Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development

Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroinflammation is still a question of great biologic interest. For its pattern of expression and its known signaling cascades involving important regulators of inflammation as Fyn kinase and ALK, RPTPβ/ζ is a target receptor for PTN and MK in neuroinflammation. Pharmacologic modulation of the PTN, MK, RPTPβ/ζ and/or its downstream effectors, Fyn and ALK, is a novel therapeutic strategy to modulate neuroinflammation, from central or peripheral origin, in different pathological contexts. Author Contributions GH and EG wrote the manuscript and built Figure 1 and Table 1. MPR-A wrote the manuscript and built Figure 2. Funding This work has been supported by grants SAF2014-56671-R from Ministerio de Economía y Competitividad of Spain, PNSD001I2015 from National Plan on Drug abuse, Ministerio de Sanidad, Servicios Sociales e Igualdad of Sp...
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research

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