calpain and Death--Sudden--Cardiac

This article reviews what our colleagues have found as to how ischemic injury or cell death develop in myocardium through Ca(2+)-dependent protease calpain and how compensatory responses evolve through activation of intracellular signaling molecules including PKC isoforms, MAP kinase family enzymes and PI3 kinase. We also addressed how restraint or other psychological stress evokes hypertension and cardiovascular responses in signaling molecules or genes. Unexpectedly, carbon monoxide protects heart and cardiogenic cells against ischemia-resperfusion injury. When I think back, the unresolved cases of autopsies provided ideas for experimental study, which then taught us how the other cases died.

Topics: Animals; Ankyrins; Calcium; Calpain; Carbon Monoxide; Carrier Proteins; Central Nervous System Stimulants; Connexin 43; Death, Sudden, Cardiac; Gap Junctions; Humans; Ischemic Preconditioning, Myocardial; Methamphetamine; Microfilament Proteins; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardial Ischemia; Myocardial Reperfusion Injury; Nitric Oxide; Phosphatidylinositol 3-Kinases; Protein Kinase C; Reactive Oxygen Species; Restraint, Physical; Stress, Psychological

Topics: Animals; Apoptosis; Calcium-Calmodulin-Dependent Protein Kinases; Calpain; Death, Sudden, Cardiac; Forensic Medicine; Humans; Myocardial Ischemia; Stress, Psychological

Topics: Apoptosis Inducing Factor; Calpain; Cardiomyopathies; Cell Death; Death, Sudden, Cardiac; Humans; Muscle Cells; Protein Transport

Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Calpains, a family of cysteine proteases have been implicated in cells death following TBI. Using immunohistochemistry calpain expression was analyzed in post mortem brain tissue obtained from patients who died after TBI, and findings were compared with the brain tissue from patients who died from sudden cardiac arrest. In the injured cortex an increase in calpain expression was observed in all resident brain cells: neurons, glial and endothelial cells in comparison to the control group (all p < 0.001). Calpain expression was analyzed in different post-traumatic intervals, from day 0 until 10 days post-injury, in order to establish a time course of expression in the brain cortex after TBI. Expression was detected in the cortex 5 hours after the accident, peaked at 72 hours, and substantially reduced by 10 days after TBI. Calpain expression in the cortex significantly changed during the time from TBI to death (p < 0.001), and the most prominent expression was detected in the cortex 3 days after TBI. Our results indicate that prolonged calpain expression in resident brain cells (neurons, glial and endothelial cells) plays an important role in neuronal degeneration following TBI.

Topics: Adult; Aged; Brain Injuries; Calpain; Cerebral Cortex; Death, Sudden, Cardiac; Female; Humans; Male; Middle Aged; Neuroglia; Neurons; Protein Subunits