Cerebrospinal fluid matrix-remodeling biomarkers in neonates with myelomeningocele: MMP-9, TIMP-1, and TGF-β1

Ibrahim Alataş1, Larisa Andrada Ay2, Hakkı Kemal Erdinç3

  • 1Department of Neurosurgery, Spina Bifida and Fetal Center, İstanbul Beykent University, Istanbul, Turkey.

Abstract

Insights

Elevated matrix metalloproteinase-9 (MMP-9) in cerebrospinal fluid of neonates with myelomeningocele suggests abnormal extracellular matrix remodeling contributes to neural tube defects. MMP-9 may serve as a biomarker for this condition.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Biochemistry

Background:

  • Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) regulate extracellular matrix (ECM) remodeling and neural tissue homeostasis.
  • Transforming growth factor β1 (TGF-β1) influences inflammation, ECM deposition, and tissue repair.
  • Dysregulation of these pathways is implicated in congenital spinal dysraphism.

Purpose of the Study:

  • To quantify cerebrospinal fluid (CSF) levels of MMP-9, TIMP-1, and TGF-β1 in neonates with myelomeningocele.
  • To evaluate the potential of these molecules as pathogenic mediators or biomarkers in myelomeningocele.

Main Methods:

  • Preoperative CSF samples were collected from 48 neonates with myelomeningocele and 24 age-matched controls.
  • MMP-9, TIMP-1, and TGF-β1 concentrations were measured using ELISA.
  • Intergroup differences and biomarker correlations were analyzed.

Main Results:

  • CSF MMP-9 levels were significantly elevated in neonates with myelomeningocele compared to controls (57.12 ± 64.19 ng/mL vs. 11.29 ± 6.79 ng/mL; p < 0.05).
  • TIMP-1 and TGF-β1 levels did not differ significantly between groups.
  • MMP-9 showed positive correlations with TIMP-1 and TGF-β1, suggesting coordinated regulation.

Conclusions:

  • Elevated CSF MMP-9 in neonates with myelomeningocele indicates dysregulated ECM remodeling associated with neural tube malformation.
  • MMP-9 may function as a biomarker for ECM dysregulation in congenital spinal dysraphism.
  • These findings offer insights into pathogenesis and potential therapeutic targets.

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