Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Ectopic Expression of Cation Chloride Cotransporters KCC2 in Blood Exosomes, used as a Biomarker of Functional Rehabilitation

Laura Caccialupi
,
Amina Rezzag
,
Marine Tessier
,
Florent Poulhes
,
Cédric Sapet
,
Olivier Zelphati
ORCID logo ,
Claudio Rivera
,
Jérôme Laurin
ORCID logo ,
Christophe Pellegrino
* ORCID logo
Version 1 : Received: 24 August 2022 / Approved: 29 August 2022 / Online: 29 August 2022 (09:36:50 CEST)

How to cite: Caccialupi, L.; Rezzag, A.; Tessier, M.; Poulhes, F.; Sapet, C.; Zelphati, O.; Rivera, C.; Laurin, J.; Pellegrino, C. Ectopic Expression of Cation Chloride Cotransporters KCC2 in Blood Exosomes, used as a Biomarker of Functional Rehabilitation. Preprints 2022, 2022080480. https://doi.org/10.20944/preprints202208.0480.v1 Caccialupi, L.; Rezzag, A.; Tessier, M.; Poulhes, F.; Sapet, C.; Zelphati, O.; Rivera, C.; Laurin, J.; Pellegrino, C. Ectopic Expression of Cation Chloride Cotransporters KCC2 in Blood Exosomes, used as a Biomarker of Functional Rehabilitation. Preprints 2022, 2022080480. https://doi.org/10.20944/preprints202208.0480.v1

Abstract

Background. Traumatic brain injury (TBI) is the main cause of disabilities over the industrialized countries. Cognitive decline appears in the chronic phase of the pathology consecutively to cellular and molecular processes. Here we described the use of KCC2, a neuronal-specific potassium-chloride transporters as potent biomarker to predict cognitive dysfunctions after TBI. Methods. Using neuronal and total exosomes collection from blood serum in control and TBI subjects we were able to anticipate the decline of cognitive performance. Results. After TBI, we observed a significative and persistant loss of KCC2 expression in the blood exosomes that is correlated to changes in network activity and cellular processes such as secondary neurogenesis. Also we correlated this KCC2 loss in expression to the appearance of the cognitive decline observed in mice and more particularly we correlate the KCC2 loss of expression to the appearance of the depressive-like behavior. Conclusion. According to our protocol, we were able to confirm our previous findings in agreement with the potential therapeutic effect of bumetanide in the prevention of the post traumatic depression after TBI, by restoring the KCC2 expression thus preventing the massive neuronal death of interneurons and the secondary neurogenesis effect observed in such model.

Keywords

psychiatric disease; brain injury; chloride transporter

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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