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Moderate hypothermia induces marked increase in levels and nuclear accumulation of SUMO 2/3‐conjugated proteins in neurons
Author(s) -
Wang Liangli,
Ma Qing,
Yang Wei,
Mackensen G. Burkhard,
Paschen Wulf
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07916.x
Subject(s) - hypothermia , neuroprotection , western blot , endogeny , biology , neuron , pharmacology , chemistry , microbiology and biotechnology , medicine , biochemistry , neuroscience , gene
Deep hypothermia protects the brain from ischemic damage and is therefore used during major cardiovascular surgeries requiring cardiopulmonary bypass and a period of circulatory arrest. Here, we demonstrated that small ubiquitin‐like modifier ( SUMO 1‐3) conjugation is markedly activated in the brain during deep to moderate hypothermia. Animals were subjected to normothermic (37°C) or deep to moderate (18°C, 24°C, 30°C) hypothermic cardiopulmonary bypass, and the effects of hypothermia on SUMO conjugation were evaluated by Western blot and immunohistochemistry. Exposure to moderate 30°C hypothermia was sufficient to markedly increase levels and nuclear accumulation of SUMO 2/3‐conjugated proteins in these cells. Deep hypothermia induced nuclear translocation of the SUMO ‐conjugating enzyme Ubc9, suggesting that the increase in nuclear levels of SUMO 2/3‐conjugated proteins observed in brains of hypothermic animals is an active process. Exposure of primary neuronal cultures to deep hypothermia induced only a moderate rise in levels of SUMO 2/3‐conjugated proteins. This suggests that neurons in vivo have a higher capacity than neurons in vitro to activate this endogenous potentially neuroprotective pathway upon exposure to hypothermia. Identifying proteins that are SUMO 2/3 conjugated during hypothermia could help to design new strategies for preventive and therapeutic interventions to make neurons more resistant to a transient interruption of blood supply.