| First Author | Fais RS | Year | 2019 |
| Journal | Sci Rep | Volume | 9 |
| Issue | 1 | Pages | 16224 |
| PubMed ID | 31700106 | Mgi Jnum | J:297956 |
| Mgi Id | MGI:6479448 | Doi | 10.1038/s41598-019-52831-0 |
| Citation | Fais RS, et al. (2019) The inflammasome NLRP3 plays a dual role on mouse corpora cavernosa relaxation. Sci Rep 9(1):16224 |
| abstractText | NLRP3 plays a role in vascular diseases. Corpora cavernosa (CC) is an extension of the vasculature. We hypothesize that NLRP3 plays a deleterious role in CC relaxation. Male C57BL/6 (WT) and NLRP3 deficient (NLRP3(-/-)) mice were used. Intracavernosal pressure (ICP/MAP) measurement was performed. Functional responses were obtained from CC strips of WT and NLRP3(-/-) mice before and after MCC950 (NLRP3 inhibitor) or LPS + ATP (NLRP3 stimulation). NLRP3, caspase-1, IL-1beta, eNOS, nNOS, guanylyl cyclase-beta1 (GCbeta1) and PKG1 protein expressions were determined. ICP/MAP and sodium nitroprusside (SNP)-induced relaxation in CC were decreased in NLRP3(-/-) mice. Caspase-1, IL-1beta and eNOS activity were increased, but PKG1 was reduced in CC of NLRP3(-/-). MCC950 decreased non-adrenergic non-cholinergic (NANC), acetylcholine (ACh), and SNP-induced relaxation in WT mice. MCC950 did not alter NLRP3, caspase-1 and IL-1beta, but reduced GCbeta1 expression. Although LPS + ATP decreased ACh- and SNP-, it increased NANC-induced relaxation in CC from WT, but not from NLRP3(-/-) mice. LPS + ATP increased NLRP3, caspase-1 and interleukin-1beta (IL-1beta). Conversely, it reduced eNOS activity and GCbeta1 expression. NLRP3 plays a dual role in CC relaxation, with its inhibition leading to impairment of nitric oxide-mediated relaxation, while its activation by LPS + ATP causes decreased CC sensitivity to NO and endothelium-dependent relaxation. |
