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3 results on '"Shao Zhicheng"'

1. Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia.

Author

Shao Z, Noh H, Bin Kim W, Ni P, Nguyen C, Cote SE, Noyes E, Zhao J, Parsons T, Park JM, Zheng K, Park JJ, Coyle JT, Weinberger DR, Straub RE, Berman KF, Apud J, Ongur D, Cohen BM, McPhie DL, Rapoport JL, Perlis RH, Lanz TA, Xi HS, Yin C, Huang W, Hirayama T, Fukuda E, Yagi T, Ghosh S, Eggan KC, Kim HY, Eisenberg LM, Moghadam AA, Stanton PK, Cho JH, and Chung S

Subjects
Animals, Cadherins genetics, Female, Humans, Induced Pluripotent Stem Cells, Interneurons pathology, Male, Mice, Mice, Knockout, Prefrontal Cortex pathology, Protocadherins, Schizophrenia pathology, Synapses genetics, Synapses metabolism, Cadherins metabolism, Interneurons metabolism, Prefrontal Cortex metabolism, Schizophrenia metabolism, Signal Transduction physiology
Abstract

We generated cortical interneurons (cINs) from induced pluripotent stem cells derived from 14 healthy controls and 14 subjects with schizophrenia. Both healthy control cINs and schizophrenia cINs were authentic, fired spontaneously, received functional excitatory inputs from host neurons, and induced GABA-mediated inhibition in host neurons in vivo. However, schizophrenia cINs had dysregulated expression of protocadherin genes, which lie within documented schizophrenia loci. Mice lacking protocadherin-α showed defective arborization and synaptic density of prefrontal cortex cINs and behavioral abnormalities. Schizophrenia cINs similarly showed defects in synaptic density and arborization that were reversed by inhibitors of protein kinase C, a downstream kinase in the protocadherin pathway. These findings reveal an intrinsic abnormality in schizophrenia cINs in the absence of any circuit-driven pathology. They also demonstrate the utility of homogenous and functional populations of a relevant neuronal subtype for probing pathogenesis mechanisms during development.

Published
2019
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2. Dysregulated protocadherin-pathway activity as an intrinsic defect in iPSC-derived cortical interneurons from patients with schizophrenia

Author

Shao, Zhicheng, Noh, Haneul, Kim, Woong Bin, Ni, Peiyan, Nguyen, Christine, Cote, Sarah E., Noyes, Elizabeth, Zhao, Joyce, Parsons, Teagan, Park, James M., Zheng, Kelvin, Park, Joshua J., Coyle, Joseph T., Weinberger, Daniel R., Straub, Richard E., Berman, Karen F., Apud, Jose, Ongur, Dost, Cohen, Bruce M., McPhie, Donna L., Rapoport, Judith L., Perlis, Roy H., Lanz, Thomas A., Xi, Hualin Simon, Yin, Changhong, Huang, Weihua, Hirayama, Teruyoshi, Fukuda, Emi, Yagi, Takeshi, Ghosh, Sulagna, Eggan, Kevin C., Kim, Hae-Young, Eisenberg, Leonard M., Moghadam, Alexander A., Stanton, Patric K., Cho, Jun-Hyeong, and Chung, Sangmi

Subjects
Male, Mice, Knockout, interneurons, induced pluripotent stem cells, virus diseases, Prefrontal Cortex, urologic and male genital diseases, Cadherins, female genital diseases and pregnancy complications, Article, Protocadherins, Mice, nervous system, Synapses, Schizophrenia, Animals, Humans, Female, protocadherin, neoplasms, Signal Transduction
Abstract

We generated cortical interneurons (cINs) from induced pluripotent stem cells derived from 14 healthy controls and 14 subjects with schizophrenia. Both healthy control cINs and schizophrenia cINs were authentic, fired spontaneously, received functional excitatory inputs from host neurons, and induced GABA-mediated inhibition in host neurons in vivo. However, schizophrenia cINs had dysregulated expression of protocadherin genes, which lie within documented schizophrenia loci. Mice lacking protocadherin-α showed defective arborization and synaptic density of prefrontal cortex cINs and behavioral abnormalities. Schizophrenia cINs similarly showed defects in synaptic density and arborization that were reversed by inhibitors of protein kinase C, a downstream kinase in the protocadherin pathway. These findings reveal an intrinsic abnormality in schizophrenia cINs in the absence of any circuit-driven pathology. They also demonstrate the utility of homogenous and functional populations of a relevant neuronal subtype for probing pathogenesis mechanisms during development.

Published
2019

3. Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia

Author

Shao, Zhicheng, Noh, Haneul, Bin Kim, Woong, Ni, Peiyan, Nguyen, Christine, Cote, Sarah E, Noyes, Elizabeth, Zhao, Joyce, Parsons, Teagan, Park, James M, Zheng, Kelvin, Park, Joshua J, Coyle, Joseph T, Weinberger, Daniel R, Straub, Richard E, Berman, Karen F, Apud, Jose, Ongur, Dost, Cohen, Bruce M, McPhie, Donna L, Rapoport, Judith L, Perlis, Roy H, Lanz, Thomas A, Xi, Hualin Simon, Yin, Changhong, Huang, Weihua, Hirayama, Teruyoshi, Fukuda, Emi, Yagi, Takeshi, Ghosh, Sulagna, Eggan, Kevin C, Kim, Hae-Young, Eisenberg, Leonard M, Moghadam, Alexander A, Stanton, Patric K, Cho, Jun-Hyeong, and Chung, Sangmi

Subjects
Male, animal structures, Knockout, Induced Pluripotent Stem Cells, Prefrontal Cortex, Regenerative Medicine, Mice, Interneurons, Animals, Humans, 2.1 Biological and endogenous factors, Psychology, Aetiology, neoplasms, Neurology & Neurosurgery, Neurosciences, virus diseases, Cadherins, Stem Cell Research, female genital diseases and pregnancy complications, Protocadherins, Brain Disorders, Mental Health, nervous system, Synapses, Neurological, Schizophrenia, Female, Cognitive Sciences, Signal Transduction
Abstract

We generated cortical interneurons (cINs) from induced pluripotent stem cells derived from 14 healthy controls and 14 subjects with schizophrenia. Both healthy control cINs and schizophrenia cINs were authentic, fired spontaneously, received functional excitatory inputs from host neurons, and induced GABA-mediated inhibition in host neurons in vivo. However, schizophrenia cINs had dysregulated expression of protocadherin genes, which lie within documented schizophrenia loci. Mice lacking protocadherin-α showed defective arborization and synaptic density of prefrontal cortex cINs and behavioral abnormalities. Schizophrenia cINs similarly showed defects in synaptic density and arborization that were reversed by inhibitors of protein kinase C, a downstream kinase in the protocadherin pathway. These findings reveal an intrinsic abnormality in schizophrenia cINs in the absence of any circuit-driven pathology. They also demonstrate the utility of homogenous and functional populations of a relevant neuronal subtype for probing pathogenesis mechanisms during development.

Published
2019

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