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Purpose <p>Matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of metalloproteinases, regulate extracellular matrix remodeling and neural tissue homeostasis. Transforming growth factor β1 modulates inflammation, ECM deposition, and tissue repair. Dysregulation of these pathways may contribute to congenital spinal dysraphism. This study quantified cerebrospinal fluid MMP-9, TIMP-1, and TGF-β1 in neonates with myelomeningocele and evaluated their potential as pathogenic mediators or biomarkers.</p> Methods <p>Preoperative CSF samples were collected from 48 neonates with isolated myelomeningocele (Group 1) and 24 age-matched controls with sterile CSF (Group 2). MMP-9, TIMP-1, and TGF-β1 concentrations were measured via ELISA. Intergroup differences were analyzed, and Pearson correlation assessed relationships among biomarkers.</p> Results <p>CSF MMP-9 levels were significantly elevated in neonates with myelomeningocele compared to controls (57.12 ± 64.19&#xa0;ng/mL vs. 11.29 ± 6.79&#xa0;ng/mL; <i>p</i> &lt; 0.05). TIMP-1 (368.78 ± 220.08&#xa0;ng/mL vs. 450.04 ± 390.22&#xa0;ng/mL) and TGF-β1 (2.32 ± 1.44&#xa0;ng/mL vs. 2.524 ± 1.07&#xa0;ng/mL) did not differ significantly. MMP-9 correlated positively with TIMP-1 across all subjects (<i>p</i> &lt; 0.05) and with TGF-β1 within the myelomeningocele group (<i>p</i> &lt; 0.05), indicating coordinated regulation of ECM degradation and fibrogenic signaling.</p> Conclusion <p>Elevated CSF MMP-9 in neonates with myelomeningocele suggests dysregulated ECM remodeling may be associated with neural tube malformation. MMP-9 may serve as a biomarker of ECM dysregulation, providing insights into the pathogenesis of congenital spinal dysraphism and identifying possible targets for future therapeutic interventions.</p>

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

  • 期刊论文

  • 发表日期：

    2026年2月4日

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  • Ibrahim Alataş,
  • Larisa Andrada Ay,
  • Hakkı Kemal Erdinç,
  • Nursu Kara,
  • Cenk Çelik,
  • Ece Çetin,
  • Gülseli Berivan Sezen,
  • Şeyhmus Kerem Özel,
  • Merih Cetinkaya,
  • Palmet Gün Atak,
  • Uzay Görmüş

摘要

Purpose

Matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of metalloproteinases, regulate extracellular matrix remodeling and neural tissue homeostasis. Transforming growth factor β1 modulates inflammation, ECM deposition, and tissue repair. Dysregulation of these pathways may contribute to congenital spinal dysraphism. This study quantified cerebrospinal fluid MMP-9, TIMP-1, and TGF-β1 in neonates with myelomeningocele and evaluated their potential as pathogenic mediators or biomarkers.

Methods

Preoperative CSF samples were collected from 48 neonates with isolated myelomeningocele (Group 1) and 24 age-matched controls with sterile CSF (Group 2). MMP-9, TIMP-1, and TGF-β1 concentrations were measured via ELISA. Intergroup differences were analyzed, and Pearson correlation assessed relationships among biomarkers.

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 (368.78 ± 220.08 ng/mL vs. 450.04 ± 390.22 ng/mL) and TGF-β1 (2.32 ± 1.44 ng/mL vs. 2.524 ± 1.07 ng/mL) did not differ significantly. MMP-9 correlated positively with TIMP-1 across all subjects (p < 0.05) and with TGF-β1 within the myelomeningocele group (p < 0.05), indicating coordinated regulation of ECM degradation and fibrogenic signaling.

Conclusion

Elevated CSF MMP-9 in neonates with myelomeningocele suggests dysregulated ECM remodeling may be associated with neural tube malformation. MMP-9 may serve as a biomarker of ECM dysregulation, providing insights into the pathogenesis of congenital spinal dysraphism and identifying possible targets for future therapeutic interventions.