Dataset Information

Shotgun LC-MS analysis of aorta and liver tissues from WT and Gal-1 KO mice to study the role of Galectin-1 in vascular remodeling in atherosclerosis and abdominal aortic aneurysm

ABSTRACT: Pathological vascular remodeling is the underlying cause of main cardiovascular diseases (CVD) including atherosclerosis and abdominal aortic aneurysm (AAA). We analyzed the potential role of galectin-1 (Gal-1) in atherosclerosis and AAA. Atherosclerosis was induced in mice lacking Gal-1 (Lgals1-/-) and wild-type (WT) by pAAV/D377Y-mPCSK9 adenovirus injection (1011 vector genome copies) followed by western diet during 16 weeks. In a second model, atherosclerostic WT mice were treated with recombinant Gal-1 protein (rGal-1, 100 µg 3 days/week) or vehicle during 16 weeks. Moreover, the same therapeutic approach was performed in elastase-induced AAA in mice treated for 2 weeks. Finally, Gal-1 expression was assessed in human atherosclerotic plaques and AAA lesions. Gal-1 deletion led to higher atherosclerotic burden along the aorta and larger atherosclerotic plaques in the aortic root. This deleterious effect was associated to higher circulating and lesional lipid levels and lower alpha- smooth muscle actin (α-SMA) staining in the plaques. Proteomic analysis of aorta homogenates showed an upregulation of Fibronectin and VCAM-1 in Lgals1-/- mice as compared to WT aortic tissues. In vitro experiments in VSMCs from Lgals1-/- mice or transfected with Gal-1 siRNA showed increased Fibronectin, VCAM-1 and KLF4 mRNA expression along with a decrease in α-SMA mRNA expression. Treatment with rGal-1 decreased atherosclerotic plaques (size and burden) and elastase-induced aortic dilatation, associated to higher content of α-SMA staining, in both experimental models. Gal-1 protein and mRNA tissue levels were decreased in human atherosclerotic plaques and AAA as compared to control aortic tissues.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver, Abdominal Aorta

DISEASE(S): Atherosclerosis,Abdominal Aortic Aneurysm

SUBMITTER: Estefanía Núñez

LAB HEAD: Jesús Vázquez

PROVIDER: PXD024637 | Pride | 2022-04-04

REPOSITORIES: Pride

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Galectin-1 prevents pathological vascular remodeling in atherosclerosis and abdominal aortic aneurysm.

Roldán-Montero Raquel R Pérez-Sáez Juan M JM Cerro-Pardo Isabel I Oller Jorge J Martinez-Lopez Diego D Nuñez Estefania E Maller Sebastian M SM Gutierrez-Muñoz Carmen C Mendez-Barbero Nerea N Escola-Gil Joan C JC Michel Jean-Baptiste JB Mittelbrunn Maria M Vázquez Jesús J Blanco-Colio Luis M LM Rabinovich Gabriel A GA Martin-Ventura Jose L JL

Science advances 20220316 11

Pathological vascular remodeling is the underlying cause of atherosclerosis and abdominal aortic aneurysm (AAA). Here, we analyzed the role of galectin-1 (Gal-1), a β-galactoside-binding protein, as a therapeutic target for atherosclerosis and AAA. Mice lacking Gal-1 (<i>Lgals1<sup>-/-</sup></i>) developed severe atherosclerosis induced by pAAV/D377Y-mPCSK9 adenovirus and displayed higher lipid levels and lower expression of contractile markers of vascular smooth muscle cells (VSMCs) in plaques ...[more]

PMID: 35294231

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			Action	DRS
	TMT1_Aorta.raw	Raw
	TMT1_Aorta_PSMs.txt	Txt
	TMT1_Liver.raw	Raw
	TMT1_Liver_PSMs.txt	Txt
	TMT2_Aorta.raw	Raw