Neuraminidase-1 promotes heart failure after ischemia/reperfusion injury by affecting cardiomyocytes and invading monocytes/macrophages.

ABSTRACT: Neuraminidase (NEU)1 forms a multienzyme complex with beta-galactosidase (β-GAL) and protective-protein/cathepsin (PPC) A, which cleaves sialic-acids from cell surface glycoconjugates. We investigated the role of NEU1 in the myocardium after ischemia/reperfusion (I/R). Three days after inducing I/R, left ventricles (LV) of male mice (3 months-old) displayed upregulated neuraminidase activity and increased NEU1, β-GAL and PPCA expression. Mice hypomorphic for neu1 (hNEU1) had less neuraminidase activity, fewer pro-inflammatory (Lin^-CD11b⁺F4/80⁺Ly-6C^high), and more anti-inflammatory macrophages (Lin^-CD11b⁺F4/80⁺Ly-6C^low) 3 days after I/R, and less LV dysfunction 14 days after I/R. WT mice transplanted wit

SUBMITTER: Heimerl M 

PROVIDER: S-EPMC7519006 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature