Published online May 14, 2015. doi: 10.3748/wjg.v21.i18.5635
Peer-review started: October 9, 2014
First decision: November 14, 2014
Revised: November 28, 2014
Accepted: December 19, 2014
Article in press: December 22, 2014
Published online: May 14, 2015
Processing time: 221 Days and 16.8 Hours
AIM: To determine if hyperpolarisation-activated nucleotide-gated (HCN) channels exist in human colon, and to investigate the expression of HCN channels in Hirschsprung’s disease.
METHODS: We investigated HCN1, HCN2, HCN3 and HCN4 protein expression in pull-through specimens from patients with Hirschsprung’s disease (HSCR, n = 10) using the proximal-most ganglionic segment and distal-most aganglionic segment, as well as in healthy control specimens obtained at the time of sigmoid colostomy closure in children who had undergone anorectoplasty for imperforate anus (n = 10). Fluorescent immunohistochemistry was performed to assess protein distribution, which was then visualized using confocal microscopy.
RESULTS: No HCN1 channel expression was observed in any of the tissues studied. Both HCN2 and HCN4 proteins were found to be equally expressed in the aganglionic and ganglionic bowel in HSCR and controls. HCN3 channel expression was found to be markedly decreased in the aganglionic colon vs ganglionic colon and controls. HCN2-4 channels were seen to be expressed within neurons of the myenteric and submucosal plexus of the ganglionic bowel and normal controls, and also co-localised to interstitial cells of Cajal in all tissues studied.
CONCLUSION: We demonstrate HCN channel expression in human colon for the first time. Reduced HCN3 expression in aganglionic bowel suggests its potential role in HSCR pathophysiology.
Core tip: Children with Hirschsprung’s disease experience symptoms of intestinal obstruction due to a spastically contracted aganglionic segment of distal bowel, however the mechanism for this spasticity is incompletely understood. Hyperpolarisation-activated nucleotide-gated channels play a key role in regulating cell excitability in both pacemaker and non-pacing cells. We examined expression of hyperpolarisation-activated nucleotide-gated (HCN) 1-4 in both Hirschsprung’s disease (HSCR) colon and healthy controls. While HCN-1 expression was absent, and HCN-2 and HCN-4 were expressed at similar levels in diseased and healthy bowel, we found HCN-3 to be reduced in aganglionic bowel in HSCR. We suggest deficient HCN3 channels may be involved in the pathophysiology of HSCR.