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  1. Article ; Online: GAS1 is present in the cerebrospinal fluid and is expressed in the choroid plexus of the adult rat.

    Ayala-Sarmiento, Alberto E / Estudillo, Enrique / Pérez-Sánchez, Gilberto / Sierra-Sánchez, Arturo / González-Mariscal, Lorenza / Martínez-Fong, Daniel / Segovia, José

    Histochemistry and cell biology

    2016  Volume 146, Issue 3, Page(s) 325–336

    Abstract: Growth arrest specific 1 (GAS1) is a GPI-anchored protein that inhibits proliferation when overexpressed in tumors but during development it promotes proliferation and survival of different organs and tissues. This dual ability is caused by its capacity ... ...

    Abstract Growth arrest specific 1 (GAS1) is a GPI-anchored protein that inhibits proliferation when overexpressed in tumors but during development it promotes proliferation and survival of different organs and tissues. This dual ability is caused by its capacity to interact both by inhibiting the signaling induced by the glial cell line-derived neurotrophic factor and by facilitating the activity of the sonic hedgehog pathway. GAS1 is expressed as membrane bound in different organs and as a secreted form by glomerular mesangial cells. In the developing central nervous system, GAS1 is found in neural progenitors; however, it continues to be expressed in the adult brain. Here, we demonstrate that soluble GAS1 is present in the cerebrospinal fluid (CSF) and it is expressed in the choroid plexus (CP) of the adult rat, the main producer of CSF. Additionally, we confirm the presence of GAS1 in blood plasma and liver of the adult rat, the principal source of blood plasma proteins. The pattern of expression of GAS1 is perivascular in both the CP and the liver. In vitro studies show that the fibroblast cell line NIH/3T3 expresses one form of GAS1 and releases two soluble forms into the supernatant. Briefly, in the present work, we show the presence of GAS1 in adult rat body fluids focusing in the CSF and the CP, and suggest that secreted GAS1 exists as two different isoforms.
    MeSH term(s) Animals ; Cell Cycle Proteins/cerebrospinal fluid ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Choroid Plexus/metabolism ; GPI-Linked Proteins/cerebrospinal fluid ; GPI-Linked Proteins/metabolism ; Mice ; NIH 3T3 Cells ; Rats ; Rats, Wistar
    Chemical Substances Cell Cycle Proteins ; GPI-Linked Proteins ; Gas1 protein, rat
    Language English
    Publishing date 2016-05-25
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1222930-1
    ISSN 1432-119X ; 0301-5564 ; 0948-6143
    ISSN (online) 1432-119X
    ISSN 0301-5564 ; 0948-6143
    DOI 10.1007/s00418-016-1449-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The transfection of BDNF to dopamine neurons potentiates the effect of dopamine D3 receptor agonist recovering the striatal innervation, dendritic spines and motor behavior in an aged rat model of Parkinson's disease.

    Razgado-Hernandez, Luis F / Espadas-Alvarez, Armando J / Reyna-Velazquez, Patricia / Sierra-Sanchez, Arturo / Anaya-Martinez, Veronica / Jimenez-Estrada, Ismael / Bannon, Michael J / Martinez-Fong, Daniel / Aceves-Ruiz, Jorge

    PloS one

    2015  Volume 10, Issue 2, Page(s) e0117391

    Abstract: The progressive degeneration of the dopamine neurons of the pars compacta of substantia nigra and the consequent loss of the dopamine innervation of the striatum leads to the impairment of motor behavior in Parkinson's disease. Accordingly, an efficient ... ...

    Abstract The progressive degeneration of the dopamine neurons of the pars compacta of substantia nigra and the consequent loss of the dopamine innervation of the striatum leads to the impairment of motor behavior in Parkinson's disease. Accordingly, an efficient therapy of the disease should protect and regenerate the dopamine neurons of the substantia nigra and the dopamine innervation of the striatum. Nigral neurons express Brain Derived Neurotropic Factor (BDNF) and dopamine D3 receptors, both of which protect the dopamine neurons. The chronic activation of dopamine D3 receptors by their agonists, in addition, restores, in part, the dopamine innervation of the striatum. Here we explored whether the over-expression of BDNF by dopamine neurons potentiates the effect of the activation of D3 receptors restoring nigrostriatal innervation. Twelve-month old Wistar rats were unilaterally injected with 6-hydroxydopamine into the striatum. Five months later, rats were treated with the D3 agonist 7-hydroxy-N,N-di-n-propy1-2-aminotetralin (7-OH-DPAT) administered i.p. during 4½ months via osmotic pumps and the BDNF gene transfection into nigral cells using the neurotensin-polyplex nanovector (a non-viral transfection) that selectively transfect the dopamine neurons via the high-affinity neurotensin receptor expressed by these neurons. Two months after the withdrawal of 7-OH-DPAT when rats were aged (24 months old), immunohistochemistry assays were made. The over-expression of BDNF in rats receiving the D3 agonist normalized gait and motor coordination; in addition, it eliminated the muscle rigidity produced by the loss of dopamine. The recovery of motor behavior was associated with the recovery of the nigral neurons, the dopamine innervation of the striatum and of the number of dendritic spines of the striatal neurons. Thus, the over-expression of BDNF in dopamine neurons associated with the chronic activation of the D3 receptors appears to be a promising strategy for restoring dopamine neurons in Parkinson's disease.
    MeSH term(s) Animals ; Biomechanical Phenomena/drug effects ; Biomechanical Phenomena/genetics ; Brain-Derived Neurotrophic Factor/genetics ; Dendritic Spines/drug effects ; Dendritic Spines/physiology ; Disease Models, Animal ; Dopamine Agonists/pharmacology ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/pathology ; Gait/drug effects ; Gait/genetics ; Male ; Motor Activity/drug effects ; Motor Activity/genetics ; Muscles/drug effects ; Muscles/physiopathology ; Neostriatum/drug effects ; Neostriatum/physiopathology ; Parkinson Disease/genetics ; Parkinson Disease/pathology ; Parkinson Disease/physiopathology ; Psychomotor Performance/drug effects ; Rats ; Rats, Wistar ; Receptors, Dopamine D3/metabolism ; Recovery of Function/drug effects ; Recovery of Function/genetics ; Regeneration/drug effects ; Regeneration/genetics ; Transfection ; Tyrosine 3-Monooxygenase/metabolism
    Chemical Substances Brain-Derived Neurotrophic Factor ; Dopamine Agonists ; Receptors, Dopamine D3 ; Tyrosine 3-Monooxygenase (EC 1.14.16.2)
    Language English
    Publishing date 2015-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0117391
    Database MEDical Literature Analysis and Retrieval System OnLINE

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