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α V β 3 Integrin regulates astrocyte reactivity
by
Alvarez, Alvaro
, Burgos-Bravo, Francesca
, Herrera-Molina, Rodrigo
, Rojas, Fabiola
, Quest, Andrew F G
, Pérez-Nuñez, Ramón
, Rojas-Mancilla, Edgardo
, Leyton, Lisette
, Lagos-Cabré, Raúl
, Schneider, Pascal
, Kong, Milene
, van Zundert, Brigitte
, Herrera-Marschitz, Mario
, Cárdenas, Areli
in
Animals
/ Animals, Genetically Modified
/ Animals, Newborn
/ Astrocytes - drug effects
/ Astrocytes - physiology
/ Cell Movement - drug effects
/ Cell Movement - genetics
/ Cell Movement - physiology
/ Cells, Cultured
/ Connexins - genetics
/ Connexins - metabolism
/ Disease Models, Animal
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - genetics
/ Humans
/ Integrin alphaVbeta3 - genetics
/ Integrin alphaVbeta3 - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neurodegenerative Diseases - genetics
/ Neurodegenerative Diseases - pathology
/ Rats
/ Receptors, Purinergic P2 - genetics
/ Receptors, Purinergic P2 - metabolism
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Superoxide Dismutase - genetics
/ Superoxide Dismutase - metabolism
/ Thy-1 Antigens - pharmacology
/ Tumor Necrosis Factor-alpha - pharmacology
/ Wound Healing - physiology
2017
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α V β 3 Integrin regulates astrocyte reactivity
by
Alvarez, Alvaro
, Burgos-Bravo, Francesca
, Herrera-Molina, Rodrigo
, Rojas, Fabiola
, Quest, Andrew F G
, Pérez-Nuñez, Ramón
, Rojas-Mancilla, Edgardo
, Leyton, Lisette
, Lagos-Cabré, Raúl
, Schneider, Pascal
, Kong, Milene
, van Zundert, Brigitte
, Herrera-Marschitz, Mario
, Cárdenas, Areli
in
Animals
/ Animals, Genetically Modified
/ Animals, Newborn
/ Astrocytes - drug effects
/ Astrocytes - physiology
/ Cell Movement - drug effects
/ Cell Movement - genetics
/ Cell Movement - physiology
/ Cells, Cultured
/ Connexins - genetics
/ Connexins - metabolism
/ Disease Models, Animal
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - genetics
/ Humans
/ Integrin alphaVbeta3 - genetics
/ Integrin alphaVbeta3 - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neurodegenerative Diseases - genetics
/ Neurodegenerative Diseases - pathology
/ Rats
/ Receptors, Purinergic P2 - genetics
/ Receptors, Purinergic P2 - metabolism
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Superoxide Dismutase - genetics
/ Superoxide Dismutase - metabolism
/ Thy-1 Antigens - pharmacology
/ Tumor Necrosis Factor-alpha - pharmacology
/ Wound Healing - physiology
2017
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α V β 3 Integrin regulates astrocyte reactivity
by
Alvarez, Alvaro
, Burgos-Bravo, Francesca
, Herrera-Molina, Rodrigo
, Rojas, Fabiola
, Quest, Andrew F G
, Pérez-Nuñez, Ramón
, Rojas-Mancilla, Edgardo
, Leyton, Lisette
, Lagos-Cabré, Raúl
, Schneider, Pascal
, Kong, Milene
, van Zundert, Brigitte
, Herrera-Marschitz, Mario
, Cárdenas, Areli
in
Animals
/ Animals, Genetically Modified
/ Animals, Newborn
/ Astrocytes - drug effects
/ Astrocytes - physiology
/ Cell Movement - drug effects
/ Cell Movement - genetics
/ Cell Movement - physiology
/ Cells, Cultured
/ Connexins - genetics
/ Connexins - metabolism
/ Disease Models, Animal
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - genetics
/ Humans
/ Integrin alphaVbeta3 - genetics
/ Integrin alphaVbeta3 - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neurodegenerative Diseases - genetics
/ Neurodegenerative Diseases - pathology
/ Rats
/ Receptors, Purinergic P2 - genetics
/ Receptors, Purinergic P2 - metabolism
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Superoxide Dismutase - genetics
/ Superoxide Dismutase - metabolism
/ Thy-1 Antigens - pharmacology
/ Tumor Necrosis Factor-alpha - pharmacology
/ Wound Healing - physiology
2017
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Journal Article
α V β 3 Integrin regulates astrocyte reactivity
2017
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Overview
Neuroinflammation involves cytokine release, astrocyte reactivity and migration. Neuronal Thy-1 promotes DITNC1 astrocyte migration by engaging α
β
Integrin and Syndecan-4. Primary astrocytes express low levels of these receptors and are unresponsive to Thy-1; thus, inflammation and astrocyte reactivity might be necessary for Thy-1-induced responses.
Wild-type rat astrocytes (TNF-activated) or from human SOD1
transgenic mice (a neurodegenerative disease model) were used to evaluate cell migration, Thy-1 receptor levels, signaling molecules, and reactivity markers.
Thy-1 induced astrocyte migration only after TNF priming. Increased expression of α
β
Integrin, Syndecan-4, P2X7R, Pannexin-1, Connexin-43, GFAP, and iNOS were observed in TNF-treated astrocytes. Silencing of β
Integrin prior to TNF treatment prevented Thy-1-induced migration, while β
Integrin over-expression was sufficient to induce astrocyte reactivity and allow Thy-1-induced migration. Finally, hSOD1
astrocytes behave as TNF-treated astrocytes since they were reactive and responsive to Thy-1.
Therefore, inflammation induces expression of α
β
Integrin and other proteins, astrocyte reactivity, and Thy-1 responsiveness. Importantly, ectopic control of β
Integrin levels modulates these responses regardless of inflammation.
Subject
/ Animals, Genetically Modified
/ Cell Movement - drug effects
/ Gene Expression Regulation - drug effects
/ Gene Expression Regulation - genetics
/ Humans
/ Integrin alphaVbeta3 - genetics
/ Integrin alphaVbeta3 - metabolism
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neurodegenerative Diseases - genetics
/ Neurodegenerative Diseases - pathology
/ Rats
/ Receptors, Purinergic P2 - genetics
/ Receptors, Purinergic P2 - metabolism
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
/ Superoxide Dismutase - genetics
/ Superoxide Dismutase - metabolism
/ Thy-1 Antigens - pharmacology
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