Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Vascular insult accompanied by overexpressed heme oxygenase-1 as a pathophysiological mechanism in experimental neurolathyrism with hind-leg paraparesis.

Authors: Kawaguchi, K  Lambein, F  Kusama-Eguchi, K 
Citation: Kawaguchi K, etal., Biochem Biophys Res Commun. 2012 Nov 9;428(1):160-6. doi: 10.1016/j.bbrc.2012.10.032. Epub 2012 Oct 12.
Pubmed: (View Article at PubMed) PMID:23068093
DOI: Full-text: DOI:10.1016/j.bbrc.2012.10.032

Neurolathyrism (NL) is a motor neuron disease characterized by spastic paraparesis in the hind legs. beta-N-oxalyl-l-alpha,beta-diaminopropionic acid (l-beta-ODAP), a component amino acid of the grass pea (Lathyrus sativus L.), has been proposed as the cause of this disease. In our NL rat model, we previously reported that transient intra-parenchymal hemorrhage occurred in the lower spinal cord during the early treatment period. We show here a possible pathological role of the hemorrhage in motor neuron damage and paraparesis pathology. In the lumbo-sacral spinal cord, blood vessel integrity was lost with numerous TdT-mediated dUTP nick end-labeling-positive blood vessel-like structures occurring simultaneously with the hemorrhage. We observed a coincident >10-fold increase in heme oxygenase-1 (HO-1) only in the lower spinal cord. The early period of paraparesis in the lower leg was greatly suppressed by pretreatment with zinc protoporphyrin IX, a HO-1 inhibitor. In vitro, l-beta-ODAP was toxic to human umbilical vein endothelial cells compared to l-glutamate. The present data shed light on the role and the mechanism of vascular insult in causing dysfunction and moribund motor neurons in experimental NL.


Disease Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 10766441
Created: 2016-02-05
Species: All species
Last Modified: 2016-02-05
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.