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Human oligodendrocytes express Cx31.3: function and interactions with Cx32 mutants.

Irene Sargiannidou¹, Meejin Ahn, Alan D Enriquez

¹Clinical Neurosciences Section, Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus.

Neurobiology of Disease

|March 21, 2008

Summary

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Human oligodendrocytes express connexin31.3 (Cx31.3), a protein similar to mouse Cx29. Mutations in connexin32 (Cx32) linked to Charcot-Marie-Tooth disease do not affect Cx31.3 expression or function in the brain.

Area of Science:

Neuroscience
Cell Biology
Genetics

Background:

Oligodendrocytes, the myelin-producing cells of the central nervous system (CNS), utilize gap junction (GJ) proteins like connexin32 (Cx32), Cx47, and Cx29.
X-linked Charcot-Marie-Tooth disease (CMT) involves CNS phenotypes potentially linked to dominant Cx32 mutations affecting other connexins.

Purpose of the Study:

To investigate the expression of Cx31.3, the human ortholog of murine Cx29, in the human brain.
To determine the relationship between Cx31.3, Cx32, and Cx47 in human oligodendrocytes.
To assess whether Cx32 mutants associated with CNS disorders impact Cx31.3 expression and function in vitro.

Main Methods:

Immunohistochemical localization of Cx31.3 in human brain tissue.
Co-expression analysis of Cx31.3 with Cx32 in human oligodendrocytes.

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In vitro studies using HeLa cells to examine Cx31.3 localization and hemichannel/GJ formation.

Assessment of Cx31.3 trafficking and function in the presence of Cx32 mutants.

Main Results:

Cx31.3 was found in human gray matter along small myelinated fibers, mirroring Cx29 localization in rodents.
Cx31.3 was co-expressed with Cx32 in a subset of human oligodendrocytes.
In HeLa cells, Cx31.3 localized to the cell membrane, forming hemichannels but not GJs.
Intracellular retention of CNS-associated Cx32 mutants did not alter the localization or function of co-expressed Cx31.3.

Conclusions:

Human Cx31.3 shares characteristics with its murine ortholog, Cx29.
Cx32 mutants implicated in CNS phenotypes do not affect Cx31.3 trafficking or function.
The pathogenic mechanisms of Cx32 mutants in oligodendrocytes may involve toxic effects independent of Cx31.3 interaction.