Departmental Affiliation and City, State, Zip for All Authors

Student, Fort Worth, TX, 76107; Professor, Fort Worth, TX, 76107; Graduate Student, Fort Worth TX, 76107

Scientific Abstract

INTERMITTENT HYPOXIA INCREAES MICROGLIAL EXPRESSION OF BDNF Amanda Garcia*, Dana Al-Hamidi*, Robert T. Mallet* *Department of Integrative Physiology, UNT Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, Texas 76107 Inflammation is a crucial component of various devastating diseases that negatively impact the central nervous system, including stroke, alcohol withdrawal, diabetic neuropathy, and dementia. The objective of this investigation is to target the specific anti-inflammatory pathways that result from controlled oxygen deprivation. For this investigation microglial-derived EOC20 cells were exposed to four different conditions: 1) Normoxia with glucose-rich media 2) Intermittent hypoxic conditioning 3) Oxygen and glucose deprivation 4) Oxygen and glucose deprivation with intermittent hypoxic conditioning. Bradford protein assays were utilized to measure the protein concentration in the extract. Immunoblots were used to identify the protective protein BDNF. The immunoblots were incubated with rabbit anti-BDNF followed by anti-rabbit IgG. The density was measured via ImageJ and normalized against alpha-tubulin. An overexpression of BDNF was observed in microglia exposed to intermittent hypoxic training, however the protein expression of only three groups were analyzed for this experiment. An increase of samples would be needed to further evaluate the significance of these results. If IHT is indeed proven to increase expression of neuroprotective proteins, then it could potentially be used in the medical field as a treatment or a preventative measure against inflammatory diseases of the central nervous system. Keywords: Inflammation, central nervous system, intermittent hypoxia, immunoblot, oxygen glucose deprivation, BDNF, alcohol withdrawal, alpha-tubulin, protective protein, ImageJ, neuroprotective

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INTERMITTENT HYPOXIA INCREASES MICROGLIAL EXPRESSION OF BDNF

INTERMITTENT HYPOXIA INCREAES MICROGLIAL EXPRESSION OF BDNF Amanda Garcia*, Dana Al-Hamidi*, Robert T. Mallet* *Department of Integrative Physiology, UNT Health Science Center, 3500 Camp Bowie Blvd., Fort Worth, Texas 76107 Inflammation is a crucial component of various devastating diseases that negatively impact the central nervous system, including stroke, alcohol withdrawal, diabetic neuropathy, and dementia. The objective of this investigation is to target the specific anti-inflammatory pathways that result from controlled oxygen deprivation. For this investigation microglial-derived EOC20 cells were exposed to four different conditions: 1) Normoxia with glucose-rich media 2) Intermittent hypoxic conditioning 3) Oxygen and glucose deprivation 4) Oxygen and glucose deprivation with intermittent hypoxic conditioning. Bradford protein assays were utilized to measure the protein concentration in the extract. Immunoblots were used to identify the protective protein BDNF. The immunoblots were incubated with rabbit anti-BDNF followed by anti-rabbit IgG. The density was measured via ImageJ and normalized against alpha-tubulin. An overexpression of BDNF was observed in microglia exposed to intermittent hypoxic training, however the protein expression of only three groups were analyzed for this experiment. An increase of samples would be needed to further evaluate the significance of these results. If IHT is indeed proven to increase expression of neuroprotective proteins, then it could potentially be used in the medical field as a treatment or a preventative measure against inflammatory diseases of the central nervous system. Keywords: Inflammation, central nervous system, intermittent hypoxia, immunoblot, oxygen glucose deprivation, BDNF, alcohol withdrawal, alpha-tubulin, protective protein, ImageJ, neuroprotective

Manuscript Number

1034