Journal: Nitric oxide : biology and chemistry
Article Title: Downregulation of neuronal nitric oxide synthase (nNOS) within the paraventricular nucleus in Ins2 Akita -type-1 diabetic mice contributes to sympatho-excitation.
doi: 10.1016/j.niox.2024.11.001
Figure Lengend Snippet: Fig. 7. Proposed model for the up-regulation of the PIN by post-translational regulation in the PVN. Elevated central Ang II levels via AT1R in the PVN increase the expression of PIN via decreasing the ubiquitination. Increased expression of PIN destabilizes nNOS dimers, which renders nNOS catalytically inactive, either by interfering with the assembly or dimer stability. A reduced level of functional nNOS reduces NO production in the PVN, causing an increase in sympatho-excitation and associated blood pressure.
Article Snippet: The following primary antibodies were used: nNOS (sc-5302, 1:500), ACE (sc-23908, 1:250), ACE2 (sc-20998, 1:250), Ang II type 1 receptor (AT1R) (sc-515884, 1:250), Mas receptor (sc-390453, 1:250), protein inhibitor of nNOS (PIN) (sc-13969, 1:500), and β-actin (sc-47778, 1:1000) (Santa Cruz Biotechnology, Santa Cruz, CA).
Techniques: Expressing, Ubiquitin Proteomics, Functional Assay