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25 results on '"Gollihue, Jenna L."'

5. Soluble TNF mediates amyloid-independent, diet-induced alterations to immune and neuronal functions in an Alzheimer’s disease mouse model

Author

MacPherson, Kathryn P., primary, Eidson, Lori N., additional, Houser, Madelyn C., additional, Weiss, Blaine E., additional, Gollihue, Jenna L., additional, Herrick, Mary K., additional, de Sousa Rodrigues, Maria Elizabeth, additional, Sniffen, Lindsey, additional, Weekman, Erica M., additional, Hamilton, Adam M., additional, Kelly, Sean D., additional, Oliver, Danielle L., additional, Yang, Yuan, additional, Chang, Jianjun, additional, Sampson, Timothy R., additional, Norris, Christopher M., additional, and Tansey, Malú Gámez, additional

Published
2023
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6. Targeting Astrocyte Signaling Alleviates Cerebrovascular and Synaptic Function Deficits in a Diet-Based Mouse Model of Small Cerebral Vessel Disease

Author

Sompol, Pradoldej, primary, Gollihue, Jenna L., additional, Weiss, Blaine E., additional, Lin, Ruei-Lung, additional, Case, Sami L., additional, Kraner, Susan D., additional, Weekman, Erica M., additional, Gant, John C., additional, Rogers, Colin B., additional, Niedowicz, Dana M., additional, Sudduth, Tiffany L., additional, Powell, David K., additional, Lin, Ai-Ling, additional, Nelson, Peter T., additional, Thibault, Olivier, additional, Wilcock, Donna M., additional, and Norris, Christopher M., additional

Published
2023
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8. Q134R: Small chemical compound with NFAT inhibitory properties improves behavioral performance and synapse function in mouse models of amyloid pathology

Author

Sompol, Pradoldej, primary, Gollihue, Jenna L., additional, Kraner, Susan D., additional, Artiushin, Irina A., additional, Cloyd, Ryan A., additional, Chishti, Emad A., additional, Koren, Shon A., additional, Nation, Grant K., additional, Abisambra, Jose F., additional, Huzian, Orsolya, additional, Nagy, Lajos I., additional, Santha, Miklos, additional, Hackler, Laszlo, additional, Puskas, Laszlo G., additional, and Norris, Christopher M., additional

Published
2021
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10. Novel small chemical compound with NFAT modulatory properties alleviates synaptic dysfunction and improves cognition in mouse models of amyloid pathology

Author

Sompol, Pradoldej, primary, Gollihue, Jenna L., additional, Cloyd, Ryan, additional, Koren, Shon, additional, Nation, Grant K., additional, Abisambra, Jose F., additional, Artiushin, Irina A., additional, Kraner, Susan D., additional, Huzian, Orsolya, additional, Hackler, Laszlo, additional, Puskas, Laszlo G., additional, and Norris, Christopher M., additional

Published
2020
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12. Astrocyte activation and neurovascular function in a diet‐based model of vascular contributions to cognitive impairment and dementia (VCID)

Author

Sompol, Pradoldej, primary, Edelmann, Stephanie E., additional, Lin, Ruei‐Lung, additional, Gant, Christopher C., additional, Kraner, Susan D., additional, Weiss, Blaine E., additional, Farr, N. Drew, additional, Gollihue, Jenna L., additional, Thibault, Olivier, additional, Wilcock, Donna M., additional, and Norris, Christopher M., additional

Published
2020
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15. Mitochondrial Transplantation After Spinal Cord Injury

Author

Gollihue, Jenna L.

Subjects
Neuroscience and Neurobiology
Abstract

Contusion spinal cord injury (SCI) results in devastating life-long debilitation in which there are currently no effective treatments. The primary injury site presents a complex environment marked by subsequent secondary pathophysiological cascades involving excessive reactive oxygen and nitrogen species (ROS/RNS) production, glutamate-induced excitotoxicity, calcium dysregulation, and delayed neuronal apoptosis. Many of these cascades involve mitochondrial dysfunction, thus a single mitochondrial-centric therapy that targets a variety of these factors could be far reaching in its potential benefits after SCI. As such, this dissertation examines whether transplantation of exogenous mitochondria after SCI can attenuate secondary injury cascades to decrease the spread and severity of the injury. Our first experiment tested the dose-dependent effects of mitochondrial transplantation on the ability to maintain acute overall bioenergetics after SCI. We compared transplantation of mitochondria originating from two different sources-cultured PC12 cells or rat soleus leg muscle. 24 hours after injury, State III oxygen consumption rates were maintained to over 80% of sham levels when 100ug of mitochondria was transplanted, regardless of the origin of the mitochondria. Complex I enzyme activity assays corroborated our findings that the 100ug dosage gave optimal benefits compared to vehicle injection. We also analyzed the rostral-caudal distribution and cell-type colocalization of transplanted transgenically-labeled tGFP mitochondria after SCI. There were greater volumes and rostral-caudal spread of tGFP mitochondria at the 24 hour time point compared to 7 days post injection. tGFP mitochondria had the greatest propensity to colocalize with macrophages and pericytes. Colocalization was evident in endothelial cells, oligodendrocytes and astrocytes, though no such colabeling was present in neurons. Further, colocalization of tGFP was always greater at the 24 hour time compared to 48 hour or 7days post injection time points. These data indicate that there is a cell-type difference in incorporation potential of exogenous mitochondria which changes over time. Finally, we tested the effects of mitochondrial transplantation on long term functional recovery. Animals were injected with either vehicle, 100ug cell-derived mitochondria, or 100ug muscle-derived mitochondria immediately after contusion SCI. Functional analyses including BBB overground locomotor scale and von Frey mechanical sensitivity tests did not show any differences between treatment groups. Likewise, there were no differences in tissue sparing when mitochondria were transplanted compared to vehicle injections, though there were higher neuronal cell counts in tGFP mitochondria injected groups caudal of the injury site. These studies present the potential of mitochondrial transplantation for therapeutic intervention after SCI. While our acute measures do not correspond into long term recovery, we show that at 24 hours transplanted mitochondria do have an effect on bioenergetics and that they are taken into host cells. We believe that further investigation into caveats and technical refinement is necessary at this time to translate the evident acute bioenergetic recovery into long term functional recovery.

Published
2017
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17. P4‐218: Q134R: NOVEL SMALL CHEMICAL COMPOUND WITH NFAT INHIBITORY PROPERTIES AMELIORATES SYNAPTIC DEFICITS IN A MOUSE MODEL OF ALZHEIMER'S DISEASE

Author

Norris, Christopher M., primary, Sompol, Pradoldej, additional, Gollihue, Jenna L., additional, Cloyd, Ryan, additional, Koren, Shon, additional, Nation, Grant K., additional, Abisambra, Joe F., additional, Kraner, Susan D., additional, Artiushin, Irina A., additional, Huzian, Orsolya, additional, and Puskas, Laszlo G., additional

Published
2018
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24. MITOCHONDRIAL TRANSPLANTATION AFTER SPINAL CORD INJURY: EFFECTS ON TISSUE BIOENERGETICS AND FUNCTIONAL NEUROPROTECTION

Author

Gollihue, Jenna L.

Subjects
PC-12 mitochondria, central pattern generators, co-localization, transgenic labeling, oxidative phosphorylation, Neuroscience and Neurobiology
Abstract

Contusion spinal cord injury (SCI) results in devastating life-long debilitation in which there are currently no effective treatments. The primary injury site presents a complex environment marked by subsequent secondary pathophysiological cascades involving excessive reactive oxygen and nitrogen species (ROS/RNS) production, glutamate-induced excitotoxicity, calcium dysregulation, and delayed neuronal apoptosis. Many of these cascades involve mitochondrial dysfunction, thus a single mitochondrial-centric therapy that targets a variety of these factors could be far reaching in its potential benefits after SCI. As such, this dissertation examines whether transplantation of exogenous mitochondria after SCI can attenuate secondary injury cascades to decrease the spread and severity of the injury. Our first experiment tested the dose-dependent effects of mitochondrial transplantation on the ability to maintain acute overall bioenergetics after SCI. We compared transplantation of mitochondria originating from two different sources-cultured PC12 cells or rat soleus leg muscle. 24 hours after injury, State III oxygen consumption rates were maintained to over 80% of sham levels when 100ug of mitochondria was transplanted, regardless of the origin of the mitochondria. Complex I enzyme activity assays corroborated our findings that the 100ug dosage gave optimal benefits compared to vehicle injection. We also analyzed the rostral-caudal distribution and cell-type colocalization of transplanted transgenically-labeled tGFP mitochondria after SCI. There were greater volumes and rostral-caudal spread of tGFP mitochondria at the 24 hour time point compared to 7 days post injection. tGFP mitochondria had the greatest propensity to colocalize with macrophages and pericytes. Colocalization was evident in endothelial cells, oligodendrocytes and astrocytes, though no such colabeling was present in neurons. Further, colocalization of tGFP was always greater at the 24 hour time compared to 48 hour or 7days post injection time points. These data indicate that there is a cell-type difference in incorporation potential of exogenous mitochondria which changes over time. Finally, we tested the effects of mitochondrial transplantation on long term functional recovery. Animals were injected with either vehicle, 100ug cell-derived mitochondria, or 100ug muscle-derived mitochondria immediately after contusion SCI. Functional analyses including BBB overground locomotor scale and von Frey mechanical sensitivity tests did not show any differences between treatment groups. Likewise, there were no differences in tissue sparing when mitochondria were transplanted compared to vehicle injections, though there were higher neuronal cell counts in tGFP mitochondria injected groups caudal of the injury site. These studies present the potential of mitochondrial transplantation for therapeutic intervention after SCI. While our acute measures do not correspond into long term recovery, we show that at 24 hours transplanted mitochondria do have an effect on bioenergetics and that they are taken into host cells. We believe that further investigation into caveats and technical refinement is necessary at this time to translate the evident acute bioenergetic recovery into long term functional recovery.

Published
2017

25. Mitochondrial transplantation strategies as potential therapeutics for central nervous system trauma.

Author

Gollihue JL, Patel SP, and Rabchevsky AG

Abstract

Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of "mitochondrial medicine" is emerging in which injury/disease states are targeted therapeutically at the level of the mitochondrion, including specific antioxidants, bioenergetic substrate additions, and membrane uncoupling agents. Consequently, novel mitochondrial transplantation strategies represent a potentially multifactorial therapy leading to increased adenosine triphosphate production, decreased oxidative stress, mitochondrial DNA replacement, improved bioenergetics and tissue sparing. Herein, we describe briefly the history of mitochondrial transplantation and the various techniques used for both in vitro and in vivo delivery, the benefits associated with successful transference into both peripheral and central nervous system tissues, along with caveats and pitfalls that hinder the advancements of this novel therapeutic., Competing Interests: None declared

Published
2018
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