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Mutant SOD1G93A in bone marrow-derived cells exacerbates 3-nitropropionic acid induced striatal damage in mice.
Neurosci Lett. 2007 May 17; 418(2):175-80.NL

Abstract

3-Nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, produces selective lesions in striatal neurons that resemble those observed in Huntington's disease neuropathology. In this study, we evaluated the role of peripheral bone marrow-derived cells (BMDCs) in the 3-NP-induced striatal damage by transplanting bone marrow cells with human SOD1 G93A mutation (mSOD1(G93A)) which induces amyotrophic lateral sclerosis through an unknown gain of toxicity and mitochondrial dysfunction. We assessed striatal damage after 3-NP treatment in the recipient C57BL/6 wild-type (WT) mice that received bone marrow cells from WT or mSOD1(G93A) transgenic donor mice (WT-->WT or mSOD(G93A)-->WT). After intraperitoneal injection of 3-NP, six of the eight mSOD1(G93A)-->WT mice had bilateral striatal lesions while only one out of eight WT-->WT mice had a striatal lesion. The lesion volume was significantly higher in the mSOD1(G93A)-->WT mice than in the WT-->WT mice. However, following an intrastriatal injection of 3-NP, there was no significant difference in the lesion volumes between the WT-->WT mice and mSOD1(G93A)-->WT mice. Thus, the exacerbation of 3-NP-induced striatal damage in mSOD(G93A)-->WT mice was only seen after systemic administration of 3-NP, but not after intrastriatal injection. These results demonstrate that altered SOD1 activity (mSOD(G93A)) in BMDCs affects striatal damage probably through a mechanism involving a systemic factor.

Authors+Show Affiliations

Department of Neurology, Boston University School of Medicine, 715 Albany Street, E301 Boston, MA, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17418947

Citation

Huang, Qing-Yuan, et al. "Mutant SOD1G93A in Bone Marrow-derived Cells Exacerbates 3-nitropropionic Acid Induced Striatal Damage in Mice." Neuroscience Letters, vol. 418, no. 2, 2007, pp. 175-80.
Huang QY, Yu L, Ferrante RJ, et al. Mutant SOD1G93A in bone marrow-derived cells exacerbates 3-nitropropionic acid induced striatal damage in mice. Neurosci Lett. 2007;418(2):175-80.
Huang, Q. Y., Yu, L., Ferrante, R. J., & Chen, J. F. (2007). Mutant SOD1G93A in bone marrow-derived cells exacerbates 3-nitropropionic acid induced striatal damage in mice. Neuroscience Letters, 418(2), 175-80.
Huang QY, et al. Mutant SOD1G93A in Bone Marrow-derived Cells Exacerbates 3-nitropropionic Acid Induced Striatal Damage in Mice. Neurosci Lett. 2007 May 17;418(2):175-80. PubMed PMID: 17418947.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mutant SOD1G93A in bone marrow-derived cells exacerbates 3-nitropropionic acid induced striatal damage in mice. AU - Huang,Qing-Yuan, AU - Yu,Liqun, AU - Ferrante,Robert J, AU - Chen,Jiang-Fan, Y1 - 2007/03/21/ PY - 2007/01/08/received PY - 2007/02/28/revised PY - 2007/03/10/accepted PY - 2007/4/10/pubmed PY - 2007/7/26/medline PY - 2007/4/10/entrez SP - 175 EP - 80 JF - Neuroscience letters JO - Neurosci Lett VL - 418 IS - 2 N2 - 3-Nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, produces selective lesions in striatal neurons that resemble those observed in Huntington's disease neuropathology. In this study, we evaluated the role of peripheral bone marrow-derived cells (BMDCs) in the 3-NP-induced striatal damage by transplanting bone marrow cells with human SOD1 G93A mutation (mSOD1(G93A)) which induces amyotrophic lateral sclerosis through an unknown gain of toxicity and mitochondrial dysfunction. We assessed striatal damage after 3-NP treatment in the recipient C57BL/6 wild-type (WT) mice that received bone marrow cells from WT or mSOD1(G93A) transgenic donor mice (WT-->WT or mSOD(G93A)-->WT). After intraperitoneal injection of 3-NP, six of the eight mSOD1(G93A)-->WT mice had bilateral striatal lesions while only one out of eight WT-->WT mice had a striatal lesion. The lesion volume was significantly higher in the mSOD1(G93A)-->WT mice than in the WT-->WT mice. However, following an intrastriatal injection of 3-NP, there was no significant difference in the lesion volumes between the WT-->WT mice and mSOD1(G93A)-->WT mice. Thus, the exacerbation of 3-NP-induced striatal damage in mSOD(G93A)-->WT mice was only seen after systemic administration of 3-NP, but not after intrastriatal injection. These results demonstrate that altered SOD1 activity (mSOD(G93A)) in BMDCs affects striatal damage probably through a mechanism involving a systemic factor. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/17418947/Mutant_SOD1G93A_in_bone_marrow_derived_cells_exacerbates_3_nitropropionic_acid_induced_striatal_damage_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(07)00312-6 DB - PRIME DP - Unbound Medicine ER -