TGF-β2 And Golgi Apparatus Alteration In Ischemic Gerbils And Subcellular Compartmentalization Of TGF-β2 In Golgi Apparatus

OBJECTIVETGF-β2,a prominent TGF-βisoform in neurons,has been show to be benificial active in ischemic stroke.Golgi apparatus(GA)is a pivotal organelle in which proteins are processed and prepared for secretion,but there are very few reports about the mophological alterations and effect of GA in the ischemic insult.The present study investigated TGF-β2 protein expression in hippocampal neuron cells,and evaluated the potential mechanisms of the neuroprotective activity of it in ischemic stroke in gerbils.And the experimental was also designed to observe whether the GA mophology is abnormal and whether TGF-β2 subcellular localization is in the neuron GA after transient forebrain ischemia.METHODSTGF-β2-immunoreactivity in the hippocampus neurons was studied in gerbils subjected to 10 min forebrain ischemia,due to experimentally induced bilateral carotid artery occlusion(BCAO).The studies were performed in different postischemic periods and sham-operation(6h,1,3 and 7 day after ischemia)with immunohistochemical methods to observe the expression of TGF-β2 and alteration of morphology in Golgi complex during ischemic injury.In addition,the subcellular localization of TGF-β2 is determined in trans-Golgi network by Confocal Immunofluorographs with TGN38.RESULTSIn the ischemic animals,results showed that TGF-β2 isoform persistent express and it peaks at 3 days,then decreased but not significantly in gerbils 7 days postocclusion.No significant alterations to the Golgi were noted at the point of 6h,1 and 3 day following TFI,but there are a few neurons in which the GA lost the normal network-like configuration and its elements decreased in cortical cells from gerbils survived 7 days postocclusion.In addition,TGF-β2 was colocalized with TGN38 in the trans-Golgi network.CONCLUSIONS1.TGF-β2 protein expression increased in neurons after ischemic, which may represent an endogenous adaptative response of the brain damage and exert neuroprotection against ischemic injury.2.Fragmentation of GA is not common phenomenon in the ischemic, but intact GA structual of neurons is beneficial for cell survival.3.TGF-β2 was determined its subcellular compartmentalization in trans-Golgi network,and its secretion via Golgi apparatus after ischmic is supposed to beneficial active for GA.