Irreversible Inflammation is Associated with Decreased Levels of the α1-, β1-, and α2-Subunits of sGC in Human Odontoblasts

The nitric oxide (NO) receptor enzyme soluble guanylate cyclase (sGC) contains one prosthetic heme group as an alpha beta heterodimer, and two heterodimer isoforms (alpha(1)beta(1), alpha(2)beta(1)) were characterized to have enzyme activity. To test the irreversible inflammation-dependent regulation of sGC in odontoblasts, we incubated decalcified frozen sections of healthy and inflamed human third molars with antibodies against beta-actin, nitrotyrosine, inducible nitric oxide synthase (iNOS), alpha(1)-, beta(1)-, and alpha(2)-subunits of sGC and analyzed them at protein levels by quantitative immunohistochemistry. The irreversible inflammation induced an increase in the signal intensities for nitrotyrosine and iNOS and a decrease for the alpha(1)-, beta(1)-, and alpha(2)-subunits of sGC in odontoblasts. Inflammatory mediators, reactive oxygen, and nitrogen species may impair the expression of the alpha(1)-, beta(1)-, and alpha(2)-subunits in odontoblasts. The decrease of sGC at the protein level in inflamed odontoblasts is compatible with a critical role for sGC to mediate biological effects of NO in health.