| First Author | Mishima K | Year | 2019 |
| Journal | PLoS One | Volume | 14 |
| Issue | 10 | Pages | e0223496 |
| PubMed ID | 31596895 | Mgi Jnum | J:280373 |
| Mgi Id | MGI:6364650 | Doi | 10.1371/journal.pone.0223496 |
| Citation | Mishima K, et al. (2019) Attenuation of renal fibrosis after unilateral ureteral obstruction in mice lacking the N-type calcium channel. PLoS One 14(10):e0223496 |
| abstractText | The N-type Ca2+ channel (Cav2.2) is distributed in sympathetic nerves that innervate the tubules, the vessels, and the juxtaglomerular granular cells of the kidney. However, the role of N-type Ca2+ channels in renal disease remains unknown. To address this issue, Cav2.2 knockout mice were utilized. Immunoreactive Cav2.2 was undetectable in normal kidneys of C57BL/6N mice, but it became positive in the interstitial S100-positive nerve fibers after unilateral ureteral obstruction (UUO). There were no significant differences in mean blood pressure, heart rate, and renal function between wild-type littermates and Cav2.2-knockout mice at baseline, as well as after UUO. Cav2.2 deficiency significantly reduced the EVG-positive fibrotic area, alpha-SMA expression, the production of type I collagen, and the hypoxic area in the obstructed kidneys. The expression of tyrosine hydroxylase, a marker for sympathetic neurons, was significantly increased in the obstructed kidneys of wild-type mice, but not in Cav2.2-knockout mice. These data suggest that increased Cav2.2 is implicated in renal nerve activation leading to the progression of renal fibrosis. Blockade of Cav2.2 might be a novel therapeutic approach for preventing renal fibrosis. |
