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Beckmann A, Recktenwald J, Ferdinand A, et al. First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization. Biology (Basel). 2021;10(12)doi: 10.3390/biology10121307.
Beckmann, A., Recktenwald, J., Ferdinand, A., Grißmer, A., & Meier, C. (2021). First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization. Biology, 10(12), . https://doi.org/10.3390/biology10121307
Beckmann, Anja, et al. "First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization." Biology vol. 10,12 (2021). doi: https://doi.org/10.3390/biology10121307
Beckmann A, Recktenwald J, Ferdinand A, Grißmer A, Meier C. First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization. Biology (Basel). 2021 Dec 09;10(12). doi: 10.3390/biology10121307. PMID: 34943223; PMCID: PMC8698406.
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Biology (Basel). 2021 Dec 09;10(12). doi: 10.3390/biology10121307.

First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization.

Biology

Anja Beckmann, Johanna Recktenwald, Alice Ferdinand, Alexander Grißmer, Carola Meier

Affiliations

  1. Department of Anatomy and Cell Biology, Saarland University, 66421 Homburg/Saar, Germany.

PMID: 34943223 PMCID: PMC8698406 DOI: 10.3390/biology10121307

Abstract

In a short-term model of hyperosmotic stress, primary murine astrocytes were stimulated with a hyperosmolar sucrose solution for five minutes. Astrocytic gap junctions, which are mainly composed of Connexin (Cx) 43, displayed immediate ultrastructural changes, demonstrated by freeze-fracture replica immunogold labeling: their area, perimeter, and distance of intramembrane particles increased, whereas particle numbers per area decreased. Ultrastructural changes were, however, not accompanied by changes in Cx43 mRNA expression. In contrast, transcription of the gap junction regulator zonula occludens (ZO) protein 1 significantly increased, whereas its protein expression was unaffected. Phosphorylation of Serine (S) 368 of the Cx43 C-terminus has previously been associated with gap junction disassembly and reduction in gap junction communication. Hyperosmolar sucrose treatment led to enhanced phosphorylation of Cx43S368 and was accompanied by inhibition of gap junctional intercellular communication, demonstrated by a scrape loading-dye transfer assay. Taken together, Cx43 gap junctions are fast reacting elements in response to hyperosmolar challenges and can therefore be considered as one of the first responders to hyperosmolarity. In this process, phosphorylation of Cx43S368 was associated with disassembly of gap junctions and inhibition of their function. Thus, modulation of the gap junction assembly might represent a target in the treatment of brain edema or trauma.

Keywords: Cx43; FRIL; freeze fracture; hyperosmolar; sucrose; ultrastructure

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