Profiles
Ming-Lei Guo
Courses Taught
- Neuroscience Special Topics
Graduate Education
- Ph.D., Fudan University, P. R. China
Postdoctoral Education
- Postdoctoral training, University of Kansas Medical Center
- Postdoctoral training, University of Missouri-Kansas City
Lab Location
Lewis Hall, Rooms 2149 and 2151
Research Interests
A: The role of microglia in the development of drug addiction
Drug addiction (substance use disorder, SUD) has been long recognized as brain diseases with alterations on neuroplasticity (neuron-centered hypothesis). Recently, accumulating evidence show that microglia activation can promote the development of SUD. Cocaine can activate microglia in vitro and in vivo and microglia inhibition could block cocaine-mediated reward effects. Microglia inhibition has been suggested as a novel therapeutic approach for SUD treatment. Our interests are to identify detailed mechanism underlying microglia activation induced by cocaine with a focus on autophagy and NLRP3 inflammasome. We employ various in vitro and in vivo approaches including behavioral tests to explore the roles of microglia and neuroimmune signaling in the development of SUDs. One powerful approach is that we have setup mouse self-administration model in EVMS. The long-term goal of this project is to identify novel neuroimmune signaling which can be targeted for SUD treatment.
B: Mechanisms responsible for exaggerated microglia activation in chronic HIV (+) persons with cocaine and cART
In the era of cART, HIV infected individuals can live longer comparable to general negative population. Still, the quality of their life is deeply compromised due to the high prevalence of HAND and HIV-associated dyslipidemia. Inflammation in brain and peripheral system underlie such pathological changes in HIV (+) persons on cART. Drug abuse (cocaine), high comorbidity with HIV infection, exaggerated the neurological symptoms (memory and cognitive impairment) in those persons. Enhanced microglia activation has been revealed in the context of HIV infection, cocaine, and antiretrovirals. Our interests are to explore the detailed molecular pathways responsible for enhanced microglia activation (NLRP3 inflammasome) and how the dysregulated neuroimmune signaling induce neuronal injuries. Various animal models have been employed for this project such as HIV-TAT mice and HIV-Tg rats.
Keywords: Microglia, neuroinflammation, autophagy, HIV, NLRP3 inflammasome
Relevant Publications
- Guo L, Reed KM, Carter A, Cheng Y, Roodsari SK, Martinez Pineda D, Wellman LL, Sanford LD, Guo ML. Sleep-Disturbance-Induced Microglial Activation Involves CRH-Mediated Galectin 3 and Autophagy Dysregulation. Cells. 2022 Dec 30;12(1):160.
- Tripathi A, Thangaraj A, Chivero ET, Periyasamy P, Callen S, Burkovetskaya ME, Guo ML*, Buch S. Antiretroviral-Mediated Microglial Activation Involves Dysregulated Autophagy and Lysosomal Dysfunction. Cells. 2019, 8(10). *Co-corresponding author
- Guo ML, Liao K, Periyasamy P, Yang L, Cai Y, Callen SE, Buch S. Cocaine mediated microglial activation involves ER stress/Autophagy axis. Autophagy. 2015, 11: 995-1009
- Guo ML, Xue B, Jin DZ, Mao LM, Wang JQ. Dynamic downregulation of Nogo receptor expression in the rat forebrain by amphetamine. Neurochem Int. 2013, 63:195-200.
- Guo ML, Fibuch EE, Liu XY, Choe ES, Bush S, Mao LM, Wang JQ. CaMKIIalpha interacts with M4 muscarinic receptors to control receptor and psychomotor function. EMBO J. 2010, 29:2070-81.
Courses Taught
- Neuroscience Special Topics
Graduate Education
- Ph.D., Fudan University, P. R. China
Postdoctoral Education
- Postdoctoral training, University of Kansas Medical Center
- Postdoctoral training, University of Missouri-Kansas City
Lab Location
Lewis Hall, Rooms 2149 and 2151
Research Interests
A: The role of microglia in the development of drug addiction
Drug addiction (substance use disorder, SUD) has been long recognized as brain diseases with alterations on neuroplasticity (neuron-centered hypothesis). Recently, accumulating evidence show that microglia activation can promote the development of SUD. Cocaine can activate microglia in vitro and in vivo and microglia inhibition could block cocaine-mediated reward effects. Microglia inhibition has been suggested as a novel therapeutic approach for SUD treatment. Our interests are to identify detailed mechanism underlying microglia activation induced by cocaine with a focus on autophagy and NLRP3 inflammasome. We employ various in vitro and in vivo approaches including behavioral tests to explore the roles of microglia and neuroimmune signaling in the development of SUDs. One powerful approach is that we have setup mouse self-administration model in EVMS. The long-term goal of this project is to identify novel neuroimmune signaling which can be targeted for SUD treatment.
B: Mechanisms responsible for exaggerated microglia activation in chronic HIV (+) persons with cocaine and cART
In the era of cART, HIV infected individuals can live longer comparable to general negative population. Still, the quality of their life is deeply compromised due to the high prevalence of HAND and HIV-associated dyslipidemia. Inflammation in brain and peripheral system underlie such pathological changes in HIV (+) persons on cART. Drug abuse (cocaine), high comorbidity with HIV infection, exaggerated the neurological symptoms (memory and cognitive impairment) in those persons. Enhanced microglia activation has been revealed in the context of HIV infection, cocaine, and antiretrovirals. Our interests are to explore the detailed molecular pathways responsible for enhanced microglia activation (NLRP3 inflammasome) and how the dysregulated neuroimmune signaling induce neuronal injuries. Various animal models have been employed for this project such as HIV-TAT mice and HIV-Tg rats.
Keywords: Microglia, neuroinflammation, autophagy, HIV, NLRP3 inflammasome
Relevant Publications
- Guo L, Reed KM, Carter A, Cheng Y, Roodsari SK, Martinez Pineda D, Wellman LL, Sanford LD, Guo ML. Sleep-Disturbance-Induced Microglial Activation Involves CRH-Mediated Galectin 3 and Autophagy Dysregulation. Cells. 2022 Dec 30;12(1):160.
- Tripathi A, Thangaraj A, Chivero ET, Periyasamy P, Callen S, Burkovetskaya ME, Guo ML*, Buch S. Antiretroviral-Mediated Microglial Activation Involves Dysregulated Autophagy and Lysosomal Dysfunction. Cells. 2019, 8(10). *Co-corresponding author
- Guo ML, Liao K, Periyasamy P, Yang L, Cai Y, Callen SE, Buch S. Cocaine mediated microglial activation involves ER stress/Autophagy axis. Autophagy. 2015, 11: 995-1009
- Guo ML, Xue B, Jin DZ, Mao LM, Wang JQ. Dynamic downregulation of Nogo receptor expression in the rat forebrain by amphetamine. Neurochem Int. 2013, 63:195-200.
- Guo ML, Fibuch EE, Liu XY, Choe ES, Bush S, Mao LM, Wang JQ. CaMKIIalpha interacts with M4 muscarinic receptors to control receptor and psychomotor function. EMBO J. 2010, 29:2070-81.