title: Neuronic autophagy contributes to p-connexin 43 degradation in hippocampal astrocytes following traumatic brain injury in rats.
abstract: Connexins, gap junction proteins, have short half‑lives of only a few hours; therefore, degradation of these proteins can rapidly modulate their function. Autophagy is a type of degradation pathway that has been implicated in several diseases and was reported to be induced following traumatic brain injury (TBI). The aim of the present study was to investigate the involvement of neuronic autophagy in proteolysis of phosphorylated connexin 43 (p‑Cx43) in hippocampal astrocytes following TBI in rats. Western blot analysis and immunofluorescence showed a TBI‑induced increase in levels of astrocytic p‑Cx43 following treatment with 3‑methyladenine, an inhibitor of autophagy, in the hippocampus. Internalized gap junctions were observed in the neuronic cytoplasm using transmission electron microscopy. These results demonstrated that neuronic autophagy may regulate cellular levels of p‑Cx43 in hippocampal astrocytes following TBI. This therefore indicated that the persistence of p‑Cx43 accumulation was due to insufficient degradation capacity of constitutive autophagy.
authors.affiliation: Department of Interventional Neuroradiology, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Li Qian
authors.initials: LQ
authors.lastname: Sun
authors.affiliation: Department of Histology and Embryology, School of Basic Medical Science, Hebei United University, Tangshan, Hebei 063000, P.R. China.
authors.forename: Jun Ling
authors.initials: JL
authors.lastname: Gao
authors.affiliation: Department of Histology and Embryology, School of Basic Medical Science, Hebei United University, Tangshan, Hebei 063000, P.R. China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Cui
authors.affiliation: Department of Histology and Embryology, School of Basic Medical Science, Hebei United University, Tangshan, Hebei 063000, P.R. China.
authors.forename: Man Man
authors.initials: MM
authors.lastname: Zhao
authors.affiliation: Department of Ophthalmology, Tangshan Ophthalmology Hospital, Tangshan, Hebei 063000, P.R. China.
authors.forename: Xiao Bin
authors.initials: XB
authors.lastname: Jing
authors.affiliation: Department of Histology and Embryology, School of Basic Medical Science, Hebei United University, Tangshan, Hebei 063000, P.R. China.
authors.forename: Ran
authors.initials: R
authors.lastname: Li
authors.affiliation: Department of Histology and Embryology, School of Basic Medical Science, Hebei United University, Tangshan, Hebei 063000, P.R. China.
authors.forename: Yan Xia
authors.initials: YX
authors.lastname: Tian
authors.affiliation: Department of Neurosurgery, Tangshan Gongren Hospital, Tangshan, Hebei 063000, P.R. China.
authors.forename: Jian Zhong
authors.initials: JZ
authors.lastname: Cui
authors.affiliation: Department of Interventional Neuroradiology, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Zhong-Xue
authors.initials: ZX
authors.lastname: Wu
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D001343:Autophagy; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D018031:Connexin 43 / Q000378:metabolism*; D017629:Gap Junctions / Q000378:metabolism / Q000648:ultrastructure; D006624:Hippocampus / Q000378:metabolism*; D008247:Lysosomes / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D059748:Proteolysis; D051381:Rats
chemical_list: D018031:Connexin 43; D008869:Microtubule-Associated Proteins; C526109:Anxa3 protein, rat