Proteomic Analysis of Cerebral Cortex Extracts from Sus scrofa with Induced Hemorrhagic Stroke

Abstract

Cerebrovascular diseases, including stroke and micro stroke, are the main causes of death in contemporary society. Hemorrhagic stroke is the fast emerging defficiency in the brain function resulting from disturbance of blood supply to the brain caused by the rapture of blood vessels (Lopez et al. in Proteomics Clin Appl 6:190-200, 2012). The influence of a model hemorrhagic stroke on white pigs with the change in the protein profile of their cortical samples 24 h and 2 months after the stroke was examined using mass-spectrometric analysis. Different proteins (n = 30) were identified, and their content was elevated. These proteins are involved in the mechanisms of neuroprotection, including compensation of oxidative stress (TXN, SNCA, PRDX6, ENO1), prevention of unwanted protein aggregation and apoptosis (PTMA, SNCA, SNCB), release of neurotransmitters (GAPDH, PEBP1) and assembly of the cytoskeleton (ACTA2, PTMA, TUBA4A, TUBA1D), etc. Also, a group of seven Ras family proteins involved in the regulation of cell proliferation and differentiation was found in the samples taken 24 h following the stroke. The relative concentrations of most of the proteins in the samples taken 2 months after the stroke demonstrate intermediate values between the control sample and the sample taken in 24 h, indicating the extinction of change in the protein profile with time. During the first 24 h after the stroke, there is an increase in protein fractions participating in exocytosis, synaptic plasticity/signaling, and support of neurotransmitter transport. Such shift in the weight of protein functional clusters can be attributed to activation of compensatory mechanisms in the body focused on neuroprotection.

Dynamic protein changes in the perihaemorrhagic zone of Surgically Treated Intracerebral Haemorrhage Patients

“…Although there are no previous studies on the proteome of human brain following ICH, a study in a pig model of ICH showed differences in proteomic expression of whole tissue at 24 h and at 60 days compared to controls 38 . Another study in a rat model of acute ICH showed differential protein expression 39 , as did a tissue proteomic study of collagenase-induced ICH in rats at 2 days post-ICH 40 .…”

Pervasive Genomic Damage in Experimental Intracerebral Hemorrhage: Therapeutic Potential of a Mechanistic-Based Carbon Nanoparticle

“…ICH releases blood cells and their breakdown products into the brain parenchyma. This release subsequently damages neurons and neural tissues. − In addition to the initial injury and mass effects, processes associated with brain injury during ICH include red blood cell (RBC) lysis, which results in the release of free hemoglobin (Hb). , Free Hb is unstable and undergoes unchecked auto-oxidation to release hemin and globin chains. While the amino acids of globin chains are recycled for protein synthesis, the fate of hemin may be converted into biliverdin, which can act as an antioxidant, or into redox-active iron, which can be reused for Hb synthesis or as free hemin.…”

Proteomic Markers in the Muscles and Brain of Pigs Recovered from Hemorrhagic Stroke

“…Further autologous venous blood (from the ear vein of the same pig, 300 mkl) was injected into the damaged area ( Figure 1 a). This surgery allowed us to obtain a reproducible model of intracerebral hemorrhage with necessary precision, as was described in [ 9 ]. Sham surgery was performed without damaging the brain structures.…”