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SELECTBIO Conferences Extracellular Vesicles (EVs) & Nanoparticles 2024: Diagnostics, Delivery, Therapeutics

Shilpa Buch's Biography

Shilpa Buch, Professor and Senior Executive Vice Chair for Research, University of Nebraska Medical Center

I am currently a Professor & Executive Vice Chair for Research and the Director of the Nebraska Center for Substance Abuse research at the University of Nebraska. I received my PhD in 1982 in Microbiology from Maharaja Sayajirao Univ in Baroda, India and moved to Canada for postdoctoral training. I began my independent research career as an Assistant Professor at the Hospital for Sick Kids, Toronto, following which, I moved to Kansas University and embarked on a research area focused on understanding how addictive drugs co-operate with HIV-1 to exacerbate neurological complications. I rose through the ranks at Kansas and in 2007, made a move as a full Professor to University of Nebraska in Omaha. Research approaches used in my lab involve a multipronged approach comprising of a variety of complementary model systems ranging from cell cultures to rodent models to the higher more relevant macaque model of SIV pathogenesis. More recently, my research interest is centered on exploring how exosomes act as conduits to transport key signaling mediators (small noncoding RNAs/microRNAs) to distant recipient cells as a means to regulate gene expression and cellular cross talk. I lead an active research program involving collaborations both nationally and internationally, with over 225 peer-reviewed publications. I have consistently held NIH funding throughout my career and continue to serve on NIH study sections. During my career, I have had the good fortune of being recognized by various national and International societies with the Wybran (2012) and the Distinguished services (2023; 2013) Awards, both of which hold a special meaning for me. I have also been awarded the UNMC Scientist laureate award (2016) in addition to the Kansas City scientist award. Aligning closely with my passion for mentoring, has enabled me to take an active leading role in the Women’s Mentoring Program at UNMC (2015-2017). I have also received the Women in Neuroscience award at the International Society of Neurovirology in 2016. I have played an active role as a Secretary of the Society on Neuroimmune Pharmacology and have been invited as a speaker & as a Chair at various meetings and have also organized several symposia. To further hone my leadership skills, I graduated from the Executive Leadership for Academic Medicine Program that fosters the growth and career trajectories of women leaders nationally.

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HIV and Opioid-Mediated Aging and Cognitive Decline: Implications for Astrocyte EVs

Thursday, 4 April 2024 at 09:00

Add to Calendar ▼2024-04-04 09:00:002024-04-04 10:00:00Europe/LondonHIV and Opioid-Mediated Aging and Cognitive Decline: Implications for Astrocyte EVsExtracellular Vesicles (EVs) and Nanoparticles 2024: Diagnostics, Delivery, Therapeutics in Miami, FloridaMiami,

Although cART usage has increased the lifespan of HIV+ individuals, paradoxically, its dependence is also associated with increased risk of comorbidity of HIV-Associated Neurocognitive Disorders (HAND). Heroin abuse can accelerate the process of HAND pathogenesis, specifically age-sensitive brain functional networks in patients. Based on our previous findings that astrocytes play a major role in HIV Tat & Morphine-mediated amyloidosis & senescence-like phenotype, and since these senescence associated secretory phenotype (SASP) cargoes can be released in extracellular vesicles (EVs), we sought to assess whether HIV Tat protein and morphine-stimulated astrocyte derived EVs (ADEVs) containing these toxic cargoes could induce synaptodegeneration in neurons invitro and when administered in the brains of naïve mice. This study aims to focus on the cellular cross-talk mediated by ADEVs in inducing synaptodendritic injury. Methods: We assessed the novel role of long noncoding (lnc) RNA BACE1 antisense (AS) in HIV-Tat/morphine mediated astrocytic senescence and amyloidosis and in mediating neuronal injury. Additionally, we assessed the behavioral deficits as well as ageing phenotype in morphine dependent, as well as Tat-ADEV injected mice. Results: Both HIV-Tat and Morphine-induced senescence phenotype (p16, p21, ROS, cell cycle arrest, ß- gal activity, cytokines) and accumulation of amyloids in human astrocytes in culture. Furthermore, using gene silencing approach, we showed that this phenomenon was regulated by lncRNA BACE1AS. Next, EVs isolated from HIV-Tat or morphine exposed human astrocytes were demonstrated to shuttle the SASP cargoes and also that, the EV numbers were regulated by lncRNA BACE1AS. These EVs upon being uptaken by the neurons both in vitro and in vivo, were shown to induce neuronal senescence & synaptodendritic injury. Interestingly, validation in vivo demonstrated that morphine administered mice exhibited ageing phenotype in the frontal cortex and hippocampus and this was associated with cognitive decline. There was also synaptodegeneration in the hippocampi of mice injected with  these ADEVs. Conclusion(s): This study underscores the role of lncRNA BACE1AS in astrocytic senescence and amyloidosis and the role of ADEVs in mediating synaptodegeneration leading to cognitive impairments associated with HAND.

Add to Calendar ▼2024-04-03 00:00:002024-04-04 00:00:00Europe/LondonExtracellular Vesicles (EVs) and Nanoparticles 2024: Diagnostics, Delivery, TherapeuticsExtracellular Vesicles (EVs) and Nanoparticles 2024: Diagnostics, Delivery, Therapeutics in Miami, FloridaMiami,