Weiqiao Zhang1, Zhijie Zhang2, Liping Wu2, Yongming Qiu3, Yingying Lin3. 1. Department of Neurosurgery, Yuyao People's Hospital of Zhejiang Province, Yuyao City, Zhejiang, China. Electronic address: zhang951154@sina.com. 2. Department of Neurosurgery, Yuyao People's Hospital of Zhejiang Province, Yuyao City, Zhejiang, China. 3. Department of Neurosurgery, Renji Hospital, School of Medicine, Shanghai Jiao-tong University, Shanghai, China.
Abstract
BACKGROUND: Ischemia stroke is a destructive cerebrovascular disease and a major cause of death and lifelong neurological disability. N-Acetyl-l-aspartyl-l-glutamate (NAAG) is a neurotransmitter in the mammalian brain and involves a variety of physiological and pathological functions including ischemia brain injury. Full understanding of the functions of NAAG peptidase (GCPII) in the pathogenesis of ischemia brain injury is extremely valuable for effective therapies to ischemia stroke. METHODS: The expressions of GCPII and NAAG agonist metabotropic glutamate receptor (mGluR3) and TGFb1 were examined by real-time polymerase chain reaction and western blot. Moreover, GCPII knockdown cells were constructed using lentivirus-mediated transfection. Function and molecular mechanisms of GCPII knockdown on apoptosis induced from hypoxic-ischemic-induced injury in neuronal cells were analyzed. RESULTS: In this study, we found that the expressions of GCPII and mGluR3 were upregulated in CoCl2-induced hypoxia environment in neuronal cells. Moreover, knockdown of GCPII in neuronal cells ameliorated apoptosis from hypoxic-ischemic-induced injury through suppressing expressions of caspase 3 and caspase 9. CONCLUSIONS: Our results highlighted the roles of GCPII in the ischemia brain injury, and might provide an important target in therapeutic implications.
BACKGROUND:Ischemia stroke is a destructive cerebrovascular disease and a major cause of death and lifelong neurological disability. N-Acetyl-l-aspartyl-l-glutamate (NAAG) is a neurotransmitter in the mammalian brain and involves a variety of physiological and pathological functions including ischemia brain injury. Full understanding of the functions of NAAG peptidase (GCPII) in the pathogenesis of ischemia brain injury is extremely valuable for effective therapies to ischemia stroke. METHODS: The expressions of GCPII and NAAG agonist metabotropic glutamate receptor (mGluR3) and TGFb1 were examined by real-time polymerase chain reaction and western blot. Moreover, GCPII knockdown cells were constructed using lentivirus-mediated transfection. Function and molecular mechanisms of GCPII knockdown on apoptosis induced from hypoxic-ischemic-induced injury in neuronal cells were analyzed. RESULTS: In this study, we found that the expressions of GCPII and mGluR3 were upregulated in CoCl2-induced hypoxia environment in neuronal cells. Moreover, knockdown of GCPII in neuronal cells ameliorated apoptosis from hypoxic-ischemic-induced injury through suppressing expressions of caspase 3 and caspase 9. CONCLUSIONS: Our results highlighted the roles of GCPII in the ischemia brain injury, and might provide an important target in therapeutic implications.
Authors: Shengtao Yang; Dibyadeep Datta; Alvaro Duque; Yury M Morozov; Jon Arellano; Barbara S Slusher; Min Wang; Amy F T Arnsten Journal: Mol Psychiatry Date: 2022-06-22 Impact factor: 13.437
Authors: Dibyadeep Datta; Shannon N Leslie; Elizabeth Woo; Nishita Amancharla; Ayah Elmansy; Miguel Lepe; Adam P Mecca; Barbara S Slusher; Angus C Nairn; Amy F T Arnsten Journal: Front Aging Neurosci Date: 2021-11-15 Impact factor: 5.750