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Moyamoya disease (MMD) involves abnormal blood vessel growth. Researchers found that elevated tubulin proteins TUBA4A and TUBB4B contribute to MMD progression by affecting vascular smooth muscle cells, offering potential therapeutic targets.

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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Proteomics

Background:

  • Moyamoya disease (MMD) is a cerebrovascular disorder causing progressive intracranial arterial stenosis, leading to stroke.
  • The underlying pathogenesis of MMD is not fully understood, hindering effective diagnosis and treatment.

Purpose of the Study:

  • To investigate the molecular mechanisms and identify potential biomarkers and therapeutic targets for Moyamoya disease.

Main Methods:

  • Data-independent acquisition (DIA) proteomics on serum from MMD patients and controls.
  • ELISA validation, vascular organoid generation from induced pluripotent stem cells (iPSCs), histological staining, transcriptomics, and single-cell RNA sequencing (scRNA-seq).

Main Results:

  • Abnormal accumulation of vascular smooth muscle cells (VSMCs) in MMD patient arteries.
  • Significant upregulation of TUBA4A and TUBB4B in MMD serum.
  • TUBA4A and TUBB4B promote VSMC proliferation, migration, and phenotypic switching via the GJA1/PI3K/AKT/KLF4 pathway.
  • MMD vascular organoids show increased synthetic VSMCs with elevated TUBA4A and TUBB4B.

Conclusions:

  • Overexpression of TUBA4A and TUBB4B contributes to pathological vascular remodeling in MMD.
  • The GJA1/PI3K/AKT/KLF4 pathway is implicated in MMD pathogenesis.
  • TUBA4A and TUBB4B represent potential therapeutic targets for MMD intervention.