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3. Early activation of STAT3 regulates reactive astrogliosis induced by diverse forms of neurotoxicity.

Author

O'Callaghan, James P, Kelly, Kimberly A, VanGilder, Reyna L, Sofroniew, Michael V, and Miller, Diane B

Subjects
Brain, Hippocampus, Corpus Striatum, Astrocytes, Animals, Mice, Knockout, Mice, Rats, Gliosis, Aza Compounds, Glial Fibrillary Acidic Protein, Lipopolysaccharides, Nerve Tissue Proteins, Gene Expression Regulation, Up-Regulation, Gene Deletion, Models, Biological, Female, Male, STAT3 Transcription Factor, Janus Kinase 2, Heterocyclic Compounds, 4 or More Rings, Heterocyclic Compounds, or More Rings, Knockout, Models, Biological, General Science & Technology
Abstract

Astrogliosis, a cellular response characterized by astrocytic hypertrophy and accumulation of GFAP, is a hallmark of all types of central nervous system (CNS) injuries. Potential signaling mechanisms driving the conversion of astrocytes into "reactive" phenotypes differ with respect to the injury models employed and can be complicated by factors such as disruption of the blood-brain barrier (BBB). As denervation tools, neurotoxicants have the advantage of selective targeting of brain regions and cell types, often with sparing of the BBB. Previously, we found that neuroinflammation and activation of the JAK2-STAT3 pathway in astrocytes precedes up regulation of GFAP in the MPTP mouse model of dopaminergic neurotoxicity. Here we show that multiple mechanistically distinct mouse models of neurotoxicity (MPTP, AMP, METH, MDA, MDMA, KA, TMT) engender the same neuroinflammatory and STAT3 activation responses in specific regions of the brain targeted by each neurotoxicant. The STAT3 effects seen for TMT in the mouse could be generalized to the rat, demonstrating cross-species validity for STAT3 activation. Pharmacological antagonists of the neurotoxic effects blocked neuroinflammatory responses, pSTAT3tyr705 and GFAP induction, indicating that damage to neuronal targets instigated astrogliosis. Selective deletion of STAT3 from astrocytes in STAT3 conditional knockout mice markedly attenuated MPTP-induced astrogliosis. Monitoring STAT3 translocation in GFAP-positive cells indicated that effects of MPTP, METH and KA on pSTAT3tyr705 were localized to astrocytes. These findings strongly implicate the STAT3 pathway in astrocytes as a broadly triggered signaling pathway for astrogliosis. We also observed, however, that the acute neuroinflammatory response to the known inflammogen, LPS, can activate STAT3 in CNS tissue without inducing classical signs of astrogliosis. Thus, acute phase neuroinflammatory responses and neurotoxicity-induced astrogliosis both signal through STAT3 but appear to do so through different modules, perhaps localized to different cell types.

Published
2014

5. Brain organochlorines and Lewy pathology: The Honolulu‐Asia aging study

Author

Ross, G Webster, Duda, John E, Abbott, Robert D, Pellizzari, Edo, Petrovitch, Helen, Miller, Diane B, O'Callaghan, James P, Tanner, Caroline M, Noorigian, Joseph V, Masaki, Kamal, Launer, Lenore, and White, Lon R

Subjects
Neurodegenerative, Aging, Brain Disorders, Dementia, Neurosciences, Acquired Cognitive Impairment, Parkinson's Disease, Aetiology, 2.1 Biological and endogenous factors, Neurological, Aged, Aged, 80 and over, Asian, Brain, Cohort Studies, Hawaii, Humans, Hydrocarbons, Chlorinated, Lewy Bodies, Male, Clinical Sciences, Human Movement and Sports Sciences, Neurology & Neurosurgery
Abstract

Although organochlorines have been reported more frequently in Parkinson's disease (PD) brains than in controls, the association with brain Lewy pathology is unknown. Honolulu-Asia Aging Study (HAAS) participants, exposed to organochlorines from a variety of sources during midlife, represent a population well suited to determining the relationship of brain organochlorines with Lewy pathology in decedents from the longitudinal HAAS. The study design included the measurement of 21 organochlorine levels in frozen occipital lobe samples from HAAS decedents. Alpha-synuclein immunostaining performed on 225 brains was used to identify Lewy bodies and Lewy neurites. With the potential for spurious associations to appear between Lewy pathology and 17 organochlorine compounds found in at least 1 brain, initial assessments identified heptachlor epoxide isomer b, methoxychlor, and benzene hexachloride b as being most important. The prevalence of Lewy pathology was 75% (6 of 8) among brains with any 2 of the 3 compounds, 48.8% (79 of 162) among those with 1, and 32.7% (18 of 55) for those with neither (P = .007 test for trend). Although findings persisted after removing cases with PD and dementia with Lewy bodies and after adjustment for age at death, body mass index, pack-years of cigarette smoking, and coffee intake (P = .013), the results were insignificant when correcting for multiple testing. Although consistent with earlier accounts of an association between organochlorines and clinical PD, associations with Lewy pathology warrant further study.

Published
2012

29. Mild steel welding fume causes manganese accumulation and subtle neuroinflammatory changes but not overt neuronal damage in discrete brain regions of rats after short-term inhalation exposure

Author

Antonini, James M., Sriram, Krishnan, Benkovic, Stanley A., Roberts, Jenny R., Stone, Samuel, Chen, Bean T., Schwegler-Berry, Diane, Jefferson, Amy M., Billig, Brenda K., Felton, Christopher M., Hammer, Mary Ann, Ma, Fang, Frazer, David G., O’Callaghan, James P., and Miller, Diane B.

Published
2009
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33. NeuroAIDS, Drug Abuse, and Inflammation: Building Collaborative Research Activities

Author

Berman, Joan W., Carson, Monica J., Chang, Linda, Cox, Brian M., Fox, Howard S., Gonzalez, R. Gilberto, Hanson, Glen R., Hauser, Kurt F., Ho, Wen-Zhe, Hong, Jau-Shyong, Major, Eugene O., Maragos, William F., Masliah, Eliezer, McArthur, Justin C., Miller, Diane B., Nath, Avindra, O’Callaghan, James P., Persidsky, Yuri, Power, Christopher, Rogers, Thomas J., and Royal, III, Walter

Published
2006
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34. Work, obesity, and occupational safety and health

Author

Schulte, Paul A., Wagner, Gregory R., Ostry, Aleck, Blanciforti, Laura A., Cutlip, Robert G., Krajnak, Kristine M., Luster, Michael, Munson, Albert E., O'Callaghan, James P., Parks, Christine G., Simeonova, Petia P., and Miller, Diane B.

Subjects
Obesity -- Health aspects, Workers -- Health aspects, Occupational health and safety, Work environment, Government, Health care industry
Abstract

There is increasing evidence that obesity and overweight may be related, in part, to adverse work conditions. In particular, the risk of obesity may increase in high-demand, low-control work environments, and for those who work Iong hours. In addition, obesity may modify the risk for vibration-induced injury and certain occupational musculoskeletal disorders. We hypothesized that obesity may also be a co-risk factor for the developmentof occupational asthma and cardiovascular disease that and it may modify the worker's response to occupational stress, immune response to chemical exposures, and risk of disease from occupational neurotoxins. We developed 5 conceptual models of the interrelationship of work, obesity, and occupational safety and health and highlighted the ethical, legal, and social issues related to fuller considerationof obesity's role in occupational health and safety. doi: 10.2105/AJ PH.2006.086900

Published
2007

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