Tags

Type your tag names separated by a space and hit enter

Role of neuronal and inducible nitric oxide synthases in the guinea pig ileum myenteric plexus during in vitro ischemia and reperfusion.
Neurogastroenterol Motil 2013; 25(2):e114-26NM

Abstract

BACKGROUND

Intestinal ischemia and reperfusion (I/R) injury leads to abnormalities in motility, namely delay of transit, caused by damage to myenteric neurons. Alterations of the nitrergic transmission may occur in these conditions. This study investigated whether an in vitro I/R injury may affect nitric oxide (NO) production from the myenteric plexus of the guinea pig ileum and which NO synthase (NOS) isoform is involved.

METHODS

The distribution of the neuronal (n) and inducible (i) NOS was determined by immunohistochemistry during 60 min of glucose/oxygen deprivation (in vitro ischemia) followed by 60 min of reperfusion. The protein and mRNA levels of nNOS and iNOS were investigated by Western-immunoblotting and real time RT-PCR, respectively. NO levels were quantified as nitrite/nitrate.

KEY RESULTS

After in vitro I/R the proportion of nNOS-expressing neurons and protein levels remained unchanged. nNOS mRNA levels increased 60 min after inducing ischemia and in the following 5 min of reperfusion. iNOS-immunoreactive neurons, protein and mRNA levels were up-regulated during the whole I/R period. A significant increase of nitrite/nitrate levels was observed in the first 5 min after inducing I/R and was significantly reduced by N(ω) -propyl-l-arginine and 1400 W, selective inhibitors of nNOS and iNOS, respectively.

CONCLUSIONS & INFERENCES

Our data demonstrate that both iNOS and nNOS represent sources for NO overproduction in ileal myenteric plexus during I/R, although iNOS undergoes more consistent changes suggesting a more relevant role for this isoform in the alterations occurring in myenteric neurons following I/R.

Authors+Show Affiliations

Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy. cristina.giaroni@uninsubria.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23279126

Citation

Giaroni, C, et al. "Role of Neuronal and Inducible Nitric Oxide Synthases in the Guinea Pig Ileum Myenteric Plexus During in Vitro Ischemia and Reperfusion." Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, vol. 25, no. 2, 2013, pp. e114-26.
Giaroni C, Marchet S, Carpanese E, et al. Role of neuronal and inducible nitric oxide synthases in the guinea pig ileum myenteric plexus during in vitro ischemia and reperfusion. Neurogastroenterol Motil. 2013;25(2):e114-26.
Giaroni, C., Marchet, S., Carpanese, E., Prandoni, V., Oldrini, R., Bartolini, B., ... Frigo, G. (2013). Role of neuronal and inducible nitric oxide synthases in the guinea pig ileum myenteric plexus during in vitro ischemia and reperfusion. Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, 25(2), pp. e114-26. doi:10.1111/nmo.12061.
Giaroni C, et al. Role of Neuronal and Inducible Nitric Oxide Synthases in the Guinea Pig Ileum Myenteric Plexus During in Vitro Ischemia and Reperfusion. Neurogastroenterol Motil. 2013;25(2):e114-26. PubMed PMID: 23279126.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of neuronal and inducible nitric oxide synthases in the guinea pig ileum myenteric plexus during in vitro ischemia and reperfusion. AU - Giaroni,C, AU - Marchet,S, AU - Carpanese,E, AU - Prandoni,V, AU - Oldrini,R, AU - Bartolini,B, AU - Moro,E, AU - Vigetti,D, AU - Crema,F, AU - Lecchini,S, AU - Frigo,G, Y1 - 2013/01/02/ PY - 2013/1/3/entrez PY - 2013/1/3/pubmed PY - 2013/9/11/medline SP - e114 EP - 26 JF - Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society JO - Neurogastroenterol. Motil. VL - 25 IS - 2 N2 - BACKGROUND: Intestinal ischemia and reperfusion (I/R) injury leads to abnormalities in motility, namely delay of transit, caused by damage to myenteric neurons. Alterations of the nitrergic transmission may occur in these conditions. This study investigated whether an in vitro I/R injury may affect nitric oxide (NO) production from the myenteric plexus of the guinea pig ileum and which NO synthase (NOS) isoform is involved. METHODS: The distribution of the neuronal (n) and inducible (i) NOS was determined by immunohistochemistry during 60 min of glucose/oxygen deprivation (in vitro ischemia) followed by 60 min of reperfusion. The protein and mRNA levels of nNOS and iNOS were investigated by Western-immunoblotting and real time RT-PCR, respectively. NO levels were quantified as nitrite/nitrate. KEY RESULTS: After in vitro I/R the proportion of nNOS-expressing neurons and protein levels remained unchanged. nNOS mRNA levels increased 60 min after inducing ischemia and in the following 5 min of reperfusion. iNOS-immunoreactive neurons, protein and mRNA levels were up-regulated during the whole I/R period. A significant increase of nitrite/nitrate levels was observed in the first 5 min after inducing I/R and was significantly reduced by N(ω) -propyl-l-arginine and 1400 W, selective inhibitors of nNOS and iNOS, respectively. CONCLUSIONS & INFERENCES: Our data demonstrate that both iNOS and nNOS represent sources for NO overproduction in ileal myenteric plexus during I/R, although iNOS undergoes more consistent changes suggesting a more relevant role for this isoform in the alterations occurring in myenteric neurons following I/R. SN - 1365-2982 UR - https://www.unboundmedicine.com/medline/citation/23279126/Role_of_neuronal_and_inducible_nitric_oxide_synthases_in_the_guinea_pig_ileum_myenteric_plexus_during_in_vitro_ischemia_and_reperfusion_ L2 - https://doi.org/10.1111/nmo.12061 DB - PRIME DP - Unbound Medicine ER -