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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Apoptosis, Brain Ischemia, Cerebrovascular Circulation, Hypothermia, Induced, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Proto-Oncogene Proteins c-akt, Reperfusion Injury, Signal Transduction, Suppression, Genetic.
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Does genetic suppression of Akt1 activity aggravate cerebral ischemia/reperfusion injury after deep hypothermic low flow in transgenic mice? Context: We investigated the genetic role of the PI3K/Akt signaling pathway in Akt1 (+/-) mice after cerebral ischemia/reperfusion injury following post-surgery deep hypothermic low flow. 3-week-old Akt1 (+/-) and wild-type C57/B6 mice were randomly and equally divided into sham-surgery and surgery groups. Surgery group mice were subjected to gradual body temperature reduction and bilateral common carotid artery occlusion for 120 min at 18.5 ± 0.5 °C, followed by artery reopening and rewarming. Occlusion was not performed in sham-surgery group animals. Regional cerebral blood flow was determined by laser Doppler flowmetry. Using reverse transcriptase-PCR, apoptotic assays, immunohistology, and Western blot analyses, we determined the apoptotic level of cerebral cells and the expression of Akt signaling pathway components. Regional cerebral blood flow was decreased by ≥ 86% during bilateral common carotid artery occlusion. Akt1 (+/-) mice experienced showed mortality after 24 h of cerebral I/R, and displayed increased numbers of apoptotic cerebral cells and apoptotic protein expression levels. Western analysis revealed Akt1 hypoactivity, which led to less efficient apoptotic signaling pathway inhibition.
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Akt1 suppresses the mitochondrial apoptosis signaling pathway, and Akt1 haplo-insufficiency exacerbates cerebral ischemia/reperfusion after deep hypothermic low flow conditions in mice. Akt may be a potential molecular therapeutic target for brain protection during surgery in congenital heart disease patients. Final Decision: yes