HSP20 And Golgi Apparatus Alteration Following Transient Forebrain Ischemia And Subcellular Compartmentalization Of HSP20 In Golgi Apparatus

Objective: HSP20 is abundant in brain, playing a crucial role in neuronal cell survival.Golgi apparatus (GA) is a very important organelle that involves in the metabolism of numerous proteins. Little is known, however, about the alteration of HSP20 after ischemia and the relationship between HSP20 and GA. Therefore, our present study was designed to check HSP20 expressional alterations and investigated whether HSP20 is associated with GA in the brain after ischemia.Methods: Gerbils models of bilateral carotid artery occlusion (BCAO) were established by occluding both carotid arteries for 10 min. Histological alteration and HSP20, GA immunoreactivities were examined in the brain tissue after 10 minutes transient forebrain ischemia in gerbils. The expressions of HSP20 in brain tissue were detected by using Immunohistochemical technique and Western blot technique at the 6th hour, 1st day, 3rd and 7th day after IR. The expressions of TGN38 in brain tissue were also detected by using Western blot technique. Confocal Immunofluorographs of HSP20 and TGN38 were also taken in gerbils models postocclusion.Results: (1) Staning with HE: The tissues of normal group and sham-operated group was integrate, but that of I/R were changed with gliocyte hyperplasia and hypertrophia, interstitial edema, cellular edema, gliocyte and neuron edema, neuron necrosis.(2) Immunohistochemical Methods: low expression of HSP20 was measured in the normal group and sham-operated group. HSP20 was increased immediately after ischemic insult, reached a maximum at 3 days, then declined in the 7days postocclusion; immunofluorescence showed that HSP20 was colocalized with TGN38, a marker molecule for GA.(3) Gain from Western blot: low expression of HSP20 was measured in the normal group and sham-operated group. HSP20 was increased immediately after ischemic insult, reached a maximum at 3 days, then declined in the 7days postocclusion; (similar to Immunohistochemical); But the expressions of TGN38 in brain tissue were not changed specifically.Conclusions:(1) The expression of HSP20 was increased after brain I/R injury and may exert neuroprotective effects.(2) HSP20 was presented in the Golgi apparatus, suggesting that both continuous protein synthesis and transportation via the Golgi complex were required for HSP20 and HSP20 may be essential for physiological functions involving GA.(3) The expressions of TGN38 in brain tissue were not changed specifically after brain I/R injury in seven days .