Hongxia Zhou, MD
Professor, Environmental Health Sciences
Robert Stempel College of Public Health and Social Work
FIU Center for Translational Science
Office: CTS 239
Phone: 305-348-7778
Email: hozhou@fiu.edu
Overview
Devoted to reveal the causes and identify the treatments for neurodegenerative diseases including amyotrophic lateral sclerosis (ALS).
My research is focused on the molecular mechanisms of neurodegeneration in neurologic diseases including ALS. Using genetic approaches, we have created a few lines of novel transgenic and knockin rats as relevant models for in vivo study on neurodegeneration.
1) Neurodegeneration in ALS is partially reversible in a rat model. Using a tetracycline-inducible gene expression system, we examined the reversibility of neurodegeneration in an ALS model. We found that neurons are prevented from demise in paralyzed rats after the ALS-causing gene TDP-43 is stopped from further expression. Motor function is partially recovered in the rats due to functional compensation from survived neurons. As no effective treatment is currently available for ALS, our finding will encourage every effort to search for therapeutic treatments for the disease.
2) Reactive astrocytes secrete neurotoxic factors such as LCN2 to promote neuron death in neurodegenerative diseases. Astrocytes often become reactive in neurodegenerative diseases and reactive astrocytes are believed to be harmful to neurons. How reactive astrocytes exert a toxicity on neurons is not clear. We used multidisciplinary approach in search of potent molecules mediating astrocytic neurotoxicity. We identified that reactive astrocytes secrete lipocalin 2 (LCN2) as a potent mediator of astrocytic neurotoxicity. LCN2 is known to stimulate quiescent astrocytes and microglia to become reactive. Caution must be taken when glial replacement is tested for therapeutic effects against neurological diseases.
Along with my long-term collaborator Dr. Xugang Xia, I am leading my research team to reveal disease mechanisms and identify effective treatment for neurodegenerative diseases.
Dr. Hongxia Zhou is a professor at the Center for Translational Sciences and in the Robert Stempel College of Public Health and Social Work at Florida International University. Dr. Zhou received Doctor’s degree of medicine from Freiburg University in Germany and completed postdoctoral training at the University of Massachusetts Medical College. She spent 10 years at Thomas Jefferson University where she established a core lab for creating transgenic and knockin rats. She moved to the University of Central Florida in 2016 and joined FIU in 2019. Her research is focused on the molecular mechanisms of neuron death in neurodegenerative diseases.
Neurodegeneration in ALS is partially reversible in a rat model. Using a tetracycline-inducible gene expression system, we examined the reversibility of neurodegeneration in an ALS model. We found that neurons are prevented from demise in paralyzed rats after the ALS-causing gene TDP-43 is stopped from further expression. Motor function is partially recovered in the rats due to functional compensation from survived neurons. As no effective treatment is currently available for ALS, our finding encourages all efforts to develop effective treatments for the disease.
Reactive astrocytes secrete neurotoxic factors such as LCN2 to promote neuron death in neurodegenerative diseases. Astrocytes often become reactive in neurodegenerative diseases and activated astrocytes are believed to produce toxicity on neurons. Using multidisciplinary approach, we identified that reactive astrocytes secrete lipocalin 2 (LCN2) as a potent mediator of astrocytic neurotoxicity. LCN2 is known to stimulate quiescent astrocytes and microglia to become reactive.
Research Interests
Keywords: neurodegenerative diseases; amyotrophic lateral sclerosis; gene manipulation in rat model; neurochemistry; molecular biology
Molecular mechanisms of neurodegeneration in neurologic diseases
Recent Publications
Research Interests
- Pulmonary Vascular Disease
- Dry Powder Inhalers; Spray Drying; Inhalation
- Monocrotaline; Type II Bone Morphogenetic Protein Receptor; Pulmonary Hypertension
- Renalase; NAD(P)H Oxidase (H2o2-forming); Apocynin
- Myosin Light Chain Kinase; Cadherin 5; ML 7
- Persistent Fetal Circulation Syndrome; Ductus Arteriosus; Pulmonary Hypertension
Abstracts
Education
Professional Honors
