Teng Guan

University of Manitoba

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Jiming Kong

University of Manitoba

Yisong Qian

Nanchang University

Yunman Li

China Pharmaceutical University

Xuzhen Tang

WuXi AppTec (China)

Ying Guo

Heilongjiang University

Hongbin Sun

China Pharmaceutical University

Menghao Huang

Indiana University – Purdue University Indianapolis

Guohui Zhang

Washington University in St. Louis

Longfei Huang

Capital Institute of Pediatrics

Qiang Yu

Jiangsu University

Cooperative Institutions

University of Manitoba

China Pharmaceutical University

Sun Yat-sen University

Chinese Academy of Medical Sciences & Peking Union Medical College

Hebei North University

Children's Hospital Research Institute of Manitoba

Chinese Academy of Sciences

Nanchang University

Army Medical University

Zhejiang University

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Neuroprotection of Maslinic Acid, a Novel Glycogen Phos-phorylase Inhibitor, in Type 2 Diabetic Rats

Chinese Journal of Natural Medicines (2010)

Teng Guan Yisong Qian Menghao Huang Longfei Huang Xuzhen Tang

Phos

10.3724/sp.j.1009.2010.00293

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Citations (7)

Selective Susceptibility of Oligodendrocytes to Carbon Monoxide Poisoning: Implication for Delayed Neurologic Sequelae (DNS)

Frontiers in Psychiatry (2020)

Xiaofei Tian Teng Guan Ying Guo Guohui Zhang Jiming Kong

Delayed neurologic sequelae (DNS) are recurrent-transient neuropsychiatric consequences of carbon monoxide (CO) intoxication. Pathologically DNS features damages to the brain white matter. Here we test a hypothesis that direct cytotoxicity of CO to oligodendrocytes plays a role in the development of DNS. In an in vitro model of CO poisoning with the carbon monoxide releasing molecule-2 (CORM-2) as a CO donor, we show that CORM-2 at concentrations higher than 200 µM significantly inhibited viability and caused significant death of PC12 cells. Similar minimum toxicity concentration was observed on primary brain cells including neurons, astrocytes, and microglia. Interestingly, oligodendrocytes showed cytotoxicity to CORM-2 at a much lower concentration (100 µM). We further found that CORM-2 at 100 µM inhibited proteolipid protein (PLP) production and reduced myelin coverage on axons in an in vitro model of myelination. Our results show that direct cytotoxicity is a mechanism of CO poisoning and DNS may result from a high susceptibility of oligodendrocytes to CO poisoning.

Carbon monoxide poisoning

CO poisoning

10.3389/fpsyt.2020.00815

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BNIP3 and OGD‐induced oligodendrocyte death: Role in white matter injury in cerebral ischemia

The FASEB Journal (2012)

Teng Guan Chengren Li Jiming Kong

We sought to identify potential role of BNIP3, a proapoptotic member of the Bcl‐2 family of death‐regulating proteins that promote programmed cell death, in Oxygen–glucose deprivation (OGD) treated primary cultures of rat oligodendrocyte lineage cells (OLs). OGD induced cytotoxic injury to various maturational stages of OLs. Survival assays revealed that oligodendrocyte precursor cells (OPCs) and later‐stage precursors were highly vulnerable, whereas more mature OLs were relatively resistant. Exposure of OLs to OGD resulted in a significant increase in BNIP3 expression. Knockdown of BNIP3 with shRNA reduced OGD‐triggered OL apoptosis. Thirty minutes ischemic preconditioning (IPC) of later‐stage precursors and more mature OLs down‐regulated the BNIP3 expression and shown cytoprotection. Interestingly, OPCs were more susceptible to OGD after IPC pretreatment, concurrent with highly BNIP3 expression. These studies unveil BNIP3 as an important mediator in OLs death and reveal a novel mechanism of action of IPC on stage‐specific OLs cultures, which may contribute to a better understanding of white matter injury in cerebral ischemia.

Cytoprotection

10.1096/fasebj.26.1_supplement.521.11

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C1q is essential for myelination in the central nervous system (CNS)

iScience (2023)

Qiang Yu Nan Zhang Teng Guan Ying Guo Hassan Marzban

Myelin sheath in the central nervous system (CNS) is essential for efficient action potential conduction. Microglia, the macrophages in the CNS, are suggested to regulate myelin development. However, the specific involvement of microglia in initial myelination is yet to be elucidated. Here, first, by culturing neural stem cells, we demonstrated that myelin sheath formation only occurred in the presence of a microglia-conditioned medium. Furthermore, the absence of C1q, a microglia-derived factor, resulted in myelination failure in the neural stem cell culture. Additionally, adding native human C1q protein was sufficient to induce myelination in vitro. Finally, in the C1q conditional knockout mouse model (C1qaFL/FL: Cx3cr1CreER), C1q deficiency prior to the onset of myelination led to reduced myelin thickness and elevated g-ratio during initial myelination. This study uncovers the pivotal role of microglia-derived C1q in developmental myelination and could potentially pave the way for new therapeutic strategies for treating demyelinating diseases.

Demyelinating Disorder

10.1016/j.isci.2023.108518

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Citations (6)

4,8-dicarboxyl-8,9-iridoid-1-glycoside Promotes Neural Stem Cell Differentiation Through MeCP2

Dose-Response (2022)

WeiBing Wang Zhen Liu Baosheng Jing HaiMin Mai Hong Jiao

Borojó (Borojoa patinoi Cuatrec) fruit has recently been shown to have a variety of health benefit, but the mechanisms have been little studied. The aim of this study was to investigate the effect of 4,8-dicarboxyl-8,9-iridoid-1-glycoside (388) on proliferation and differentiation of embryonic neural stem cells (NSCs).NSCs were treated with 388 and stem cell differentiation was determined by western blotting and immunofluorescence staining. The role of MeCP2 in 388-mediated embryonic NSCs differentiation was examined.The results showed that in the presence of mitogen when NSCs proliferated and maintained their multipotency, treatment with 388 did not affect the viability of NSCs. Following mitogen withdrawal to initiate NSC differentiation, treatment with 388 at the doses of 10 and 50 μg/mL significantly increased neural differentiation in both cortex and spinal cord-derived culture. 388 also significantly up-regulated MeCP2 expression. The expression of the neuronal and oligodendrocytic markers was enhanced after addition of 388 in the differentiation culture. However, knockdown of MeCP2 results in inhibition of NSC differentiation, and the pro-differentiation effect of 388 was mostly abolished.This study confirmed that 388 stimulates differentiation of NSCs and identifies its mechanism of action by upregulating MeCP2.

Neural cell

10.1177/15593258221112959

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Citations (3)

Astrocytic glutamate transporter-dependent neuroprotection against glutamate toxicity: An in vitro study of maslinic acid

European Journal of Pharmacology (2010)

Yisong Qian Teng Guan Xuzhen Tang Longfei Huang Menghao Huang

Glutamate aspartate transporter

Excitotoxicity

10.1016/j.ejphar.2010.10.095

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Citations (33)

Necrostatin‐1 prevents the proapoptotic protein Bcl‐2/adenovirus E1B 19‐kDa interacting protein 3 from integration into mitochondria

Journal of Neurochemistry (2020)

Jiao Mu Jiequn Weng Chaoxian Yang Teng Guan Li Deng

Necrostatin-1 (Nec-1) has previously been shown to protect neurons from death in traumatic and ischemic brain injuries. This study tests the hypothesis that Nec-1 protects neural cells against traumatic and ischemic brain injuries through inhibition of the Bcl-2/adenovirus E1B 19-kDa interacting protein 3 (BNIP3). We have used biochemical and morphological techniques to determine the inhibition of Nec-1 on BNIP3-induced cell death and to identify its mechanism of action in in vivo and in vitro models of neurodegeneration. Here we show that Nec-1 significantly increased neuronal viability following prolonged exposure to hypoxia in vitro, and attenuated myelin damage and neuronal death in traumatic brain injury and cerebral ischemia in Sprague-Dawley rats. Nec-1 alleviated traumatic brain injury-induced up-regulation of BNIP3 in mature oligodendrocytes. In isolated mitochondria, Nec-1 prevented BNIP3 from integrating into mitochondria by modifying its binding sites on the mitochondria. Consequently, Nec-1 robustly inhibited BNIP3-induced collapse of mitochondrial membrane potential and reduced the opening probability of mitochondrial permeability transition pores. Nec-1 also preserved mitochondrial ultrastructure and suppressed BNIP3-induced nuclear translocation of apoptosis-inducing factor. In conclusion, Nec-1 protects neurons and oligodendrocytes against traumatic and ischemic brain injuries by targeting the BNIP3-induced cell death pathway, and is a novel inhibitor for BNIP3. Cover Image for this issue: https://doi.org/10.1111/jnc.15056.

10.1111/jnc.14993

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Citations (11)

Mevalonate Cascade and Neurodevelopmental and Neurodegenerative Diseases: Future Targets for Therapeutic Application

Current Molecular Pharmacology (2016)

Hassan Marzban Jiming Kong Shahram E. Mehr Jerry Vriend Jiasi Li

The mevalonate cascade is a key metabolic pathway that regulates a variety of cellular functions and is thereby implicated in the pathophysiology of most brain diseases, including neurodevelopmental and neurodegenerative disorders. Emerging lines of evidence suggest that statins and Rho GTPase inhibitors are efficacious and have advantageous properties in treatment of different pathologic conditions that are relevant to the central nervous system. Beyond the original role of statins in lowering cholesterol synthesis, they have anti-inflammatory, antioxidant and modulatory effects on signaling pathways. Additionally, Rho GTPase inhibitors and statins share the mevalonate pathway as a common target of their therapeutic actions. In this review, we discuss potential mechanisms through which these drugs, via their role in the mevalonate pathway, exert their neuroprotective effects in neurodegenerative and neurodevelopmental disorders.

Mevalonate pathway

Small GTPase

10.2174/1874467209666160112125446

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Citations (18)

Mitochondrial dysfunction in aging

Ageing Research Reviews (2023)

Ying Guo Teng Guan Kashfia Shafiq Qiang Yu Xin Jiao

Senescence

Organelle

10.1016/j.arr.2023.101955

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