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α-Methyl-prednisolone normalizes the PKC mediated brain angiogenesis in dystrophic mdx mice

Tiziana Annese1, Simona Ruggieri1, Michela De Giorgis1

  • 1Department of Basic Medical Sciences, Neurosciences and Sensory Organs, Section of Human Anatomy and Histology, University of Bari Medical School Bari, University of Bari, Italy.

Brain Research Bulletin
|February 4, 2019
PubMed

Insights

Duchenne Muscular Dystrophy (DMD) brains show altered angiogenesis due to increased protein kinase C (PKC) and reduced tight junctions. Alpha-methyl-prednisolone (PDN) treatment normalized these factors, suggesting a new therapeutic mechanism for DMD.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Duchenne Muscular Dystrophy (DMD) can cause mental disability linked to neuronal and metabolic changes.
  • Altered angiogenesis and brain vascularization are implicated in DMD pathophysiology.

Purpose of the Study:

  • To investigate the effect of alpha-methyl-prednisolone (PDN) on angiogenic markers (HIF1α, VEGFA, VEGFR-2/FLK1) and protein kinase C (PKC) in the mdx mouse model of DMD.
  • To explore PDN's impact on brain tight junctions, specifically Occludin, in the context of DMD.

Main Methods:

  • Utilized the mdx mouse model, an established experimental model for Duchenne Muscular Dystrophy.
  • Quantified mRNA and protein levels of HIF1α, VEGFA, FLK1, PKC, and Occludin.
  • Assessed Occludin phosphorylation to evaluate tight junction integrity.

Main Results:

  • mdx mice exhibited overexpression of HIF1α, VEGFA, and FLK1, alongside increased PKC and reduced Occludin expression, indicating altered brain angiogenesis.
  • PDN treatment significantly decreased HIF1α, VEGF, FLK1, and PKC levels (mRNA and protein).
  • PDN administration restored Occludin expression and reduced its phosphorylation, suggesting improved tight junction function.

Conclusions:

  • PDN normalizes aberrant angiogenesis in the brains of mdx mice by suppressing PKC signaling.
  • This study reveals a novel mechanism of action for PDN in potentially mitigating neurological aspects of DMD.
Keywords:
AngiogenesisDuchenne Muscular DystrophyPKCPrednisoloneVEGFAVEGFR-2 (FLK1)

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