File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Distribution of carbon monoxide-producing neurons in human colon and in Hirschsprung's disease patients

TitleDistribution of carbon monoxide-producing neurons in human colon and in Hirschsprung's disease patients
Authors
KeywordsCarbon monoxide
Heme oxygenase
Hirschsprung's disease
Nitric oxide
Issue Date2002
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath
Citation
Human Pathology, 2002, v. 33 n. 10, p. 1030-1036 How to Cite?
AbstractHirschsprung's disease (HSCR) is characterized by the absence of ganglion cells and impaired relaxation of the gut. Nitric oxide (NO) and, more recently, carbon monoxide (CO) have been identified as inhibitory neurotransmitters causing relaxation. A deficiency in NO has been reported in aganglionic gut; we hypothesized that CO could also be involved in impaired gut motility in HSCR. The aim of the study was to determine the distribution of CO-and NO-producing enzymes in the normal and aganglionic gut. We performed laser capture microdissection, reverse transcription-polymerase chain reaction, and immunohistochemistry on colon biopsies of normal controls (n = 9) and patients with HSCR (n = 10). The mRNA expression of heme oxygenase-2 (HO-2), immunoreactivities of HO-2 and NO synthase, was determined and compared. Results show a high level of expression of HO-2 mRNA localized in the myenteric plexus. Expression of HO-2 mRNA was also detected in the mucosa, submucosa, and muscular layer. Down-regulation of HO-2 mRNA expression was detected in the aganglionic colon. Immunoreactivities of HO-2 and NO synthase were localized mainly to the ganglion plexus and to nerve fibers within the muscle in the control colons and normoganglionic colons. HO-2-containing neurons were more abundant than NO synthase-containing neurons in the myenteric plexus. Nearly all of the NO synthase-containing neurons also contained HO-2. HO-2 and NO synthase were selectively absent in the myenteric and submucosal regions and in the muscle of the aganglionic colon. Our findings suggest involvement of both CO and NO in the pathophysiology of HSCR. Copyright 2002, Elsevier Science (USA). All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/48679
ISSN
2015 Impact Factor: 2.791
2015 SCImago Journal Rankings: 1.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_HK
dc.contributor.authorLui, VCHen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2008-05-22T04:21:08Z-
dc.date.available2008-05-22T04:21:08Z-
dc.date.issued2002en_HK
dc.identifier.citationHuman Pathology, 2002, v. 33 n. 10, p. 1030-1036en_HK
dc.identifier.issn0046-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48679-
dc.description.abstractHirschsprung's disease (HSCR) is characterized by the absence of ganglion cells and impaired relaxation of the gut. Nitric oxide (NO) and, more recently, carbon monoxide (CO) have been identified as inhibitory neurotransmitters causing relaxation. A deficiency in NO has been reported in aganglionic gut; we hypothesized that CO could also be involved in impaired gut motility in HSCR. The aim of the study was to determine the distribution of CO-and NO-producing enzymes in the normal and aganglionic gut. We performed laser capture microdissection, reverse transcription-polymerase chain reaction, and immunohistochemistry on colon biopsies of normal controls (n = 9) and patients with HSCR (n = 10). The mRNA expression of heme oxygenase-2 (HO-2), immunoreactivities of HO-2 and NO synthase, was determined and compared. Results show a high level of expression of HO-2 mRNA localized in the myenteric plexus. Expression of HO-2 mRNA was also detected in the mucosa, submucosa, and muscular layer. Down-regulation of HO-2 mRNA expression was detected in the aganglionic colon. Immunoreactivities of HO-2 and NO synthase were localized mainly to the ganglion plexus and to nerve fibers within the muscle in the control colons and normoganglionic colons. HO-2-containing neurons were more abundant than NO synthase-containing neurons in the myenteric plexus. Nearly all of the NO synthase-containing neurons also contained HO-2. HO-2 and NO synthase were selectively absent in the myenteric and submucosal regions and in the muscle of the aganglionic colon. Our findings suggest involvement of both CO and NO in the pathophysiology of HSCR. Copyright 2002, Elsevier Science (USA). All rights reserved.en_HK
dc.format.extent1829368 bytes-
dc.format.extent89249 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpathen_HK
dc.relation.ispartofHuman Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCarbon monoxideen_HK
dc.subjectHeme oxygenaseen_HK
dc.subjectHirschsprung's diseaseen_HK
dc.subjectNitric oxideen_HK
dc.subject.meshNeurons - metabolism - *pathologyen_HK
dc.subject.meshCarbon Monoxide - metabolismen_HK
dc.subject.meshColon - cytology - innervationen_HK
dc.subject.meshHirschsprung Disease - pathologyen_HK
dc.titleDistribution of carbon monoxide-producing neurons in human colon and in Hirschsprung's disease patientsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0046-8177&volume=33&issue=10&spage=1030&epage=1036&date=2002&atitle=Distribution+of+carbon+monoxide-producing+neurons+in+human+colon+and+in+Hirschsprung%27s+disease+patientsen_HK
dc.identifier.emailChen, Y: ychenc@hkucc.hku.hken_HK
dc.identifier.emailLui, VCH: vchlui@hkucc.hku.hken_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp01318en_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1053/hupa.2002.128251en_HK
dc.identifier.pmid12395377-
dc.identifier.scopuseid_2-s2.0-0036802401en_HK
dc.identifier.hkuros75798-
dc.identifier.hkuros117336-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036802401&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1030en_HK
dc.identifier.epage1036en_HK
dc.identifier.isiWOS:000178903200012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, Y=36463185300en_HK
dc.identifier.scopusauthoridLui, VCH=7004231344en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats