Proteomic assessment of C57BL/6 hippocampi after non-selective pharmacological inhibition of all nitric oxide synthase activity

Nitric oxide is the smallest gaseous signaling molecule responsible for maintaining homeostasis in a myriad of tissues and molecular pathways in neurological and cardiovascular pathologies. In recent years, there has been increasing interest in the potential interaction between arterial stiffness (AS), an independent cardiovascular risk factor, and neurodegenerative syndromes given increasingly epidemiological study reports. For this reason, we previously sought to investigate the mechanistic convergence between AS and neurodegeneration via the progressive non-selective inhibition of all nitric oxide synthase (NOS) isoforms with N(G)-nitro-L-arginine methyl ester (L-NAME) in C57BL/6 mice. Our results showed progressively increased arterial stiffness in vivo and impaired visuospatial learning and memory in L-NAME treated C57BL/6 mice. In this study, we sought to further investigate the progressive molecular signatures in hippocampal tissue via LC-MS/MS proteomic analysis