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153. Posttraumatic stress disorder

Author

Conn, P M, Wynn, Gary, Benedek, David, Johnson, Luke, Choi, Kwang, Zhang, Lei, Hu, X.-Z., Pollard, Harvey, Ursano, Robert, Conn, P M, Wynn, Gary, Benedek, David, Johnson, Luke, Choi, Kwang, Zhang, Lei, Hu, X.-Z., Pollard, Harvey, and Ursano, Robert

Abstract

This chapter provides an overview of the most up-to-date understanding of the neuroscience of posttraumatic stress disorder (PTSD). A variety of topics are covered throughout this chapter in a systematic fashion with the goal that each section can be read and understood as a stand-alone piece of a greater whole. The first section presents an overview of the neurobiology of traumatic stress from receptors to structural brain changes. After this general overview, a discussion of the various animal models of PTSD is provided. These models include fear conditioning, fear-potentiated startle, and models of unpredictable stress. This review of animal models is then followed by a discussion of biomarkers, PTSD and somatic health, neuroimaging, and treatment. Following these in-depth topics, this chapter provides some possible avenues for future research including exploration of the neuroscience of sleep and PTSD or through new technologies such as magnetoencephalography.

Published
2017

154. Defects in inositol 1,4,5-trisphosphate receptor expression, [Ca.sup.2+] signaling, and insulin secretion in the anx7(+/-) knockout mouse

Author

Srivastava, Meera, Atwater, Illani, Glasman, Mirta, Leighton, Ximena, Goping, Gertrude, Caohuy, Hung, Miller, Georgina, Pichel, Jose, Westphal, Heiner, Mears, David, Rojas, Eduardo, and Pollard, Harvey B.

Subjects
Mammals -- Genetic aspects, Pancreatic beta cells -- Research, Pancreas -- Secretions, Science and technology
Abstract

The mammalian anx7 gene codes for a [Ca.sup.2+]-activated GTPase, which supports [Ca.sup.2+]/GTP-dependent secretion events and [Ca.sup.2+] channel activities in vitro and in vivo. To test whether anx7 might be involved in [Ca.sup.2+] signaling in secreting pancreatic [Beta] cells, we knocked out the anx7 gene in the mouse and tested the insulin-secretory properties of the [Beta] cells. The nullizygous anx7 (-/-) phenotype is lethal at embryonic day 10 because of cerebral hemorrhage. However, the heterozygous anx7 (+/-) mouse, although expressing only low levels of ANX7 protein, is viable and fertile. The anx7 (+/-) phenotype is associated with a substantial defect in insulin secretion, although the insulin content of the islets, is 8- to 10-fold higher in the mutants than in the normal littermate control. We infer from electrophysiological studies that both glucose-stimulated secretion and voltage-dependent [Ca.sup.2+] channel functions are normal. However, electrooptical recordings indicate that the (+/-) mutation has caused a change in the ability of inositol 1,4,5-trisphosphate ([IP.sub.3])-generating agonists to release intracellular calcium. The principle molecular consequence of lower anx7 expression is a profound reduction in [IP.sub.3] receptor expression and function in pancreatic islets. The profound increase in islets, [Beta] cell number, and size may be a means of compensating for less efficient insulin secretion by individual defective pancreatic [Beta] cells. This is a direct demonstration of a connection between glucose-activated insulin secretion and [Ca.sup.2+] signaling through [IP.sub.3]-sensitive [Ca.sup.2+] stores.

Published
1999

166. Pharmacological Ascorbic Acid Suppresses Syngeneic Tumor Growth and Metastases in Hormone-refractory Prostate Cancer

Author

POLLARD, HARVEY B., LEVINE, MARK A., EIDELMAN, OFER, and POLLARD, MORRIS

Subjects
Male, Lung Neoplasms, Body Weight, Prostatic Neoplasms, Ascorbic Acid, Adenocarcinoma, Article, Antioxidants, Rats, ROC Curve, Lymphatic Metastasis, Animals, Intercellular Signaling Peptides and Proteins, Rats, Wistar, Neoplasm Transplantation
Abstract

AIM: The aim of this study was to test for the influence of ascorbic acid on tumorigenicity and metastases of implanted PAIII prostate cancer adenocarcinoma cells in syngeneic LW rats. MATERIALS AND METHODS: Hormone-refractory prostate cancer PAIII cells were implanted subcutaneously into immunologically intact, Lobund-Wistar (LW) rats. Intraperitoneal pharmacological doses of ascorbic acid were administered each day for the ensuing 30 days. On the 40th day, animals were sacrificed. Local tumor weights were measured, and metastases were counted. RESULTS: At the end of the 40 day experimental period, the primary tumors were found to be significantly reduced in weight (p=0.026). In addition, sub-pleural lung metastases were even more profoundly reduced in number and size (p=0.009). Grossly enlarged ipsilateral lymph node metastases declined from 7 of 15 rats to 1 of 15 rats. CONCLUSION: Pharmacological doses of ascorbic acid suppress tumor growth and metastases in hormone-refractory prostate cancer.

Published
2010

167. Chemical Rescue of ΔF508-CFTR Mimics Genetic Repair in Cystic Fibrosis Bronchial Epithelial Cells*S⃞

Author

Singh, Om V., Pollard, Harvey B., and Zeitlin, Pamela L.

Subjects
Inflammation, Research, Cell Membrane, Computational Biology, Cystic Fibrosis Transmembrane Conductance Regulator, Biological Transport, Bronchi, Epithelial Cells, Genetic Therapy, Endoplasmic Reticulum, Cytosol, Gene Expression Regulation, Mutation, Humans, Endoplasmic Reticulum Chaperone BiP, Molecular Chaperones, Subcellular Fractions
Abstract

In a previous study of sodium 4-phenylbutyrate (4-PBA)-responsive proteins in cystic fibrosis (CF) IB3-1 bronchial epithelial cells, we identified 85 differentially expressed high abundance proteins from whole cellular lysate (Singh, O. V., Vij, N., Mogayzel, P. J., Jr., Jozwik, C., Pollard, H. B., and Zeitlin, P. L. (2006) Pharmacoproteomics of 4-phenylbutyrate-treated IB3-1 cystic fibrosis bronchial epithelial cells. J. Proteome Res. 5, 562-571). In the present work we hypothesize that a subset of heat shock proteins that interact with cystic fibrosis transmembrane conductance regulator (CFTR) in common during chemical rescue and genetic repair will identify therapeutic networks for targeted intervention. Immunocomplexes were generated from total cellular lysates, and three subcellular fractions (endoplasmic reticulum (ER), cytosol, and plasma membrane) with anti-CFTR polyclonal antibody from CF (IB3-1), chemically rescued CF (4-PBA-treated IB3-1), and genetically repaired CF (IB3-1/S9 daughter cells repaired by gene transfer with adeno-associated virus-(wild type) CFTR). CFTR-interacting proteins were analyzed on two-dimensional gels and identified by mass spectrometry. A set of 16 proteins known to act in ER-associated degradation were regulated in common and functionally connected to the protein processing, protein folding, and inflammatory response. Some of these proteins were modulated exclusively in ER, cytosol, or plasma membrane. A subset of 4-PBA-modulated ER-associated degradation chaperones (GRP94, HSP84, GRP78, GRP75, and GRP58) was observed to associate with the immature B form of CFTR in ER. HSP70 and HSC70 interacted with the C band (mature form) of CFTR at the cell surface. We conclude that chemically rescued CFTR associates with a specific set of HSP70 family proteins that mark therapeutic interactions and can be useful to correct both ion transport and inflammatory phenotypes in CF subjects.

Published
2008

182. Glucose-6-phosphate Reduces Calcium Accumulation in Rat Brain Endoplasmic Reticulum

Author

UNIFORMED SERVICES UNIV OF THE HEALTH SCIENCES BETHESDA MD, Cole, Jeffrey T, Kean, William S, Pollard, Harvey B, Verma, Ajay, Watson, William D, UNIFORMED SERVICES UNIV OF THE HEALTH SCIENCES BETHESDA MD, Cole, Jeffrey T, Kean, William S, Pollard, Harvey B, Verma, Ajay, and Watson, William D

Abstract

Brain cells expend large amounts of energy sequestering calcium (Ca2+), while loss of Ca2+ compartmentalization leads to cell damage or death. Upon cell entry, glucose is converted to glucose-6-phosphate (G6P), a parent substrate to several metabolic major pathways, including glycolysis. In several tissues, G6P alters the ability of the endoplasmic reticulum (ER) to sequester Ca2+. This led to the hypothesis that G6P regulates Ca2+ accumulation by acting as an endogenous ligand for sarco-endoplasmic reticulum calcium ATPase(SERCA).Whole brain ER microsomes were pooled from adult male Sprague-Dawley rats. Using radio-isotopic assays, 45Ca2+ accumulation was quantified following incubation with increasing amounts of G6P, in the presence or absence of thapsigargin, a potent SERCA inhibitor. To qualitatively assess SERCA activity, the simultaneous release of inorganic phosphate (Pi) coupled with Ca2+ accumulation was quantified. Addition of G6P significantly and decreased Ca2+ accumulation in a dose-dependent fashion (1 10mM). The reduction in Ca2+ accumulation was not significantly different that seen with addition of thapsigargin. Addition of glucose-1-phosphate or fructose-6-phosphate, or other glucose metabolic pathway intermediates, had no effect on Ca2+ accumulation. Further, the release ofPi wasmarkedly decreased, indicatingG6P-mediatedSERCAinhibition as the responsible mechanism for reduced Ca2+ uptake. Simultaneous addition of thapsigargin and G6P did decrease inorganic phosphate in comparison to either treatment alone, which suggests that the two treatments have different mechanisms of action. Therefore, G6P may be a novel, endogenous regulator of SERCA activity. Additionally, pathological conditions observed during disease states that disrupt glucose homeostasis, may be attributable to Ca2+ dystasis caused by altered G6P regulation of SERCA activity., Pub. in Frontiers in MOLECULAR NEUROSCIENCE, v5 n51, p1-8, 20 April 2012. The original document contains color images.

Published
2012

184. CFTR Controls the Activity of NF-κB by Enhancing the Degradation of TRADD.

Author

Hua Wang, Cebotaru, Liudmila, Ha Won Lee, QingFeng Yang, Pollard, Bette S., Pollard, Harvey B., and Guggino, William B.

Subjects
CYSTIC fibrosis transmembrane conductance regulator, INFLAMMATION, TUMOR necrosis factors, GENE transfection, MOLECULAR biology
Abstract

Background/Aims: Chronic lung infection in cystic fibrosis leads to an inflammatory response that persists because of the chronic presence of bacteria and ultimately leads to a catastrophic failure of lung function. Methods: We use a combination of biochemistry, cell and molecular biology to study the interaction of TRADD, a key adaptor molecule in TNFα signaling, with CFTR in the regulation of NFκB. Results: We show that Wt CFTR binds to and colocalizes with TRADD. TRADD is a key signaling intermediate connecting TNFα with activation of NFκB. By contrast, ΔF508 CFTR does not bind to TRADD. NF-κB activation is higher in CFBE expressing ΔF508 CFTR than in cells expressing Wt CFTR. However, this differential effect is abolished when TRADD levels are knocked down. Transfecting Wt CFTR into CFBE cells reduces NF-κB activity. However the reduction is abolished by the CFTR chloride transport inhibitor-172. Consistently, transfecting in the correctly trafficked CFTR conduction mutants G551D or S341A also fail to reduce NFκB activity. Thus CFTR must be functional if it is to regulate NF-κB activity. We also found that TNFα produced a greater increase in NF-κB activity in CFBE cells than in the same cell when Wt CFTR-corrected. Consistently, the effect is also abolished when TRADD is knocked down by shRNA. Thus, Wt CFTR control of TRADD modulates the physiological activation of NF-κB by TNFα. Based on studies with proteosomal and lysosomal inhibitors, the mechanism by which Wt CFTR, but not ΔF508 CFTR, suppresses TRADD is by lysosomal degradation. Conclusion: We have uncovered a novel mechanism whereby Wt CFTR regulates TNFα signaling by enhancing TRADD degradation. Thus by reducing the levels of TRADD, Wt CFTR suppresses downstream proinflammatory NFκB signaling. By contrast, suppression of NF-κB activation fails in CF cells expressing ΔF508 CFTR. [ABSTRACT FROM AUTHOR]

Published
2016
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185. “Soldier’s Heart”: A Genetic Basis for Elevated Cardiovascular Disease Risk Associated with Post-traumatic Stress Disorder.

Author

Starr, Joshua, Eidelman, Ofer, Srivastava, Meera, Pollard, Harvey B., Dalgard, Clifton L., Shivakumar, Chittari, Jacobowitz, David M., Wilkerson, Matthew D., Stein, Murray B., and Ursano, Robert J.

Subjects
POST-traumatic stress disorder, CARDIOVASCULAR diseases risk factors, TYPE 2 diabetes, GENETICS
Abstract

“Soldier’s Heart,” is an American Civil War term linking post-traumatic stress disorder (PTSD) with increased propensity for cardiovascular disease (CVD). We have hypothesized that there might be a quantifiable genetic basis for this linkage. To test this hypothesis we identified a comprehensive set of candidate risk genes for PTSD, and tested whether any were also independent risk genes for CVD. A functional analysis algorithm was used to identify associated signaling networks. We identified 106 PTSD studies that report one or more polymorphic variants in 87 candidate genes in 83,463 subjects and controls. The top upstream drivers for these PTSD risk genes are predicted to be the glucocorticoid receptor (NR3C1) and Tumor Necrosis Factor alpha (TNFA). We find that 37 of the PTSD candidate risk genes are also candidate independent risk genes for CVD. The association between PTSD and CVD is significant by Fisher’s Exact Test (P = 3 × 10−54).We also find 15 PTSD risk genes that are independently associated with Type 2 Diabetes Mellitus (T2DM; also significant by Fisher’s Exact Test (P = 1.8 × 10−16). Our findings offer quantitative evidence for a genetic link between post-traumatic stress and cardiovascular disease, Computationally, the common mechanism for this linkage between PTSD and CVD is innate immunity and NFkB-mediated inflammation. [ABSTRACT FROM AUTHOR]

Published
2016
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190. Curcumin Treatment Suppresses IKKβ Kinase Activity of Salivary Cells of Patients with Head and Neck Cancer: A Pilot Study

Author

Kim, Suejung G., primary, Veena, Mysore S., additional, Basak, Saroj K., additional, Han, Eugene, additional, Tajima, Tracey, additional, Gjertson, David W., additional, Starr, Joshua, additional, Eidelman, Ofer, additional, Pollard, Harvey B., additional, Srivastava, Meera, additional, Srivatsan, Eri S., additional, and Wang, Marilene B., additional

Published
2011
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194. Craniotomy: True Sham for Traumatic Brain Injury, or a Sham of a Sham?

Author

Cole, Jeffrey T., primary, Yarnell, Angela, additional, Kean, William S., additional, Gold, Eric, additional, Lewis, Bobbi, additional, Ren, Ming, additional, McMullen, David C., additional, Jacobowitz, David M., additional, Pollard, Harvey B., additional, O'Neill, J. Timothy, additional, Grunberg, Neil E., additional, Dalgard, Clifton L., additional, Frank, Joseph A., additional, and Watson, William D., additional

Published
2011
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198. Gender Dependence for a Subset of the Low-Abundance Signaling Proteome in Human Platelets

Author

Eidelman, Ofer, primary, Jozwik, Catherine, additional, Huang, Wei, additional, Srivastava, Meera, additional, Rothwell, Stephen W., additional, Jacobowitz, David M., additional, Ji, Xiaoduo, additional, Zhang, Xiuying, additional, Guggino, William, additional, Wright, Jerry, additional, Kiefer, Jeffrey, additional, Olsen, Cara, additional, Adimi, Nima, additional, Mueller, Gregory P., additional, and Pollard, Harvey B., additional

Published
2010
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