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Cd248a regulates pericyte development and viability in zebrafish.

Chao Wang1, Yinming Zhong2, Yi Zhang1

  • 1Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University) and Key Laboratory of Tumor Immunopathology, Ministry of Education of China, Chongqing, China.

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CD248a regulates zebrafish pericyte numbers and blood-brain barrier integrity. This study reveals CD248a protects pericytes from hypoxia-induced apoptosis, offering new insights into vascular development.

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Area of Science:

  • Developmental Biology
  • Vascular Biology
  • Zebrafish Models

Background:

  • CD248 is a known pericyte marker in mammals, crucial for neovascularization.
  • Its specific role in zebrafish pericytes is largely uncharacterized.
  • Understanding CD248 in zebrafish can provide conserved insights into vascular development.

Purpose of the Study:

  • To investigate the function of zebrafish CD248 orthologs in pericyte biology.
  • To determine the role of cd248a in embryonic pericyte development and function.
  • To elucidate the mechanisms regulating pericyte proliferation and apoptosis in zebrafish.

Main Methods:

  • Identification of zebrafish CD248 orthologs (cd248a and cd248b).
  • Generation and analysis of cd248a and cd248b mutant zebrafish.
  • Assessment of pericyte numbers, blood-brain barrier integrity, and apoptosis.
  • Pharmacological inhibition of platelet-derived growth factor receptor.

Main Results:

  • cd248a, not cd248b, is predominantly expressed in embryonic zebrafish pericytes.
  • cd248a mutants exhibit reduced pericyte numbers and compromised blood-brain barrier.
  • cd248a overexpression increases pericyte proliferation, inhibited by AG1295.
  • cd248a deficiency enhances hypoxia-induced pericyte apoptosis.

Conclusions:

  • Zebrafish cd248a plays a critical role in regulating pericyte proliferation and survival.
  • cd248a is essential for maintaining blood-brain barrier integrity during development.
  • cd248a provides a protective effect against hypoxia-induced pericyte apoptosis.