Poly (ADP-Ribose) Polymerase immunoreactivity in Motor Neurons and Astrocytes in the Spinal Cord of Sporadic Amyotrophic Lateral Sclerosis Patients.
- Author:
Seung Hyun KIM
1
;
Jenny S HENKEL
;
Ju Han KIM
;
Myung Ho KIM
;
Jozsef I ENGELHARDT
;
Laszlo SIKLOS
;
Gu KONG
;
Stanley H APPEL
Author Information
1. Department of Neurology, Pathology, College of Medicine, Hanyang University, Seoul, Korea. kimsh1@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
ALS;
PARP;
Motor neuron;
Astrocyte;
Western analysis;
RT-PCR
- MeSH:
Amyotrophic Lateral Sclerosis*;
Astrocytes*;
Autopsy;
Chromatin;
DNA Damage;
Humans;
Membranes;
Motor Neurons*;
Oxidative Stress;
RNA, Messenger;
Spinal Cord*
- From:Journal of the Korean Neurological Association
2002;20(6):668-681
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The evidence for increased oxidative stress and DNA damage in amyotrophic lateral sclerosis (ALS) prompted studies to determine if the expression of poly (ADP-ribose) polymerase (PARP) is increased in ALS. METHOD: Twenty Spinal cord specimens were obtained at the autopsy of sALS patients (n=11) and age-matched controls with non-neurological diseases (n=9). RESULTS: Using western analyses of postmortem tissue, we demonstrated that PARP-immunoreactivity (PARP-IR) was increased three-fold in spinal cord tissues of sporadic ALS (sALS) patients compared with non-neurological disease controls. Despite the increased PARP-IR, PARP mRNA expression was not increased significantly. Immunohistochemical analyses revealed PARP-IR was increased in both white and gray matter of sALS spinal cord. While PARP-IR was predominantly seen in astrocytes, large motor neurons displayed reduced staining compared with the controls. PARP-IR was increased in the pellet fraction of sALS homogenates compared with the control homogenates, representing potential PARP binding to chromatin or membranes and suggesting a possible mechanism of PARP stabilization. CONCLUSIONS: The present results demonstrate glial alterations in sALS tissue and support the role of glial alterations in sALS pathogenesis.
