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Brain Mitochondrial Subproteome of Rpn10-Binding Proteins and Its Changes Induced by the Neurotoxin MPTP and the Neuroprotector Isatin.

Abstract Mitochondria play an important role in molecular mechanisms of neuroplasticity, adaptive changes of the brain that occur in the structure and function of its cells in response to altered physiological conditions or development of pathological disorders. Mitochondria are a crucial target for actions of neurotoxins, causing symptoms of Parkinson's disease in various experimental animal models, and also neuroprotectors. Good evidence exists in the literature that mitochondrial dysfunction induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) influences functioning of the ubiquitin-proteasomal system (UPS) responsible for selective proteolytic degradation of proteins from various intracellular compartments (including mitochondria), and neuroprotective effects of certain antiparkinsonian agents (monoamine oxidase inhibitors) may be associated with their effects on UPS. The 19S proteasomal Rpn10 subunit is considered as a ubiquitin receptor responsible for delivery of ubiquitinated proteins to the proteasome proteolytic machinery. In this study, we investigated proteomic profiles of mouse brain mitochondrial Rpn10-binding proteins, brain monoamine oxidase B (MAO B) activity, and their changes induced by a single-dose administration of the neurotoxin MPTP and the neuroprotector isatin. Administration of isatin to mice prevented MPTP-induced inactivation of MAO B and influenced the profile of brain mitochondrial Rpn10-binding proteins, in which two pools of proteins were clearly recognized. The constitutive pool was insensitive to neurotoxic/neuroprotective treatments, while the variable pool was specifically influenced by MPTP and the neuroprotector isatin. Taking into consideration that the neuroprotective dose of isatin used in this study can result in brain isatin concentrations that are proapoptotic for cells in vitro, the altered repertoire of mitochondrial Rpn10-binding proteins may thus represent a part of a switch mechanism from targeted elimination of individual (damaged) proteins to more efficient ("global") elimination of damaged organelles and whole damaged cells.
PMID
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Authors

Mayor MeshTerms

Isatin

Neuroprotective Agents

Neurotoxins

Keywords
Journal Title biochemistry. biokhimiia
Publication Year Start




PMID- 28320274
OWN - NLM
STAT- MEDLINE
DA  - 20170321
DCOM- 20170322
LR  - 20170322
IS  - 1608-3040 (Electronic)
IS  - 0006-2979 (Linking)
VI  - 82
IP  - 3
DP  - 2017 Mar
TI  - Brain Mitochondrial Subproteome of Rpn10-Binding Proteins and Its Changes Induced
      by the Neurotoxin MPTP and the Neuroprotector Isatin.
PG  - 330-339
LID - 10.1134/S0006297917030117 [doi]
AB  - Mitochondria play an important role in molecular mechanisms of neuroplasticity,
      adaptive changes of the brain that occur in the structure and function of its
      cells in response to altered physiological conditions or development of
      pathological disorders. Mitochondria are a crucial target for actions of
      neurotoxins, causing symptoms of Parkinson's disease in various experimental
      animal models, and also neuroprotectors. Good evidence exists in the literature
      that mitochondrial dysfunction induced by the neurotoxin
      1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) influences functioning of the
      ubiquitin-proteasomal system (UPS) responsible for selective proteolytic
      degradation of proteins from various intracellular compartments (including
      mitochondria), and neuroprotective effects of certain antiparkinsonian agents
      (monoamine oxidase inhibitors) may be associated with their effects on UPS. The
      19S proteasomal Rpn10 subunit is considered as a ubiquitin receptor responsible
      for delivery of ubiquitinated proteins to the proteasome proteolytic machinery.
      In this study, we investigated proteomic profiles of mouse brain mitochondrial
      Rpn10-binding proteins, brain monoamine oxidase B (MAO B) activity, and their
      changes induced by a single-dose administration of the neurotoxin MPTP and the
      neuroprotector isatin. Administration of isatin to mice prevented MPTP-induced
      inactivation of MAO B and influenced the profile of brain mitochondrial
      Rpn10-binding proteins, in which two pools of proteins were clearly recognized.
      The constitutive pool was insensitive to neurotoxic/neuroprotective treatments,
      while the variable pool was specifically influenced by MPTP and the
      neuroprotector isatin. Taking into consideration that the neuroprotective dose of
      isatin used in this study can result in brain isatin concentrations that are
      proapoptotic for cells in vitro, the altered repertoire of mitochondrial
      Rpn10-binding proteins may thus represent a part of a switch mechanism from
      targeted elimination of individual (damaged) proteins to more efficient
      ("global") elimination of damaged organelles and whole damaged cells.
FAU - Medvedev, A E
AU  - Medvedev AE
AD  - Institute of Biomedical Chemistry, Moscow, 119121, Russia. [email protected]
FAU - Buneeva, O A
AU  - Buneeva OA
FAU - Kopylov, A T
AU  - Kopylov AT
FAU - Tikhonova, O V
AU  - Tikhonova OV
FAU - Medvedeva, M V
AU  - Medvedeva MV
FAU - Nerobkova, L N
AU  - Nerobkova LN
FAU - Kapitsa, I G
AU  - Kapitsa IG
FAU - Zgoda, V G
AU  - Zgoda VG
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochemistry (Mosc)
JT  - Biochemistry. Biokhimiia
JID - 0376536
RN  - 0 (Carrier Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotoxins)
RN  - 0 (Psmd4 protein, mouse)
RN  - 82X95S7M06 (Isatin)
RN  - 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
RN  - EC 1.4.3.4 (Monoamine Oxidase)
SB  - IM
MH  - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/*pharmacokinetics
MH  - Animals
MH  - Brain/*metabolism/pathology
MH  - Carrier Proteins/*metabolism
MH  - *Isatin/pharmacokinetics/pharmacology
MH  - MPTP Poisoning/*metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mitochondria/*metabolism
MH  - Monoamine Oxidase/metabolism
MH  - Nerve Tissue Proteins/*metabolism
MH  - *Neuroprotective Agents/pharmacokinetics/pharmacology
MH  - *Neurotoxins/pharmacokinetics/toxicity
EDAT- 2017/03/23 06:00
MHDA- 2017/03/23 06:01
CRDT- 2017/03/22 06:00
AID - BCM82030470 [pii]
AID - 10.1134/S0006297917030117 [doi]
PST - ppublish
SO  - Biochemistry (Mosc). 2017 Mar;82(3):330-339. doi: 10.1134/S0006297917030117.

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