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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Dynein c1h1, dynactin and syntaphilin expression in brain areas related to neurodegenerative diseases following exposure to rotenone

Author(s):
Chaves, Rodrigo S. [1] ; Melo, Thaiany Q. [1] ; D'Unhao, Aline M. [1] ; Farizatto, Karen L. G. [1] ; Ferrari, Merari F. R. [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Inst Biosci, Dept Genet & Evolutionary Biol, Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: ACTA NEUROBIOLOGIAE EXPERIMENTALIS; v. 73, n. 4, p. 541-556, 2013.
Web of Science Citations: 5
Abstract

Neurodegeneration is often accompanied by protein inclusions which may interfere with cell physiology. On the other hand, alteration in intracellular trafficking may precede impairment of neurotransmission and therefore trigger cell death. In view of this, it is hypothesized that changes in mitochondrial traffic may occur before neurodegeneration triggered by rotenone exposure and could favor this process. The effects of low concentrations of rotenone on the expression of dynein c1h1, dynactin and syntaphilin, which are proteins related to mitochondria transport and anchoring, were evaluated in cell cultures of substantia nigra, locus coeruleus and hippocampus as well as in these same brain areas in Lewis aged rats. The results indicate that low concentrations of rotenone decrease dynein c1h1 protein levels in cell cultures and brain areas of aged rats. Dynactin is decreased after exposure to 0.1 and 0.3 nM of rotenone, and increased after exposure to 0.5 nM of rotenone in cell cultures. Aged rats present increased dynactin expression. Syntaphilin expression decreased in vitro and increased in vivo after rotenone exposure. These findings suggest that changes in protein expression related to mitochondria. 1 retrograde transport and anchoring occur before neurodegeneration induced by rotenone exposure, which may be a primary factor to trigger neurodegenerative mechanisms. (AU)

FAPESP's process: 09/12200-9 - Analysis of RAB protein expression before protein aggregation associated to neurodegeneration
Grantee:Thaiany Quevedo Melo
Support type: Scholarships in Brazil - Master
FAPESP's process: 08/04480-9 - Analysis of intracellular trafficking of mitochondria before protein aggregation formation in neurodegeneration
Grantee:Merari de Fátima Ramires Ferrari
Support type: Regular Research Grants
FAPESP's process: 11/06434-7 - Degradation of hyperphosphorylated tau and organelles trafficking during neurodegenerative processes linked to protein aggregation in hypoccampal cell cultures
Grantee:Merari de Fátima Ramires Ferrari
Support type: Regular Research Grants
FAPESP's process: 11/00478-2 - Influence of calcium and MIRO proteins on mitochondrial mobility before and during protein aggregation involved in neurodegeneration
Grantee:Rodrigo dos Santos Chaves
Support type: Scholarships in Brazil - Doctorate (Direct)