Connexin 43 regulates astrocytic migration and proliferation in response to injury

Homkajorn, Benjaporn; Sims, Neil R.; Muyderman, Håkan

doi:10.1016/j.neulet.2010.09.051

Cited by 40 publications

(42 citation statements)

References 27 publications

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“…Another distinctive marker of AbA cells is the high expression of the gap junction protein Cx43, which also is found in cultured neonatal astrocytes (32) and is known to modulate their proliferation, migration, and differentiation (33). Cx43 also can form hemichannels opened to the extracellular space in inflammatory astrocytes (34,35), which can release extracellular ATP (34,36).…”

Section: Discussionmentioning

confidence: 99%

Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis

Díaz-Amarilla

Olivera-Bravo

Trías

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

170

252

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Motoneuron loss and reactive astrocytosis are pathological hallmarks of amyotrophic lateral sclerosis (ALS), a paralytic neurodegenerative disease that can be triggered by mutations in Cu-Zn superoxide dismutase (SOD1). Dysfunctional astrocytes contribute to ALS pathogenesis, inducing motoneuron damage and accelerating disease progression. However, it is unknown whether ALS progression is associated with the appearance of a specific astrocytic phenotype with neurotoxic potential. Here, we report the isolation of astrocytes with aberrant phenotype (referred as “AbA cells”) from primary spinal cord cultures of symptomatic rats expressing the SOD1 G93A mutation. Isolation was based on AbA cells’ marked proliferative capacity and lack of replicative senescence, which allowed oligoclonal cell expansion for 1 y. AbA cells displayed astrocytic markers including glial fibrillary acidic protein, S100β protein, glutamine synthase, and connexin 43 but lacked glutamate transporter 1 and the glial progenitor marker NG2 glycoprotein. Notably, AbA cells secreted soluble factors that induced motoneuron death with a 10-fold higher potency than neonatal SOD1 G93A astrocytes. AbA-like aberrant astrocytes expressing S100β and connexin 43 but lacking NG2 were identified in nearby motoneurons, and their number increased sharply after disease onset. Thus, AbA cells appear to be an as-yet unknown astrocyte population arising during ALS progression with unprecedented proliferative and neurotoxic capacity and may be potential cellular targets for slowing ALS progression.

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Section: Discussionmentioning

confidence: 99%

Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis

Díaz-Amarilla

Olivera-Bravo

Trías

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

170

252

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“…In astrocytes, Connexin-43 is required for cell migration under pro-inflammatory conditions and it interacts with many cytoskeletal proteins, such as β-actin and glial fibrillary acidic protein [40,41]. Conversely, pannexins regulate motility of different cell types, such as neutrophils or leucocytes, tumor cells, venous fibroblasts, and neurons, among others [42][43][44].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

“…The involvement of Connexin-43 in the migration of various cell types, including neuronal precursor cells, astrocytes, and cancer cells, has been reported [40,41]. In astrocytes, Connexin-43 is necessary for astrocyte migration and proliferation but only upon injury to the central nervous system [40], and no connection between these events and neuron-derived factors has been reported. Alternatively, Pannexin-1 is required for the inflammatory response and the migration of cells from the immune system towards a chemo-attractant [42,64].…”

mentioning

confidence: 99%

Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration

Álvarez

Lagos-Cabré

Kong

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

109

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Leyton, Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration, BBA -Molecular Cell Research (2016Research ( ), doi: 10.1016Research ( /j.bbamcr.2016 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT

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“…Connexin 43 regulates astrocytic migration and proliferation in response to injury. Reactive astrocytes display up-regulation of the gap junction protein Cx43, and astroglial cells with depleted expression of Cx43 show diminished ability to migrate and to proliferate in the wound area of the brain (Homkajorn et al, 2010). Drebrin as an actin binding protein whose level is greatly decreased in brains of Alzheimer's patients was found to be a binding partner of the Cx43 COOH-terminal domain in astrocytes.…”

Section: Wwwintechopencommentioning

confidence: 96%

Alteration of Neuron-Glia Interactions in Neurodegeneration: Molecular Biomarkers and Therapeutic Strategy

Салмина¹,

Петрова²,

Таранушенко³

et al. 2011

Neurodegenerative Diseases - Processes, Prevention, Protection and Monitoring

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Connexin 43 regulates astrocytic migration and proliferation in response to injury

Cited by 40 publications

References 27 publications

Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis

Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis

Integrin-mediated transactivation of P2X7R via hemichannel-dependent ATP release stimulates astrocyte migration

Alteration of Neuron-Glia Interactions in Neurodegeneration: Molecular Biomarkers and Therapeutic Strategy

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