with either saline or angiotensin II (AngII) via osmotic mini-pumps for 28 days. High or low doses of BAPN administration promoted TAA rupture-induced death equivalently in both WT and KO male (WT = 64%; KO = 73%) and female (WT = 41%; KO = 54%) mice compared with controls. Similarly, AngII infusion caused a significantly increased, but equivalent, dilation of thoracic aortas in both male and female Gal-3 and Gal-3 KO mice compared with controls. Histological analysis revealed increased elastin fragmentation and collagen accumulation in both BAPN- and AngII-infused male and female WT and KO mice compared with controls. These findings suggest that Gal-3 deficiency did not influence either BAPN- or AngII-induced TAA formation or rupture in mice.

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