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PRL-2 phosphatase is required for vascular morphogenesis and angiogenic signaling

Mathilde Poulet1,2, Jacinthe Sirois2, Kevin Boyé1

  • 1Univ. Bordeaux, INSERM, LAMC (Laboratoire de l'Angiogenèse et du Microenvironment des Cancers), U1029, F-33600, Pessac, France.

Communications Biology
|October 24, 2020
PubMed

Insights

Protein tyrosine phosphatases regulate blood vessel formation. This study shows Phosphatase of Regenerative Liver-2 (PRL-2) is crucial for developmental angiogenesis, impacting endothelial cell migration and signaling pathways.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Vascular Biology

Background:

  • Protein tyrosine phosphatases (PTPs) are key regulators of cellular processes.
  • Atypical Phosphatase of Regenerative Liver (PRL) phosphatases' role in angiogenesis is largely unknown.
  • Angiogenesis is critical for development and implicated in diseases like cancer.

Purpose of the Study:

  • To investigate the function of PRL phosphatases in developmental angiogenesis.
  • To elucidate the role of PRL-2 (Ptp4a2) in postnatal mouse retinal vascular development.
  • To understand the molecular mechanisms by which PRL-2 influences angiogenesis.

Main Methods:

  • Analysis of inducible endothelial-specific and global Ptp4a2 mutant mice.
  • Assessment of retinal vascular outgrowth, arteriovenous differentiation, and sprouting angiogenesis.
  • Investigation of endothelial cell migration and key signaling pathways (VEGF-A, DLL-4/NOTCH-1).

Main Results:

  • Endothelial cells express PRL-2 in the postnatal retina.
  • Ptp4a2 deficiency in mice led to defective retinal vascular development.
  • PRL-2 deletion impaired endothelial cell migration and inhibited VEGF-A and DLL-4/NOTCH-1 signaling.

Conclusions:

  • PRL-2 is essential for normal developmental angiogenesis.
  • PRL-2 modulates vascular development by influencing endothelial cell migration and signaling.
  • PRL-2 represents a potential therapeutic target in angiogenesis-related conditions.

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