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Prenatal stress affects viability, activation, and chemokine signaling in astroglial cultures.

Prenatal stress affects viability, activation, and chemokine signaling in astroglial cultures.
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Sowa JE, Ślusarczyk J, Trojan E, Chamera K, Leśkiewicz M, Regulska M, Kotarska K, Basta-Kaim A,


Sowa JE, Ślusarczyk J, Trojan E, Chamera K, Leśkiewicz M, Regulska M, Kotarska K, Basta-Kaim A, (click to view)

Sowa JE, Ślusarczyk J, Trojan E, Chamera K, Leśkiewicz M, Regulska M, Kotarska K, Basta-Kaim A,

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Journal of neuroimmunology 2017 08 19311() 79-87 pii 10.1016/j.jneuroim.2017.08.006

Abstract

CXCL12/SDF-1α and CX3CL1/fractalkine are constitutively expressed in the brain, which indicates their significant functions. Emerging evidence highlights the role of astrocytes and the immune system in the pathophysiology of stress-related disorders. The aim of this study was to assess whether prenatal stress affects chemokine signaling, cell viability/activation, and the iNOS pathway in astroglial cultures. Our results showed that prenatal stress lowered astrocyte viability and simultaneously increased GFAP expression. Furthermore, CX3CL1 production and the CXCL12/CXCR4-7 axis were also altered by prenatal stress. Taken together, malfunctions caused by prenatal stress may adversely influence brain development, leading to long-term effects on adult brain function and behavior.

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