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39 results on '"Jones, T. Bucky"'

2. Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.

Author

Curry-Koski, Tala, Gusek, Brikena, Potter, Ross M., Jones, T. Bucky, Dickman, Raechel, Johnson, Nathan, Stallone, John N., Rahimian, Roshanak, Vallejo-Elias, Johana, and Esfandiarei, Mitra

Abstract

Marfan syndrome (MFS) is a systemic connective tissue disorder stemming from mutations in the gene encoding Fibrillin-1 (Fbn1), a key extracellular matrix glycoprotein. This condition manifests with various clinical features, the most critical of which is the formation of aortic root aneurysms. Reduced nitric oxide (NO) production due to diminished endothelial nitric oxide synthase (eNOS) activity has been linked to MFS aortic aneurysm pathology. Caveolin-1 (Cav1), a structural protein of plasma membrane caveolae, is known to inhibit eNOS activity, suggesting its involvement in MFS aneurysm progression by modulating NO levels. In this study, we examined the role of Cav1 in aortic smooth muscle and endothelial function, aortic wall elasticity, and wall strength in male and female MFS mice (FBN1+/Cys1041Gly) by generating developing Cav1-deficient MFS mice (MFS/Cav1KO). Our findings reveal that Cav1 ablation leads to a pronounced reduction in aortic smooth muscle contraction in response to phenylephrine, attributable to an increase in NO production in the aortic wall. Furthermore, we observed enhanced aortic relaxation responses to acetylcholine in MFS/Cav1KO mice, further underscoring Cav1's inhibitory impact on NO synthesis within the aorta. Notably, van Gieson staining and chamber myography analyses showed improved elastin fiber structure and wall strength in male MFS/Cav1KO mice, whereas these effects were absent in female counterparts. Cav1's regulatory influence on aortic root aneurysm development in MFS through NO-mediated modulation of smooth muscle and endothelial function, with notable sex-dependent variations. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Regional Differences in Microbial Infiltration of Brain Tissue from Alzheimer's Disease Patients and Control Individuals.

Author

Jones, T. Bucky, Chu, Ping, Wilkey, Brooke, Lynch, Leigha, and Jentarra, Garilyn

Subjects
*ALZHEIMER'S disease, *CEREBRAL amyloid angiopathy, *ALZHEIMER'S patients, *NEUROFIBRILLARY tangles, *LIPOTEICHOIC acid
Abstract

Alzheimer's disease (AD) is characterized by cognitive decline and neuropathology including amyloid beta (Aβ) plaques and neurofibrillary tangles (tau). Factors initiating or driving these pathologies remain unclear, though microbes have been increasingly implicated. Our data and others' findings indicate that microbes may be common constituents of the brain. It is notable that Aβ and tau have antimicrobial properties, suggesting a response to microbes in the brain. We used 16S rRNA sequencing to compare major bacterial phyla in post-mortem tissues from individuals exhibiting a range of neuropathology and cognitive status in two brain regions variably affected in AD. Our data indicate that strong regional differences exist, driven in part by the varied presence of Proteobacteria and Firmicutes. We confirmed our data using ELISA of bacterial lipopolysaccharide (LPS) and lipoteichoic acid in the same brain tissue. We identified a potential association between the composition of phyla and the presence of neuropathology but not cognitive status. Declining cognition and increasing pathology correlated closely with serum LPS, but not brain levels of LPS, although brain LPS showed a strong negative correlation with cerebral amyloid angiopathy. Collectively, our data suggest a region-specific heterogeneity of microbial populations in brain tissue potentially associated with neurodegenerative pathology. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Contributors

Author

Capra, Norman F., primary, Chen, Jian, additional, Corbett, James J., additional, Dickman, J. David, additional, Dwyer, Terry M., additional, Geyer, Howard L., additional, Grow, Wade A., additional, Haines, Duane E., additional, Henkel, Craig K., additional, Jones, T. Bucky, additional, Kaufman, Jason A., additional, Ma, Terence P., additional, May, Paul J., additional, Mihailoff, Gregory A., additional, Parent, Andrew D., additional, Perkins, Eddie, additional, Simpson, Kimberly L., additional, Terrell, Allen C., additional, Warren, Susan, additional, Willis, Mary Alissa, additional, and Yezierski, Robert P., additional

Published
2018
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11. Manipulating neuroinflammatory reactions in the injured spinal cord: back to basics

Author

Popovich, Phillip G. and Jones, T. Bucky

Subjects
Pharmacology, Experimental -- Methods, Neurons -- Physiological aspects, Inflammation -- Physiological aspects, Leukocytes -- Physiological aspects, Spinal cord -- Physiological aspects, Spinal cord -- Injuries, Immunity -- Physiological aspects, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

Recruitment of inflammatory leukocytes to the injured spinal cord is a physiological response that is associated with the production of cytokines and proteinases that are involved in host defense and wound repair. Cells in the spinal cord are mainly post-mitotic and tissue regeneration is poor; thus, these inflammatory mediators can exacerbate the damage to spared tissue and thereby impair spontaneous functional recovery. Although several aspects of immune function might benefit the CNS, experimental studies indicate that acute neuroinflammation aggravates tissue injury. Until the timing and nature of the molecular signals that govern leukocyte recruitment and activation after spinal injury are defined, clinical therapies designed to boost immune cell function should be avoided.

Published
2003

14. Cerebral Artery Reactivity in Adult APOE3 and APOE4 Mice

Author

Patel, Reema G., primary, Hoxha, Brikena, additional, Ion, Elena, additional, Vallejo‐Elias, Johana, additional, Jones, Carleton “Buck”, additional, Powell, Jessica, additional, Virden, Thomas, additional, Struthers, Jason, additional, Jones, T. Bucky, additional, and Eckman, Delrae M., additional

Published
2019
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21. Altered Energy Metabolism Pathways in the Posterior Cingulate in Young Adult Apolipoprotein E ɛ4 Carriers

Author

Perkins, Michelle, primary, Wolf, Andrew B., additional, Chavira, Bernardo, additional, Shonebarger, Daniel, additional, Meckel, J.P., additional, Leung, Lana, additional, Ballina, Lauren, additional, Ly, Sarah, additional, Saini, Aman, additional, Jones, T. Bucky, additional, Vallejo, Johana, additional, Jentarra, Garilyn, additional, and Valla, Jon, additional

Published
2016
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27. Pathological CNS autoimmune disease triggered by traumatic spinal cord injury: implications for autoimmune vaccine therapy

Author

Jones, T. Bucky, Basso, D. Michele, Sodhi, Ajeet, Pan, Jonathan Z., Hart, Ronald P., MacCallum, Robert C., Lee, Sunhee, Whitacre, Caroline C., and Popovich, Phillip G.

Subjects
CD4-Positive T-Lymphocytes, Pathology, medicine.medical_specialty, Wallerian degeneration, Lymphoid Tissue, Receptors, Antigen, T-Cell, Autoimmunity, Mice, Transgenic, Demyelinating Autoimmune Diseases, CNS, Neuroprotection, Polymerase Chain Reaction, White matter, Myelin, Mice, Reflex, medicine, Image Processing, Computer-Assisted, Animals, Nerve Growth Factors, RNA, Messenger, ARTICLE, Spinal cord injury, Spinal Cord Injuries, Autoimmune disease, biology, Behavior, Animal, business.industry, General Neuroscience, Immunotherapy, Active, Myelin Basic Protein, Recovery of Function, medicine.disease, Spinal cord, Axons, Myelin basic protein, Hindlimb, medicine.anatomical_structure, Spinal Cord, Immunology, biology.protein, Disease Progression, Cytokines, business
Abstract

Lymphocytes respond to myelin proteins after spinal cord injury (SCI) and may contribute to post-traumatic secondary degeneration. However, there is increasing evidence that autoreactive T-lymphocytes may also convey neuroprotection and promote functional recovery after CNS injury. To clarify the role of myelin autoreactive lymphocytes after SCI, we performed contusion injuries in the thoracic spinal cord of transgenic (Tg) mice in which >95% of all CD4+ T-lymphocytes are reactive with myelin basic protein (MBP). We observed significantly impaired recovery of locomotor and reflex function in Tg mice compared with non-Tg (nTg) littermates. Measures of functional impairment in Tg mice correlated with significantly less white matter at the injury site, and morphometric comparisons of injured Tg and nTg spinal cords revealed increased rostrocaudal lesion expansion (i.e., secondary degeneration) in Tg mice. Rostrocaudal to the impact site in SCI–nTg mice, demyelination was restricted to the dorsal funiculus, i.e., axons undergoing Wallerian degeneration. The remaining white matter appeared normal. In contrast, lymphocytes were colocalized with regions of demyelination and axon loss throughout the white matter of SCI–Tg mice. Impaired neurological function and exacerbated neuropathology in SCI–Tg mice were associated with increased intraspinal production of proinflammatory cytokine mRNA; neurotrophin mRNA was not elevated. These data suggest that endogenous MBP-reactive lymphocytes, activated by traumatic SCI, can contribute to tissue injury and impair functional recovery. Any neuroprotection afforded by myelin-reactive T-cells is likely to be an indirect effect mediated by other non-CNS-reactive lymphocytes. Similar to the Tg mice in this study, a subset of humans that are genetically predisposed to autoimmune diseases of the CNS may be adversely affected by vaccine therapies designed to boost autoreactive lymphocyte responses after CNS trauma. Consequently, the safe implementation of such therapies requires that future studies define the mechanisms that control T-cell function within the injured CNS.

Published
2002

37. Colaboradores

Author

Capra, Norman F., Chen, Jian, Corbett, James J., Dickman, J. David, Dwyer, Terry M., Geyer, Howard L., Grow, Wade A., Haines, Duane E., Henkel, Craig K., Jones, T. Bucky, Kaufman, Jason A., Ma, Terence P., May, Paul J., Mihailoff, Gregory A., Parent, Andrew D., Perkins, Eddie, Simpson, Kimberly L., Terrell, Allen C., Warren, Susan, Willis, Mary Alissa, and Yezierski, Robert P.

Published
2019
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39. The effects of T-lymphocytes on secondary neurodegeneration and recovery of function after experimental spinal contusion injury

Author

Jones, T. Bucky

Subjects
spinal cord injury, T-lymphocytes, neuroinflammation, secondary injury
Abstract

Spinal cord injury (SCI) disrupts nerve fibers carrying information between the brain and the body. The initial trauma activates secondary degenerative processes that continue for days to weeks, causing further loss of neurons and glia and expanding the region of tissue damage. The protracted nature of secondary injury provides an opportunity to intervene and rescue cells that may otherwise undergo secondary cell death. Cells of the peripheral immune system, including T-lymphocytes reactive with myelin proteins, infiltrate the injured spinal cord and contribute to post-injury sequelae. These cells can cause demyelination and axonal transection in the CNS yet also produce neurotrophic factors that may promote neuronal survival after injury. To clarify the role of myelin-reactive T-cells in SCI, transgenic (Tg) mice with a T-cell repertoire biased toward recognition of myelin proteins, were evaluated for their ability to recover from spinal contusion injury. Recovery of overground locomotor ability and reflex function were significantly impaired in Tg mice compared with non-Tg littermates. Motor deficits were associated with reduced myelin sparing at the impact site and exacerbation of neuropathology over the rostro-caudal spinal cord. Because the kinetics and magnitude of the T-cell response to SCI differ between mice and rats, the myelin-reactive T-cell response to SCI in Lewis rats was boosted by immunization with myelin basic protein (MBP). Similar to Tg mice, immunized rats demonstrated enhanced functional deficits and exacerbated neuropathology. Interestingly, rats that were immunized with adjuvants in the absence of myelin antigen demonstrated enhanced recovery of hind limb function compared with PBS-treated controls. These results raise the possibility that other T-cells, responsive to an undefined constituent of the adjuvant confer benefit to the injured spinal cord. In conclusion, the data suggest that myelin-reactive T-cells that infiltrate the injured spinal cord contribute to secondary neurodegeneration and loss of function. However, T-cells of other antigen specificities, as yet undefined, could confer benefit in the injured spinal cord. Thus, effective neuroprotection may be achieved by limiting deleterious T-cell functions, for example by inhibiting the autoimmune response to SCI, while promoting reparative functions of T-cells in the environment of the injured spinal cord.

Published
2004

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