Neuroprotective effects of direct activation and transactivation of PDGFβ receptors

Maryam Vasefi,Michael A Beazely

doi:10.20517/2574-1209.2020.16

Abstract

Neuroprotective effects of direct activation and transactivation of PDGFβ receptors

Highlights

There are two major platelet-derived growth factor (PDGF) receptor isoforms (α and β) and four ligand isoforms (A-D) that form homo- or hetero-dimers[1]
Tseng and colleagues directly examined the neuroprotective effect of PDGF-BB against glutamate- or NMDA-induced excitotoxicity in cultured hippocampal neurons and found that PDGF-BB pretreatment can protect neurons from these insults in both dose- and timedependent manners[37]
We have previously demonstrated that direct or indirect (GPCR-mediated) activation of the PDGFβ receptor can protect neurons against NMDA receptordependent toxicity[72]

Summary

Introduction

There are two major platelet-derived growth factor (PDGF) receptor isoforms (α and β) and four ligand isoforms (A-D) that form homo- or hetero-dimers[1]. We will briefly review the direct and indirect [i.e., GPRC - receptor tyrosine kinase (RTK) transactivation] neuroprotective effects of PDGF receptor signaling, with a focus on the PDGFβ receptors. Activation of the PDGFβ receptor increases dendrite length and cell viability (via an anti-apoptotic effect) in rat primary midbrain neurons exposed to Tat[23].

Results

Conclusion