the demonstration of an aqp4/tgf-beta 1 pathway in murine astrocytes holds implications for both neuromyelitis optica and progressive multiple sclerosis

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ID: 129883
2020
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Abstract
The role exerted by Aquaporin 4 (AQP4) as a regulator of astrocyte immune functions has been poorly explored. A recent report demonstrates that under neuroinflammatory conditions, the expression of Aqp4 on murine astrocytes is mandatory for the effective control of acute inflammation in the central nervous system. Such an immunomodulatory function appears to be mediated by a promotion of the transforming growth factor beta 1 (Tgfb1) pathway. Here, these results are discussed in the context of neuromyelitis optica (NMO) and multiple sclerosis (MS) progressive forms. It is proposed that NMO and progressive MS might rely on opposite molecular mechanisms involving, in NMO, an acutely-defective AQP4/TGFB1 pathway and, in progressive MS, a chronically-stimulated AQP4/TGFB1 pathway. Data supporting the involvement of angiotensin II as a molecular link between AQP4 and TGFB1 are also reviewed.
Reference Key
nataf2020internationalthe Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Serge Nataf
Journal Intertax
Year 2020
DOI
10.3390/ijms21031035
URL
https://www.mdpi.com/1422-0067/21/3/1035
Keywords Keywords not found

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