Mon 28 May, 2012 02:33 am
Changes in annexin A8 level of oxidative modification of the cell model of Parkinson's disease
Studies have shown that Parkinson's disease (PD) substantia nigra dopamine neurons in the protein carbonyl levels were significantly elevated. Therefore, most scholars interest has focused on oxidative stress damage that oxidative stress plays an important role in the PD substantia nigra dopaminergic neuronal death. So far we have not seen of annexin A8 (ANXA8) reported occurrence of oxidative modification. This experiment by 2,4 - dinitrophenylhydrazine (DNP) derivative steps containing carbonyl oxidation protein markers, and then using 2D gel electrophoresis, identified by mass spectrometry and Western blot method of combining the first time found that ANXA8 The oxidative modification. Expect to provide clues to the pathogenesis of PD research and treatment of drug R & D
This experimental model of proteasome inhibition in PD cells, first by the DNP derivative steps containing carbonyl oxidation of protein markers, and then the oxidative modification of proteins identified by a combination of 2D gel electrophoresis, identified by mass spectrometry and Western blot technology. The oxidative modification of annexin A8 results found for the first time in the PD model of proteasome inhibition, compared with the control group oxidation was significantly lower.
Proteins 99 were identified as of ANXA8. The Annexin a group of highly homologous calcium-dependent phospholipid-binding proteins so far have been found in mammals, 13 kinds of armexin. Chromaffin granules based on ANXA8 in vitro aggregation, and thus a separation of annexin calcium-binding proteins. Apart from the adrenal medulla, has been detected in many mammalian tissues ANXA8, including brain, liver, parotid, spleen, lung and skeletal muscle. At the cellular level of annexin A8 involved in membrane transport, exocytosis, calcium homeostasis and tumor suppressor variety of biological functions. Krapfenbauer and other reference neurotoxin kainic acid treatment in rat brain tissue proteomics method detected reduced the abundance of annexin A8 in apoptosis. Yu et al further found that in the conditions of apoptotic factor stimulation, annexin A8 down to prevent galectin -3 anti-apoptotic role.This suggests that in this experiment to reduce the oxidative modification of the level of annexin the A8 may be associated with apoptosis in the PD cell model; the other hand, the oxidative modification of the residue of annexin A8 further affect the exercise of their normal biological function. Calcium-dependent signal-transduction pathway dysfunction may be involved in the pathogenesis of PD interventions may prevent the process of apoptosis signal-transduction pathway critical step. Calcium-dependent phospholipid binding protein ANXA8 possible role in PD and other nervous system degeneration is worth further study, and may provide valuable clues for molecularly targeted drug therapy in PD research and development.