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Tenascin-C inactivation impacts lung structure and function beyond lung development.

Sandrine Gremlich1, Matthias Roth-Kleiner2, Lucile Equey2

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Tenascin-C (TNC) deficiency impairs lung function in mice, causing lasting respiratory issues. These findings highlight TNC

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Area of Science:

  • Pulmonary Medicine
  • Developmental Biology
  • Extracellular Matrix Biology

Background:

  • Tenascin-C (TNC) is crucial during lung development and transiently expressed for tissue repair.
  • Previous studies indicated TNC inactivation impacts lung development.
  • The functional consequences of TNC deficiency on lung mechanics were not fully understood.

Purpose of the Study:

  • To investigate the long-term effects of Tenascin-C (TNC) deficiency on respiratory function in mice.
  • To assess lung mechanics in TNC-deficient mice from newborn to adult stages.
  • To explore the underlying molecular and structural changes associated with TNC inactivation.

Main Methods:

  • Respiratory function parameters were measured in wild-type (WT) and TNC-deficient mice at postnatal day 5 (P5) and 90 (P90).
  • Measurements were taken under basal conditions and following high tidal volume (HTV) ventilation.
  • Lung morphology, alpha smooth muscle actin (α-SMA) expression, collagen deposition, and signaling pathways (TGFβ, TLR4) were analyzed.

Main Results:

  • TNC-deficient mice exhibited increased static compliance (Cst) and inspiratory capacity (IC) at P5, persisting under HTV ventilation.
  • At P90, elevated Cst and IC were observed only under basal conditions.
  • TNC deficiency led to reduced α-SMA around small airways, thickened collagen layers, increased surfactant protein C (SP-C), and altered TGFβ/TLR4 signaling.

Conclusions:

  • TNC inactivation during lung organogenesis results in persistent functional deficits into adulthood.
  • Altered airway smooth muscle and extracellular matrix composition contribute to impaired lung function.
  • These findings are relevant for understanding pulmonary diseases like asthma and COPD characterized by airway remodeling and ventilation heterogeneity.