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Journal articles on the topic 'Adenoviral; Nervous system; Central'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

Parks, Robin J., and Jonathan L. Bramson. "Adenoviral vectors: prospects for gene delivery to the central nervous system." Gene Therapy 6, no. 8 (1999): 1349–50. http://dx.doi.org/10.1038/sj.gt.3301013.

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Davidson, Beverly L., Edward D. Allen, Karen F. Kozarsky, James M. Wilson, and Blake J. Roessler. "A model system for in vivo gene transfer into the central nervous system using an adenoviral vector." Nature Genetics 3, no. 3 (1993): 219–23. http://dx.doi.org/10.1038/ng0393-219.

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3

Schwartz, Kevin L., Susan E. Richardson, Daune MacGregor, Sanjay Mahant, Kamini Raghuram, and Ari Bitnun. "Adenovirus-Associated Central Nervous System Disease in Children." Journal of Pediatrics 205 (February 2019): 130–37. http://dx.doi.org/10.1016/j.jpeds.2018.09.036.

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4

Zou, Linglong, Heshan Zhou, Lucio Pastore, and Keyi Yang. "Prolonged Transgene Expression Mediated by a Helper-Dependent Adenoviral Vector (hdAd) in the Central Nervous System." Molecular Therapy 2, no. 2 (2000): 105–13. http://dx.doi.org/10.1006/mthe.2000.0104.

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Vincent, Arnaud J. P. E., Maria del C. Esandi, Cees J. J. Avezaat, et al. "Preclinical Testing of Recombinant Adenoviral Herpes Simplex Virus-Thymidine Kinase Gene Therapy for Central Nervous System Malignancies." Neurosurgery 41, no. 2 (1997): 442–52. http://dx.doi.org/10.1097/00006123-199708000-00023.

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6

Betz, A. Lorris, Guo-Yuan Yang, and Beverly L. Davidson. "Attenuation of Stroke Size in Rats Using an Adenoviral Vector to Induce Overexpression of Interleukin-1 Receptor Antagonist in Brain." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (1995): 547–51. http://dx.doi.org/10.1038/jcbfm.1995.68.

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Adenoviruses have been proposed as potential vectors for gene therapy in the central nervous system, but there are no reports of their use in the treatment of a brain disease. Because central administration of interleukin-1 receptor antagonist protein (IL-1ra) reduces ischemic brain damage, we determined whether a recombinant adenovirus vector carrying the human IL-1ra cDNA (Ad.RSV IL-1ra) could be used to ameliorate brain injury in permanent focal ischemia. Groups of six rats received intraventricular injections of Ad.RSV IL-1ra or a control adenovirus containing the Escherichia coli β-galactosidase gene (Ad.RSV lacZ). Histochemical staining for β-galactosidase 5 days after virus injection indicated that transgene expression was confined primarily to the cells lining the ventricle. The concentrations of IL-1ra were fivefold to 50-fold higher in the Ad.RSV IL-1ra-injected animals, achieving levels of 9.1 ± 3.3 ng/g in brain and 23.7 ± 22.5 ng/ml in CSF. In these animals, cerebral infarct volume resulting from 24 h of permanent middle cerebral artery occlusion was reduced 64%. These studies demonstrate that adenoviral vectors can be used to deliver genes that attenuate brain injury.

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Shen, J.-S., X.-L. Meng, T. Ohashi, and Y. Eto. "Adenovirus-mediated prenatal gene transfer to murine central nervous system." Gene Therapy 9, no. 12 (2002): 819–23. http://dx.doi.org/10.1038/sj.gt.3301700.

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Huang, Yhu-Chering, Sun-Lin Huang, Shih-Perng Chen, et al. "Adenovirus infection associated with central nervous system dysfunction in children." Journal of Clinical Virology 57, no. 4 (2013): 300–304. http://dx.doi.org/10.1016/j.jcv.2013.03.017.

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Viola, John J., Zvi Ram, Stuart Walbridge, et al. "Adenovirally mediated gene transfer into experimental solid brain tumors and leptomeningeal cancer cells." Journal of Neurosurgery 82, no. 1 (1995): 70–76. http://dx.doi.org/10.3171/jns.1995.82.1.0070.

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✓ Among the appealing features of adenoviruses as vectors for transfer of genes into the central nervous system (CNS) are that they are not neurotoxic, they can accommodate the insertion of several large genes, they are not associated with the hazards of insertional mutagenesis, and they can be concentrated to a high-titer preparation. The authors evaluated the feasibility of using adenovirally mediated gene transfer into cultured human glioma cells and in rat models of solid brain tumors and meningeal cancer. Replication-deficient adenoviral vector particles carrying a nuclear-localizing lacZ gene were injected into established 9L cerebral gliomas in Fischer rats. In addition, the adenoviral vector was injected into the subarachnoid space, either simultaneously with intrathecal tumor inoculation or after establishing leptomeningeal cancer. The brains and spinal cords were removed at various intervals for histochemical evaluation for β-galactosidase activity using X-Gal staining. Additional rats received a stereotactic intracerebral injection of the vector into normal brain. No clinical abnormalities were observed in the injected rats. Injection of the adenoviral vector into normal brain resulted in diffuse transduction of astrocytes, microglia, neurons, and endothelial cells at the injection site. Injection of a high-concentration vector preparation into cerebral gliomas resulted in effective tumor transduction. Intrathecal injection of the vector in rats with meningeal cancer resulted in transduction of the infiltrating tumor in the subarachnoid space when injections were given simultaneously with, or 7 days after, tumor inoculation. Transduction rates of both solid and leptomeningeal tumors correlated with the number of injected particles. These results suggest that adenoviral vectors can efficiently transduce solid brain tumors and that the vectors survive in the cerebrospinal fluid for a sufficient period of time to allow leptomeningeal tumor transduction. Adenoviral vector should be evaluated for its potential use in therapeutic gene transfer approaches in malignancies of the CNS.

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Boulis, Nicholas M., Vikas Bhatia, Theodore I. Brindle та ін. "Adenoviral nerve growth factor and β-galactosidase transfer to spinal cord: a behavioral and histological analysis". Journal of Neurosurgery: Spine 90, № 1 (1999): 99–108. http://dx.doi.org/10.3171/spi.1999.90.1.0099.

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Object. The present study characterizes the time course and loci of gene expression induced by the administration of adenoviral vectors into spinal cord. Although a marked inflammatory response to these vectors occurred, no effect on spinal cord function was seen in the 1st postoperative week. The expression of transgenic genes delivered by viral vectors is being exploited throughout the nervous system. The present study utilized adenoviral vectors containing the Rous sarcoma virus (RSV) promoter and a nuclear localization signal to achieve transgenic expression in mammalian spinal cord. Methods. Initial experiments utilizing the vector Ad.RSVlacZ (1012 particles/ml) injected into the region of the central canal resulted in viral gene expression stretching over approximately 1.2 cm of spinal cord. Gene expression was first detected 3 days following viral administration and lasted until postinjection Day 14 with peak expression at Day 7. A variety of cell types in both white and gray matter expressed lacZ. Transgenic expression of the neurotrophin nerve growth factor (NGF) was achieved using injections of Ad.RSVNGF. On histological examination mononuclear inflammatory infiltrate and gliosis were revealed surrounding the injection sites of spinal cords receiving adenovirus but not vehicle. To assess spinal cord function during viral gene expression, animals previously trained in an operant runway task were tested at 7 days postinjection (the peak of viral gene expression) and demonstrated no changes in spinal cord function. Conclusions. Results of this study using adenoviral neurotrophic gene transfer indicate that it provided an effective tool for the delivery of potentially therapeutic proteins to the injured or diseased spinal cord.

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Lewis, Travis, Joel Glasgow, Ashley Harms, David Standaert, and David Curiel. "Fiber-Modified Adenovirus for Central Nervous System Parkinson’s Disease Gene Therapy." Viruses 6, no. 8 (2014): 3293–310. http://dx.doi.org/10.3390/v6083293.

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Chen, X., X. Zhao, Y. Hu, et al. "The spread of adenoviral vectors to central nervous system through pathway of cochlea in mimetic aging and young rats." Gene Therapy 22, no. 11 (2015): 866–75. http://dx.doi.org/10.1038/gt.2015.63.

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Plumb, Troy J., Assumpció Bosch, Blake J. Roessler, Donna S. Shewach, and Beverly L. Davidson. "Hypoxanthine-guanine phosphoribosyltransferase (HPRT) expression in the central nervous system of HPRT-deficient mice following adenoviral-mediated gene transfer." Neuroscience Letters 214, no. 2-3 (1996): 159–62. http://dx.doi.org/10.1016/0304-3940(96)12932-3.

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14

Lemiale, Franck, Wing-pui Kong, Levent M. Akyürek, et al. "Enhanced Mucosal Immunoglobulin A Response of Intranasal Adenoviral Vector Human Immunodeficiency Virus Vaccine and Localization in the Central Nervous System." Journal of Virology 77, no. 18 (2003): 10078–87. http://dx.doi.org/10.1128/jvi.77.18.10078-10087.2003.

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ABSTRACT Replication-defective adenovirus (ADV) vectors represent a promising potential platform for the development of a vaccine for AIDS. Although this vector is typically administered intramuscularly, it would be desirable to induce mucosal immunity by delivery through alternative routes. In this study, the immune response and biodistribution of ADV vectors delivered by different routes were evaluated. ADV vectors expressing human immunodeficiency virus type 1 (HIV-1) Gag, Pol, and Env were delivered intramuscularly or intranasally into mice. Intranasal immunization induced greater HIV-specific immunoglobulin A (IgA) responses in mucosal secretions and sera than in animals with intramuscular injection, which showed stronger systemic cellular and IgG responses. Administration of the vaccine through an intranasal route failed to overcome prior ADV immunity. Animals exposed to ADV prior to vaccination displayed substantially reduced cellular and humoral immune responses to HIV antigens in both groups, though the reduction was greater in animals immunized intranasally. This inhibition was partially overcome by priming with a DNA expression vector expressing HIV-1 Gag, Pol, and Env before boosting with the viral vector. Biodistribution of recombinant adenovirus (rADV) vectors administered intranasally revealed infection of the central nervous system, specifically in the olfactory bulb, possibly via retrograde transport by olfactory neurons in the nasal epithelium, which may limit the utility of this route of delivery of ADV vector-based vaccines.

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Frange, Pierre, Régis Peffault de Latour, Cécile Arnaud, et al. "Adenoviral Infection Presenting as an Isolated Central Nervous System Disease without Detectable Viremia in Two Children after Stem Cell Transplantation." Journal of Clinical Microbiology 49, no. 6 (2011): 2361–64. http://dx.doi.org/10.1128/jcm.00080-11.

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16

Horellou, Philippe, Olivier Sabaté, Marie-Hélène Buc-Caron, and Jacques Mallet. "Adenovirus-Mediated Gene Transfer to the Central Nervous System for Parkinson's Disease." Experimental Neurology 144, no. 1 (1997): 131–38. http://dx.doi.org/10.1006/exnr.1996.6399.

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17

Blits, Bas, Gerard J. Boer, and Joost Verhaagen. "Pharmacological, Cell, and Gene Therapy Strategies to Promote Spinal Cord Regeneration." Cell Transplantation 11, no. 6 (2002): 593–613. http://dx.doi.org/10.3727/000000002783985521.

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In this review, recent studies using pharmacological treatment, cell transplantation, and gene therapy to promote regeneration of the injured spinal cord in animal models will be summarized. Pharmacological and cell transplantation treatments generally revealed some degree of effect on the regeneration of the injured ascending and descending tracts, but further improvements to achieve a more significant functional recovery are necessary. The use of gene therapy to promote repair of the injured nervous system is a relatively new concept. It is based on the development of methods for delivering therapeutic genes to neurons, glia cells, or nonneural cells. Direct in vivo gene transfer or gene transfer in combination with (neuro)transplantation (ex vivo gene transfer) appeared powerful strategies to promote neuronal survival and axonal regrowth following traumatic injury to the central nervous system. Recent advances in understanding the cellular and molecular mechanisms that govern neuronal survival and neurite outgrowth have enabled the design of experiments aimed at viral vector-mediated transfer of genes encoding neurotrophic factors, growth-associated proteins, cell adhesion molecules, and antiapoptotic genes. Central to the success of these approaches was the development of efficient, nontoxic vectors for gene delivery and the acquirement of the appropriate (genetically modified) cells for neurotransplantation. Direct gene transfer in the nervous system was first achieved with herpes viral and E1-deleted adenoviral vectors. Both vector systems are problematic in that these vectors elicit immunogenic and cytotoxic responses. Adeno-associated viral vectors and lentiviral vectors constitute improved gene delivery systems and are beginning to be applied in neuroregeneration research of the spinal cord. Ex vivo approaches were initially based on the implantation of genetically modified fibroblasts. More recently, transduced Schwann cells, genetically modified pieces of peripheral nerve, and olfactory ensheathing glia have been used as implants into the injured spinal cord.

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Chillon, Miguel, Assumpció Bosch, Joseph Zabner, et al. "Group D Adenoviruses Infect Primary Central Nervous System Cells More Efficiently than Those from Group C." Journal of Virology 73, no. 3 (1999): 2537–40. http://dx.doi.org/10.1128/jvi.73.3.2537-2540.1999.

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ABSTRACT Group C adenovirus-mediated gene transfer to central nervous system cells is inefficient. We found that wild-type group D viruses, or recombinant adenovirus type 2 (Ad2) (group C) modified to contain Ad17 (group D) fiber, were more efficient in infecting primary cultures of neurons. Together with studies on primary vascular endothelial cells and tissue culture cell lines, our results indicate that there is not a universally applicable adenovirus serotype for use as a gene transfer vector.

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Blits, Bas, Paul A. Dijkhuizen, Thomas P. Carlstedt, et al. "Adenoviral Vector-Mediated Expression of a Foreign Gene in Peripheral Nerve Tissue Bridges Implanted in the Injured Peripheral and Central Nervous System." Experimental Neurology 160, no. 1 (1999): 256–67. http://dx.doi.org/10.1006/exnr.1999.7204.

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20

Zheng, Hong, Keshore R. Bidasee, William G. Mayhan, and Kaushik P. Patel. "Lack of central nitric oxide triggers erectile dysfunction in diabetes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 3 (2007): R1158—R1164. http://dx.doi.org/10.1152/ajpregu.00429.2006.

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Erectile dysfunction is a serious and common complication of diabetes mellitus. The proposed mechanisms for erectile dysfunction in diabetes include central and autonomic neuropathy, endothelial dysfunction, and smooth muscle dysfunction. The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in centrally mediated penile erection. This study was designed to examine the role of nitric oxide (NO) within the central nervous system component of the behavioral responses including erection in diabetic rats. N-methyl-d-aspartic acid (NMDA)-induced erection, yawning, and stretch through the PVN can be blocked by prior administration of NO synthase (NOS) blocker, l-NMMA, in freely moving, conscious male normal rats. Four weeks after streptozotocin (STZ) and vehicle injections, NMDA-induced erection, yawning, and stretch responses through the PVN are significantly blunted in diabetic rats compared with control rats. Examination of neuronal NOS (nNOS) protein by Western blot analysis indicated a reduced amount of nNOS protein in the PVN of rats with diabetes compared with control rats. Furthermore, restoring nNOS within the PVN by gene transfer using adenoviral transfection significantly restored the erectile and yawning responses to NMDA in diabetic rats. These data demonstrate that a blunted NO mechanism within the PVN may contribute to NMDA-induced erectile dysfunction observed in diabetes mellitus.

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Persson, Annette, Xiaolong Fan, Bengt Widegren, and Elisabet Englund. "Cell type- and region- dependent coxsackie adenovirus receptor expression in the central nervous system." Journal of Neuro-Oncology 78, no. 1 (2005): 1–6. http://dx.doi.org/10.1007/s11060-005-9055-3.

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Broder, Howard, Andrea Anderson, Sylvia K. Odesa, Thomas J. Kremen, and Linda M. Liau. "Recombinant adenovirus-transduced dendritic cell immunization in a murine model of central nervous system tumor." Neurosurgical Focus 9, no. 6 (2000): 1–8. http://dx.doi.org/10.3171/foc.2000.9.6.7.

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Object Dendritic cells (DCs) are potent antigen-presenting cells that have been shown to play a critical role in the initiation of host immune responses against tumor antigens. In this study, a recombinant adenovirus vector encoding the melanoma-associated antigen, MART-1, was used to transduce murine DCs, which were then tested for their ability to activate cytotoxic T lymphocytes (CTLs) and induce protective immunity against B16 melanoma tumor cells implanted intracranially. Methods Genetic modification of murine bone marrrow–derived DCs to express MART-1 was achieved through the use of an E1-deficient, recombinant adenovirus vector (AdVMART1). Sixty-two C57BL/6 mice were immunized by subcutaneous injection of AdVMART-1-transduced DCs (23 mice), untransduced DCs (17 mice), or sterile saline (22 mice). Using the B16 murine melanoma, which naturally expresses the MART-1 antigen, all the mice were then challenged intracranially with viable, unmodified syngeneic B16 tumor cells 7 days later. Splenocytes obtained from representative animals in each group were harvested for standard cytotoxicity and enzyme-linked immunospot assays. The remaining mice were followed for survival. Immunization of C57BL/6 mice with DCs transduced with AdVMART1-DC elicited the development of antigen-specific CTL responses. As evidenced by a prolonged survival curve when compared with control-immunized mice harboring intracranial B16 tumors, AdMART1-DC vaccination was able to elicit partial protection against central nervous system (CNS) tumor challenge in vivo. However, this CNS antitumor immunity was weaker than that previously demonstrated against subcutaneous B16 tumors in which the same vaccination strategy was used. Conclusions These data suggest that immune responses generated against CNS tumors by DC-based vaccines may be different from those obtained against subcutaneous tumors.

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Ghodsi, Abdi, Colleen Stein, Todd Derksen, Gongyu Yang, Richard D. Anderson та Beverly L. Davidson. "Extensiveβ-Glucuronidase Activity in Murine Central Nervous System after Adenovirus-Mediated Gene Transfer to Brain". Human Gene Therapy 9, № 16 (1998): 2331–40. http://dx.doi.org/10.1089/hum.1998.9.16-2331.

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Stein, Colleen S., Abdi Ghodsi, Todd Derksen, and Beverly L. Davidson. "Systemic and Central Nervous System Correction of Lysosomal Storage in Mucopolysaccharidosis Type VII Mice." Journal of Virology 73, no. 4 (1999): 3424–29. http://dx.doi.org/10.1128/jvi.73.4.3424-3429.1999.

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ABSTRACT Mucopolysaccharidosis (MPS) type VII patients lack functional β-glucuronidase, leading to systemic and central nervous system dysfunction. In this study we tested whether recombinant adenovirus that encodes β-glucuronidase (Adβgluc), delivered intravenously and into the brain parenchyma of MPS type VII mice, could provide long-term transgene expression and correction of lysosomal distension. We also tested whether systemic treatment with the immunosuppressive anti-CD40 ligand antibody, MR-1, affected transgene expression. We found substantial plasma β-glucuronidase activity for over 9 weeks after gene transfer in the MR-1- treated group, with subsequent decline in activity corresponding to a delayed anti-β-glucuronidase antibody response. At 16 weeks, near wild-type amounts of β-glucuronidase activity and striking reduction of lysosomal pathology were detected in livers from mice that had received either MR-1 cotreatment or control antibody. In the lung and kidney, β-glucuronidase activity was markedly higher for the MR-1-treated group. β-Glucuronidase activity in the brain persisted independently of MR-1 treatment. Activity was intense in the injected hemisphere and was also evident in the noninjected cortex and striatum, with dramatic improvements in storage deposits in areas of both hemispheres. These results indicate that prolonged enzyme expression from transgenes delivered to deficient liver and brain can mediate pervasive correction and illustrate the potential for gene therapy of MPS and other lysosomal storage diseases.

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Luu, Wing, James Bjork, Erin Salo, et al. "Modulation of SUR1 KATP Channel Subunit Activity in the Peripheral Nervous System Reduces Mechanical Hyperalgesia after Nerve Injury in Mice." International Journal of Molecular Sciences 20, no. 9 (2019): 2251. http://dx.doi.org/10.3390/ijms20092251.

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The ATP-sensitive K+ channel (KATP) is involved in hypersensitivity during chronic pain and is presumed to be a downstream target of mu opioid receptors. Multiple subtypes of KATP channels exist in the peripheral and central nervous system and their activity may be inversely correlated to chronic pain phenotypes in rodents. In this study, we investigated the different KATP channel subunits that could be involved in neuropathic pain in mice. In chronic pain models utilizing spinal nerve ligation, SUR1 and Kir6.2 subunits were found to be significantly downregulated in dorsal root ganglia and the spinal cord. Local or intrathecal administration of SUR1-KATP channel subtype agonists resulted in analgesia after spinal nerve ligation but not SUR2 agonists. In ex-vivo nerve recordings, administration of the SUR1 agonist diazoxide to peripheral nerve terminals decreased mechanically evoked potentials. Genetic knockdown of SUR1 through an associated adenoviral strategy resulted in mechanical hyperalgesia but not thermal hyperalgesia compared to control mice. Behavioral data from neuropathic mice indicate that local reductions in SUR1-subtype KATP channel activity can exacerbate neuropathic pain symptoms. Since neuropathic pain is of major clinical relevance, potassium channels present a target for analgesic therapies, especially since they are expressed in nociceptors and could play an essential role in regulating the excitability of neurons involved in pain-transmission.

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OH, Seunguk, Rick Odland, Scott R. Wilson, et al. "Improved distribution of small molecules and viral vectors in the murine brain using a hollow fiber catheter." Journal of Neurosurgery 107, no. 3 (2007): 568–77. http://dx.doi.org/10.3171/jns-07/09/0568.

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Object A hollow fiber catheter was developed to improve the distribution of drugs administered via direct infusion into the central nervous system (CNS). It is a porous catheter that significantly increases the surface area of brain tissue into which a drug is infused. Methods Dye was infused into the mouse brain through convection-enhanced delivery (CED) using a 28-gauge needle compared with a 3-mm-long hollow fiber catheter. To determine whether a hollow fiber catheter could increase the distribution of gene therapy vectors, a recombinant adenovirus expressing the firefly luciferase reporter was injected into the mouse striatum. Gene expression was monitored using in vivo bioluminescent imaging. To assess the distribution of gene transfer, an adenovirus expressing green fluorescent protein was injected into the striatum using a hollow fiber catheter or a needle. Results Hollow fiber catheter–mediated infusion increased the volume of brain tissue labeled with dye by 2.7 times relative to needle-mediated infusion. In vivo imaging revealed that catheter-mediated infusion of adenovirus resulted in gene expression that was 10 times greater than that mediated by a needle. The catheter appreciably increased the area of brain transduced with adenovirus relative to a needle, affecting a significant portion of the injected hemisphere. Conclusions The miniature hollow fiber catheter used in this study significantly increased the distribution of dye and adenoviral-mediated gene transfer in the mouse brain compared with the levels reached using a 28-gauge needle. Compared with standard single-port clinical catheters, the hollow fiber catheter has the advantage of millions of nanoscale pores to increase surface area and bulk flow in the CNS. Extending the scale of the hollow fiber catheter for the large mammalian brain shows promise in increasing the distribution and efficacy of gene therapy and drug therapy using CED.

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Okado, Haruo, Akiko Miwa, and Toshio Terashma. "2801 Plausible differential mechanism of adenovirus-mediated gene transfer into various regions of central nervous system." Neuroscience Research 25 (January 1996): S267. http://dx.doi.org/10.1016/0168-0102(96)89307-2.

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Kuo, Hui, Donald K. Ingram, Ronald G. Crystal, and Andrea Mastrangeli. "Retrograde transfer of replication deficient recombinant adenovirus vector in the central nervous system for tracing studies." Brain Research 705, no. 1-2 (1995): 31–38. http://dx.doi.org/10.1016/0006-8993(95)01065-3.

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Cowsill, C., T. D. Southgate, G. Morrissey, et al. "Central nervous system toxicity of two adenoviral vectors encoding variants of the herpes simplex virus type 1 thymidine kinase: reduced cytotoxicity of a truncated HSV1-TK." Gene Therapy 7, no. 8 (2000): 679–85. http://dx.doi.org/10.1038/sj.gt.3301147.

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Bajocchi, Gianluigi, Sanford H. Feldman, Ronald G. Crystal, and Andrea Mastrangeli. "Direct in vivo gene transfer to ependymal cells in the central nervous system using recombinant adenovirus vectors." Nature Genetics 3, no. 3 (1993): 229–34. http://dx.doi.org/10.1038/ng0393-229.

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Broder, Howard, Andrea Anderson, Thomas J. Kremen, Sylvia K. Odesa, and Linda M. Liau. "MART-1 adenovirus-transduced dendritic cell immunization in a murine model of metastatic central nervous system tumor." Journal of Neuro-oncology 64, no. 1-2 (2003): 21–30. http://dx.doi.org/10.1007/bf02700017.

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Neuwelt, Edward A., Michael A. Pagel, Alfred Geller, and Leslie L. Muldoon. "Gene replacement therapy in the central nervous system: Viral vector-mediated therapy of global neurodegenerative disease." Behavioral and Brain Sciences 18, no. 1 (1995): 1–9. http://dx.doi.org/10.1017/s0140525x00037237.

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AbstractThis target article describes the current state of global gene replacement in the brain using viral vectors and assesses possible solutions to some of the many problems inherent in gene therapy of the central nervous system (CNS). Gene replacement therapy in the CNS is a potential means of producing a stable expression of normal human proteins in deficient cells and thus curing certain genetically inherited enzyme deficiencies and metabolic diseases as well as cancers. The two major issues to be addressed in CNS gene replacement are the delivery of genetic material to the brain and the expression of recombinant genetic material in target cells within the CNS. Focal inoculation of recombinant virions or other genetic vectors has limitations in global CNS disease. A new approach is the blood-brain barrier (BBB) disruption technique developed in this laboratory, in which hypertonic mannitol transiently shrinks the BBB endothelium, allowing passage of high molecular weight compounds and even viruses. Gene therapy of the CNS will require a viral vector system that allows long-term, nontoxic gene expression in neurons or glial cells. Retroviral vectors have limitations in CNS gene replacement, although they are suitable for expressing recombinant genes in intracerebral grafts, or toxic genes in brain tumors. Using mutant neurotropic viruses with reduced neurotoxicity (such as defective herpes simplex virus type I [HSV-1], the HSV-1 amplicon vector system we have developed, or adenovirus mutants) has potential for direct treatment of neurons. Injecting these vectors into rodent brains can lead to stable expression of foreign genetic material in postmitotic neuronal cells. We discuss our BBB disruption delivery technique, our defective HSV-1 amplicon vector system, and our feline model for the neuronal lysosomal storage disorder Gm2-gangliosidosis (Sandhoff disease), which may prove to be a useful model system for CNS gene therapy.

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Oh, Seunguk, G. Elizabeth Pluhar, Elizabeth A. McNeil, et al. "Efficacy of nonviral gene transfer in the canine brain." Journal of Neurosurgery 107, no. 1 (2007): 136–44. http://dx.doi.org/10.3171/jns-07/07/0136.

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Object The purpose of this study was to evaluate the gene transfer capability and tolerability of plasmid DNA/poly-ethylenimine (PEI) complexes in comparison with adenovirus and naked plasmid DNA in the canine brain. Methods Plasmid or adenoviral vectors encoding firefly luciferase were injected directly into the cerebral parenchyma of five adult dogs at varying doses and volumes. Serial physical and neurological examinations, as well as blood and cerebrospinal fluid (CSF) analyses, were conducted before and after the surgery for 3 days. Three days after gene delivery, a luciferase activity assay and immunofluorescence analysis were used to test the brain tissue for gene expression. Results Injection into the brain parenchyma resulted in gene transfer throughout the cerebrum with every vector tested. Luciferase expression was highest when adenovirus vectors were used. Injection of plasmid DNA/PEI complexes and naked DNA resulted in similar levels of luciferase expression, which were on average 0.5 to 1.5% of the expression achieved with adenovirus vectors. Immunofluorescent microscopy analysis revealed that plasmid DNA/PEI complexes transduced mainly neurons, whereas adenovirus transduced mainly astrocytes. No significant acute side effects or neurological complications were observed in any of the dogs. Mononuclear cell counts significantly increased in the CSF after adenovirus injection and modestly increased after injection of plasmid DNA/PEI complexes, suggesting that a mild, acute inflammatory response occurred in the central nervous system (CNS). Conclusions Compared with rodent models that are limited by very small brains, the dog is an excellent preclinical model in which to assess the distribution and safety of emerging gene transfer technologies. In this study, short-term gene transfer was evaluated as a prelude to long-term expression and safety studies. The authors conclude that the viral and nonviral vectors tested were well tolerated and effective at mediating gene transfer throughout a large portion of the canine brain. The nonviral plasmid vectors were less effective than adenovirus, yet they still achieved appreciable gene expression levels. Due to reduced gene transfer efficiency relative to viral vectors, nonviral vectors may be most useful when the expressed protein is secreted or exerts a bystander effect. Nonviral vectors offer an alternative means to genetically modify cells within the CNS of large mammals.

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Trifilo, Matthew J., and Thomas E. Lane. "Adenovirus-Mediated Expression of CXCL10 in the Central Nervous System Results in T-Cell Recruitment and Limited Neuropathology." Journal of Neurovirology 9, no. 3 (2003): 315–24. http://dx.doi.org/10.1080/13550280390201029.

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Ariza, Lorena, Lydia Giménez-Llort, Aurélie Cubizolle, et al. "Central Nervous System Delivery of Helper-Dependent Canine Adenovirus Corrects Neuropathology and Behavior in Mucopolysaccharidosis Type VII Mice." Human Gene Therapy 25, no. 3 (2014): 199–211. http://dx.doi.org/10.1089/hum.2013.152.

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CHESKY, MARISA, ROSANA SCALCO, LUCIANE FAILACE, STEVEN READ, and LUIZ FERNANDO JOBIM. "Polymerase chain reaction for the laboratory diagnosis of aseptic meningitis and encephalitis." Arquivos de Neuro-Psiquiatria 58, no. 3B (2000): 836–42. http://dx.doi.org/10.1590/s0004-282x2000000500008.

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A protocol for testing cerebrospinal fluid specimens using a range of PCR assays for the diagnosis of central nervous system infection was developed and used to test prospectively 383 specimens. PCR assays were used for the detection of adenovirus, Borrelia burgdorferi, enteroviruses, Epstein Barr virus, cytomegalovirus, herpes simplex virus, human herpes virus type 6, JC virus, Leptospira interrogans, Listeria monocytogenes, lymphocytic choriomeningitis virus, measles virus, mumps virus, Mycobacterium sp., Mycoplasma pneumoniae, Toxoplasma gondii and varicella zoster virus. Of the 383 specimens tested in this study, 46 (12.0%) were found to be positive. The microorganisms detected were CMV, enterovirus, Epstein Barr virus, herpes simplex virus, human herpes virus type 6, JC virus, L. monocytogenes, Mycobacterium genus, Toxoplasma gondii and varicella zoster virus. The introduction of the PCR protocol described has improved the diagnosis of a range of central nervous system infections in our laboratory. We believe however that further evaluation of these assays in immunocompromised patients is necessary to better determine the predictive value of positive PCR results in these patient groups.

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Havlicek, David F., Jonathan B. Rosenberg, Bishnu P. De, et al. "Cocaine vaccine dAd5GNE protects against moderate daily and high-dose “binge” cocaine use." PLOS ONE 15, no. 11 (2020): e0239780. http://dx.doi.org/10.1371/journal.pone.0239780.

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The cocaine vaccine dAd5GNE is comprised of a disrupted serotype 5 adenovirus gene therapy vector covalently conjugated to the cocaine analog GNE. The vaccine evokes a high titer of circulating anti-cocaine antibodies that prevent cocaine from reaching its cognate receptors in the central nervous system. Prior studies have demonstrated the efficacy of dAd5GNE in models of occasional, moderate cocaine use. However, previous studies have not sufficiently evaluated the efficacy of dAd5GNE in models of the repetitive and high-dose “binge” use patterns common in human addicts. In the present study, we evaluated the capacity of dAd5GNE vaccination to protect against “binge” cocaine use and circumstances where vaccinated addicts attempt to override the vaccine. We modeled repetitive daily cocaine use in vaccinated Balb/c mice and African green monkeys, and evaluated high-dose “binge” scenarios in Balb/c mice. In each model of daily use the dAd5GNE vaccine prevented cocaine from reaching the central nervous system. In the high-dose “binge” model, vaccination decreased cocaine-induced hyperactivity and reduced the number of cocaine-induced seizures. Based on this data and our prior data in rodents and nonhuman primates, we have initiated a clinical trial evaluating the dAd5GNE anti-cocaine vaccine as a potential therapy for cocaine addicts who wish to stop cocaine use. If dAd5GNE vaccination is safe and produces high anti-cocaine antibody titers in the clinic, we hypothesize that the vaccine will restrict the access of cocaine to the central nervous system and inhibit cocaine-induced “highs” even in the context of moderate daily and high-dose “binge” use that might otherwise cause a drug-induced overdose.

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Patel, Kaushik P., William G. Mayhan, Keshore R. Bidasee, and Hong Zheng. "Enhanced angiotensin II-mediated central sympathoexcitation in streptozotocin-induced diabetes: role of superoxide anion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 2 (2011): R311—R320. http://dx.doi.org/10.1152/ajpregu.00246.2010.

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Studies have shown that the superoxide mechanism is involved in angiotensin II (ANG II) signaling in the central nervous system. We hypothesized that ANG II activates sympathetic outflow by stimulation of superoxide anion in the paraventricular nucleus (PVN) of streptozotocin (STZ)-induced diabetic rats. In α-chloralose- and urethane-anesthetized rats, microinjection of ANG II into the PVN (50, 100, and 200 pmol) produced dose-dependent increases in renal sympathetic nerve activity (RSNA), arterial pressure (AP), and heart rate (HR) in control and STZ-induced diabetic rats. There was a potentiation of the increase in RSNA (35.0 ± 5.0 vs. 23.0 ± 4.3%, P < 0.05), AP, and HR due to ANG II type I (AT1) receptor activation in diabetic rats compared with control rats. Blocking endogenous AT1 receptors within the PVN with AT1 receptor antagonist losartan produced significantly greater decreases in RSNA, AP, and HR in diabetic rats compared with control rats. Concomitantly, there were significant increases in mRNA and protein expression of AT1 receptor with increased superoxide levels and expression of NAD(P)H oxidase subunits p22phox, p47phox, and p67phox in the PVN of rats with diabetes. Pretreatment with losartan (10 mg·kg−1·day−1 in drinking water for 3 wk) significantly reduced protein expression of NAD(P)H oxidase subunits (p22phox and p47phox) in the PVN of diabetic rats. Pretreatment with adenoviral vector-mediated overexpression of human cytoplasmic superoxide dismutase (AdCuZnSOD) within the PVN attenuated the increased central responses to ANG II in diabetes (RSNA: 20.4 ± 0.7 vs. 27.7 ± 2.1%, n = 6, P < 0.05). These data support the concept that superoxide anion contributes to an enhanced ANG II-mediated signaling in the PVN involved with the exaggerated sympathoexcitation in diabetes.

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Pushchina, Evgeniya V., Ilya A. Kapustyanov, Ekaterina V. Shamshurina, and Anatoly A. Varaksin. "A Confocal Microscopic Study of Gene Transfer into the Mesencephalic Tegmentum of Juvenile Chum Salmon, Oncorhynchus keta, Using Mouse Adeno-Associated Viral Vectors." International Journal of Molecular Sciences 22, no. 11 (2021): 5661. http://dx.doi.org/10.3390/ijms22115661.

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To date, data on the presence of adenoviral receptors in fish are very limited. In the present work, we used mouse recombinant adeno-associated viral vectors (rAAV) with a calcium indicator of the latest generation GCaMP6m that are usually applied for the dorsal hippocampus of mice but were not previously used for gene delivery into fish brain. The aim of our work was to study the feasibility of transduction of rAAV in the mouse hippocampus into brain cells of juvenile chum salmon and subsequent determination of the phenotype of rAAV-labeled cells by confocal laser scanning microscopy (CLSM). Delivery of the gene in vivo was carried out by intracranial injection of a GCaMP6m-GFP-containing vector directly into the mesencephalic tegmentum region of juvenile (one-year-old) chum salmon, Oncorhynchus keta. AAV incorporation into brain cells of the juvenile chum salmon was assessed at 1 week after a single injection of the vector. AAV expression in various areas of the thalamus, pretectum, posterior-tuberal region, postcommissural region, medial and lateral regions of the tegmentum, and mesencephalic reticular formation of juvenile O. keta was evaluated using CLSM followed by immunohistochemical analysis of the localization of the neuron-specific calcium binding protein HuCD in combination with nuclear staining with DAPI. The results of the analysis showed partial colocalization of cells expressing GCaMP6m-GFP with red fluorescent HuCD protein. Thus, cells of the thalamus, posterior tuberal region, mesencephalic tegmentum, cells of the accessory visual system, mesencephalic reticular formation, hypothalamus, and postcommissural region of the mesencephalon of juvenile chum salmon expressing GCaMP6m-GFP were attributed to the neuron-specific line of chum salmon brain cells, which indicates the ability of hippocampal mammal rAAV to integrate into neurons of the central nervous system of fish with subsequent expression of viral proteins, which obviously indicates the neuronal expression of a mammalian adenoviral receptor homolog by juvenile chum salmon neurons.

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Zhang, Zhongming, Yijing Zhang, Yan Wang, et al. "Genetic knockdown of brain-derived neurotrophic factor in the nervous system attenuates angiotensin II-induced hypertension in mice." Journal of the Renin-Angiotensin-Aldosterone System 20, no. 1 (2019): 147032031983440. http://dx.doi.org/10.1177/1470320319834406.

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Introduction: Brain-derived neurotropic factor (BDNF) is expressed throughout the central nervous system and peripheral organs involved in the regulation of blood pressure, but the systemic effects of BDNF in the control of blood pressure are not well elucidated. Materials and methods: We utilized loxP flanked BDNF male mice to cross with nestin-Cre female mice to generate nerve system BDNF knockdown mice, nestin-BDNF (+/–), or injected Cre adenovirus into the subfornical organ to create subfornical organ BDNF knockdown mice. Histochemistry was used to verify injection location. Radiotelemetry was employed to determine baseline blood pressure and pressor response to angiotensin II (1000 ng/kg/min). Real-time polymerase chain reaction was used to measure the expression of renin–angiotensin system components in the laminal terminalis and peripheral organs. Results: Nestin-BDNF (+/–) mice had lower renin–angiotensin system expression in the laminal terminalis and peripheral organs including the gonadal fat pad, and a lower basal blood pressure. They exhibited an attenuated hypertensive response and a weak or similar modification of renin–angiotensin system component expression to angiotensin II infusion. Subfornical organ BDNF knockdown was sufficient for the attenuation of angiotensin II-induced hypertension. Conclusion: Central BDNF, especially subfornical organ BDNF is involved in the maintenance of basal blood pressure and in augmentation of hypertensive response to angiotensin II through systemic regulation of the expression of renin–angiotensin system molecules.

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Marcondes, Maria Cecilia Garibaldi, Ryan Ojakian, Nikki Bortell, Claudia Flynn, Bruno Conti, and Howard S. Fox. "Osteopontin Expression in the Brain Triggers Localized Inflammation and Cell Death When Immune Cells Are Activated by Pertussis Toxin." Mediators of Inflammation 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/358218.

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Upregulation of osteopontin (OPN) is a characteristic of central nervous system pathologies. However, the role of OPN in inflammation is still controversial, since it can both prevent cell death and induce the migration of potentially damaging inflammatory cells. To understand the role of OPN in inflammation and cell survival, we expressed OPN, utilizing an adenoviral vector, in the caudoputamen of mice deficient in OPN, using beta-galactosidase- (β-gal-) expressing vector as control. The tissue pathology and the expression of proinflammatory genes were compared in both treatments. Interestingly, inflammatory infiltrate was only found when the OPN-vector was combined with a peripheral treatment with pertussis toxin (Ptx), which activated peripheral cells to express the OPN receptor CD44v6. Relative toβ-gal, OPN increased the levels of inflammatory markers, including IL13Rα1, CXCR3, and CD40L. In Ptx-treated OPN KOs, apoptotic TUNEL+ cells surrounding the OPN expression site increased, compared toβ-gal. Together, these results show that local OPN expression combined with a peripheral inflammatory stimulus, such as Ptx, may be implicated in the development of brain inflammation and induction of cell death, by driving a molecular pattern characteristic of cytotoxicity. These are characteristics of inflammatory pathologies of the CNS in which OPN upregulation is a hallmark.

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Conde-Sieira, Marta, Valentina Capelli, Rosa Álvarez-Otero та ін. "Hypothalamic AMPKα2 regulates liver energy metabolism in rainbow trout through vagal innervation". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, № 1 (2020): R122—R134. http://dx.doi.org/10.1152/ajpregu.00264.2019.

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Hypothalamic AMPK plays a major role in the regulation of whole body metabolism and energy balance. Present evidence has demonstrated that this canonical mechanism is evolutionarily conserved. Thus, recent data demonstrated that inhibition of AMPKα2 in fish hypothalamus led to decreased food intake and liver capacity to use and synthesize glucose, lipids, and amino acids. We hypothesize that a signal of abundance of nutrients from the hypothalamus controls hepatic metabolism. The vagus nerve is the most important link between the brain and the liver. We therefore examined in the present study whether surgical transection of the vagus nerve in rainbow trout is sufficient to alter the effect in liver of central inhibition of AMPKα2. Thus, we vagotomized (VGX) or not (Sham) rainbow trout and then intracerebroventricularly administered adenoviral vectors tagged with green fluorescent protein alone or linked to a dominant negative isoform of AMPKα2. The inhibition of AMPKα2 led to reduced food intake in parallel with changes in the mRNA abundance of hypothalamic neuropeptides [neuropeptide Y ( npy), agouti-related protein 1 ( agrp1), and cocaine- and amphetamine-related transcript ( cartpt)] involved in food intake regulation. Central inhibition of AMPKα2 resulted in the liver having decreased capacity to use and synthesize glucose, lipids, and amino acids. Notably, these effects mostly disappeared in VGX fish. These results support the idea that autonomic nervous system actions mediate the actions of hypothalamic AMPKα2 on liver metabolism. Importantly, this evidence indicates that the well-established role of hypothalamic AMPK in energy balance is a canonical evolutionarily preserved mechanism that is also present in the fish lineage.

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Suplicy, Henrique de Lacerda, and Andressa Bornschein. "Infeccions as the etiology for obesity." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 2 (2009): 159–64. http://dx.doi.org/10.1590/s0004-27302009000200007.

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The role of infection on obesity development has been questioned since the early 1980's. Several studies on animals have shown that fisiopathologic mechanisms through which infections can produce obesity do exist. At least eight types of obesity-inducing viruses have been identified in animals, especially poultry and mice. Studies on humans are far less convincing; however, two adenoviruses, Ad-36 and SMAM-1, have shown adipogenic properties. In vitro studies with 3T3-L1 cells stated the activation of the enzymatic pathway that leads to fatty tissue accumulation; in vivo studies have also detected higher levels of antibodies against such viruses on obese subjects. Although most known infections nowadays cause obesity through central nervous system lesions, the Ad-36 adenovirus infection affects fatty tissue directly, raising doubts regarding central role component in this case.

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Cauthen, Angela N., Corrie C. Brown, and Katherine R. Spindler. "In Vitro and In Vivo Characterization of a Mouse Adenovirus Type 1 Early Region 3 Null Mutant." Journal of Virology 73, no. 10 (1999): 8640–46. http://dx.doi.org/10.1128/jvi.73.10.8640-8646.1999.

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ABSTRACT Previous attempts to construct a mouse adenovirus type 1 early region 3 (E3) null mutant by initiator codon mutagenesis were unsuccessful because one of the E3 proteins, gp11K, is synthesized as a fusion protein from a late viral mRNA (A. N. Cauthen and K. R. Spindler, Virology 259:119–128, 1999). Therefore, a different mutagenesis strategy was employed that inserted termination codons into all three reading frames of the E3 proteins. This strategy produced a mutant, pmE314, that was null for the expression of E3 proteins as determined by immunoprecipitation with E3-specific antisera. This mutant grew as well as wild-type (wt) virus in both 3T6 mouse fibroblasts and mouse brain microvascular endothelial cells. However, the 50% lethal dose for pmE314 in adult NIH Swiss outbred mice was approximately 6 log units higher than that of wt virus, indicating that pmE314 was less virulent in mice. In situ hybridization experiments revealed that the absence of the E3 proteins did not alter the tropism of the mutant virus from that of wt virus. When the histopathology was evaluated, the characteristics of the pmE314 infection at both doses administered were strikingly different from those exhibited by wt virus. The central nervous system of wt-infected mice exhibited damage to the endothelium and recruitment of inflammatory cells, whereas the central nervous system of pmE314-infected mice showed no inflammatory response and only mild signs of endothelial damage.

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Charles, Peter C., Xia Chen, Marshall S. Horwitz, and Celia F. Brosnan. "Differential chemokine induction by the mouse adenovirus type-1 in the central nervous system of susceptible and resistant strains of mice." Journal of Neurovirology 5, no. 1 (1999): 55–64. http://dx.doi.org/10.3109/13550289909029746.

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Sakai, Masashi, Kouichi Tamura, Yuko Tsurumi, et al. "Expression of MAK-V/Hunk in renal distal tubules and its possible involvement in proliferative suppression." American Journal of Physiology-Renal Physiology 292, no. 5 (2007): F1526—F1536. http://dx.doi.org/10.1152/ajprenal.00451.2006.

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MAK-V/Hunk is an SNF1-related serine/threonine kinase which was previously shown to be highly expressed in the mammary gland and central nervous system. In this study, we found MAK-V/Hunk is abundantly and specifically expressed in the thick ascending limbs and distal convoluted tubules (DCT) of the kidney from the embryonic stage to the adult stage. We demonstrated that dietary salt depletion significantly enhances renal MAK-V/Hunk mRNA levels compared with a normal-salt diet. To analyze the possible renal cellular function of this kinase, we employed mouse distal convoluted tubule (mDCT) cells. The results of reverse transcriptase-polymerase chain reaction and Western blot analysis revealed that MAK-V/Hunk is expressed endogenously in mDCT cells. Overexpression of MAK-V/Hunk by adenoviral gene transfer significantly inhibited the ANG II-induced stimulation of c- fos gene transcription and suppressed the ANG II-mediated increases in transforming growth factor-β production into the medium. This phenomenon was accompanied by inhibition of ANG II-induced activation of BrdU incorporation. On the other hand, the MAK-V/Hunk knockdown by siRNA activated the ANG II-induced c- fos gene expression. In the consecutive sections stained for MAK-V/Hunk and AT1 receptor, MAK-V/Hunk-immunopositive distal tubules expressed the AT1 receptor. This is the first report on the intrarenal localization of MAK-V/Hunk and its cellular function in renal tubular cells.

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Reetz, Julia, Steve Hildebrandt, Anke Schmidt, et al. "Novel subventricular zone early progenitor cell-specific adenovirus for in vivo therapy of central nervous system disorders reinforces brain stem cell heterogeneity." Brain Structure and Function 221, no. 4 (2015): 2049–59. http://dx.doi.org/10.1007/s00429-015-1025-8.

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Lindley, Timothy E., David W. Infanger, Mark Rishniw, et al. "Scavenging superoxide selectively in mouse forebrain is associated with improved cardiac function and survival following myocardial infarction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 1 (2009): R1—R8. http://dx.doi.org/10.1152/ajpregu.00078.2008.

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Dysregulation in central nervous system (CNS) signaling that results in chronic sympathetic hyperactivity is now recognized to play a critical role in the pathogenesis of heart failure (HF) following myocardial infarction (MI). We recently demonstrated that adenovirus-mediated gene transfer of cytoplasmic superoxide dismutase (Ad-Cu/ZnSOD) to forebrain circumventricular organs, unique sensory structures that lack a blood-brain barrier and link peripheral blood-borne signals to central nervous system cardiovascular circuits, inhibits both the MI-induced activation of these central signaling pathways and the accompanying sympathoexcitation. Here, we tested the hypothesis that this forebrain-targeted reduction in oxidative stress translates into amelioration of the post-MI decline in myocardial function and increase in mortality. Adult C57BL/6 mice underwent left coronary artery ligation or sham surgery along with forebrain-targeted gene transfer of Ad-Cu/ZnSOD or a control vector. The results demonstrate marked MI-induced increases in superoxide radical formation in one of these forebrain regions, the subfornical organ (SFO). Ad-Cu/ZnSOD targeted to this region abolished the increased superoxide levels and led to significantly improved myocardial function compared with control vector-treated mice. This was accompanied by diminished levels of cardiomyocyte apoptosis in the Ad-Cu/ZnSOD but not the control vector-treated group. These effects of superoxide scavenging with Ad-Cu/ZnSOD in the forebrain paralleled increased post-MI survival rates compared with controls. This suggests that oxidative stress in the SFO plays a critical role in the deterioration of cardiac function following MI and underscores the promise of CNS-targeted antioxidant therapy for the treatment of MI-induced HF.

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Xue, Baojian, Zhongming Zhang, Terry G. Beltz, Fang Guo, Meredith Hay, and Alan Kim Johnson. "Genetic knockdown of estrogen receptor-alpha in the subfornical organ augments ANG II-induced hypertension in female mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 6 (2015): R507—R516. http://dx.doi.org/10.1152/ajpregu.00406.2014.

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The present study tested the hypotheses that 1) ERα in the brain plays a key role in the estrogen-protective effects against ANG II-induced hypertension, and 2) that the subfornical organ (SFO) is a key site where ERα mediates these protective actions. In this study, a “floxed” ERα transgenic mouse line (ERαflox) was used to create models in which ERα was knocked down in the brain or just in the SFO. Female mice with ERα ablated in the nervous system (Nestin-ERα− mice) showed greater increases in blood pressure (BP) in response to ANG II. Furthermore, females with ERα knockdown specifically in the SFO [SFO adenovirus-Cre (Ad-Cre) injected ERαflox mice] also showed an enhanced pressor response to ANG II. Immunohistochemical (IHC), RT-PCR, and Western blot analyses revealed a marked reduction in the expression of ERα in nervous tissues and, in particular, in the SFO. These changes were not present in peripheral tissues in Nestin-ERα− mice or Ad-Cre-injected ERαflox mice. mRNA expression of components of the renin-angiotensin system in the lamina terminalis were upregulated in Nestin-ERα− mice. Moreover, ganglionic blockade on day 7 after ANG II infusions resulted in a greater reduction of BP in Nestin-ERα− mice or SFO Ad-Cre-injected mice, suggesting that knockdown of ERα in the nervous system or the SFO alone augments central ANG II-induced increase in sympathetic tone. The results indicate that interfering with the action of estrogen on SFO ERα is sufficient to abolish the protective effects of estrogen against ANG II-induced hypertension.

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Croxford, J. Ludovic, Marc Feldmann, Yuti Chernajovsky, and David Baker. "Different Therapeutic Outcomes in Experimental Allergic Encephalomyelitis Dependant Upon the Mode of Delivery of IL-10: A Comparison of the Effects of Protein, Adenoviral or Retroviral IL-10 Delivery into the Central Nervous System." Journal of Immunology 166, no. 6 (2001): 4124–30. http://dx.doi.org/10.4049/jimmunol.166.6.4124.

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