Transient cerebral ischemia leads to TGF-beta2 expression in Golgi apparatus organelles.
Transforming growth factor2 (TGFbeta2) is a prototypic member of a large superfamily of multifunctional cytokines, and its potential mechanisms of the neuroprotective activity in ischemic stroke and subcellular compartmentalization are largely unknown. The present study investigated TGF-beta2 protein expression in hippocampal neuronal cells after transient forebrain ischemia (TFI). TFI was induced in male adult gerbils with bilateral occlusion of both common carotid arteries for 10 minutes. With immunohistochemical methods we observe the expression of TGF-beta2 and morphological alternation in Golgi appratus (GA) in different postischemic periods and sham-operation (6 hours, 1, 3 and 7 days). In addition, the subcellular localization of TGF-beta2 is determined in trans-Golgi network (TGN) by double-labeling confocal immunofluorographs with TGN38.The results showed that TGF-beta2 persistent express in the ischemic animals and it peaks at 3 days, then decreased 7 days postocclusion. No significant alterations to the GA were noted at the point of 6 hours,1 and 3 days 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-beta2 was colocalized with TGN38 in the TGN after TFI .Taken together, this result suggested that TGF-beta2 protein expression increased in neurons after ischemia, which may represent an endogenous adaptative response of the brain damage and its secretion via GA after ischemia is supposed to be beneficial for GA . Furthermore, fragmentation of GA is not common phenomenon in the ischemia, but intact GA structural of neurons is beneficial for cell survival.
Hu
Zhiping
Z
Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.
Fan
Jie
J
Zeng
Liuwang
L
Lu
Wei
W
Tang
Xiangqi
X
Zhang
Jie
J
Li
Ting
T
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D005849:Gerbillinae; D006056:Golgi Apparatus / Q000378:metabolism* / Q000473:pathology; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D016548:Prosencephalon / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D053781:Transforming Growth Factor beta2 / Q000378:metabolism*; D015854:Up-Regulation / Q000502:physiology; D021601:trans-Golgi Network / Q000378:metabolism / Q000473:pathology
D008562:Membrane Glycoproteins; C513045:Tgoln2 protein, rat; D053781:Transforming Growth Factor beta2