Universität zu Köln

Vay, Sabine Ulrike ORCID: 0000-0002-3289-7807, Olschewski, Daniel Navin, Petereit, Helena, Lange, Felix, Nazarzadeh, Nilufar, Gross, Elena, Rabenstein, Monika, Blaschke, Stefan Johannes, Fink, Gereon Rudolf, Schroeter, Michael and Rueger, Maria Adele (2021). Osteopontin regulates proliferation, migration, and survival of astrocytes depending on their activation phenotype. J. Neurosci. Res., 99 (11). S. 2822 - 2844. HOBOKEN: WILEY. ISSN 1097-4547

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Abstract

The glycoprotein osteopontin is highly upregulated in central nervous system (CNS) disorders such as ischemic stroke. Osteopontin regulates cell growth, cell adhesion, homeostasis, migration, and survival of various cell types. Accordingly, osteopontin is considered an essential regulator of regeneration and repair in the ischemic milieu. Astrocytes are the most abundant cells in the CNS and play significant roles in health and disease. Astrocytes are involved in homeostasis, promote neuroprotection, and regulate synaptic plasticity. Upon activation, astrocytes may adopt different phenotypes, termed A1 and A2. The direct effects of osteopontin on astrocytes, especially in distinct activation states, are yet unknown. The current study aimed to elucidate the impact of osteopontin on resting and active astrocytes. We established an inflammatory in vitro model of activated (A1) primary astrocytes derived from neonatal wistar rats by exposure to a distinct combination of proinflammatory cytokines. To model ischemic stroke in vitro, astrocytes were subjected to oxygen and glucose deprivation (OGD) in the presence or absence of osteopontin. Osteopontin modulated the activation phenotype by attenuating A1- and restoring A2-marker expression without compromising the active astrocytes' immunocompetence. Osteopontin promoted the proliferation of active and the migration of resting astrocytes. Following transient OGD, osteopontin mitigated the delayed ongoing death of primary astrocytes, promoting their survival. Data suggest that osteopontin differentially regulates essential functions of resting and active astrocytes and confirm a significant regulatory role of osteopontin in an in vitro ischemia model. Furthermore, the data suggest that osteopontin constitutes a promising target for experimental therapies modulating neuroregeneration and repair.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Vay, Sabine Ulrike UNSPECIFIED orcid.org/0000-0002-3289-7807 UNSPECIFIED Olschewski, Daniel Navin UNSPECIFIED UNSPECIFIED UNSPECIFIED Petereit, Helena UNSPECIFIED UNSPECIFIED UNSPECIFIED Lange, Felix UNSPECIFIED UNSPECIFIED UNSPECIFIED Nazarzadeh, Nilufar UNSPECIFIED UNSPECIFIED UNSPECIFIED Gross, Elena UNSPECIFIED UNSPECIFIED UNSPECIFIED Rabenstein, Monika UNSPECIFIED UNSPECIFIED UNSPECIFIED Blaschke, Stefan Johannes UNSPECIFIED UNSPECIFIED UNSPECIFIED Fink, Gereon Rudolf UNSPECIFIED UNSPECIFIED UNSPECIFIED Schroeter, Michael UNSPECIFIED UNSPECIFIED UNSPECIFIED Rueger, Maria Adele UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-577262
DOI:	10.1002/jnr.24954
Journal or Publication Title:	J. Neurosci. Res.
Volume:	99
Number:	11
Page Range:	S. 2822 - 2844
Date:	2021
Publisher:	WILEY
Place of Publication:	HOBOKEN
ISSN:	1097-4547
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language FIBRILLARY ACIDIC PROTEIN; BLOOD-BRAIN-BARRIER; REACTIVE ASTROCYTES; UP-REGULATION; EXPRESSION; MICROGLIA; CD44; PROGRESSION; DEFICIENT; INTEGRIN Multiple languages Neurosciences Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/57726