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The LINC Complex Regulates Tendon Elastic Modulus, Collagen Crimp, and Lateral Expansion During Early Postnatal

Nicholas M Pancheri1, Jordan T Daw2, Destinee Ditton1

  • 1Chemical & Biological Engineering, University of Idaho, Moscow, Idaho, USA.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|March 16, 2025
PubMed
Summary
This summary is machine-generated.

The linker of nucleoskeleton and cytoskeleton (LINC) complex regulates tendon development by sensing mechanical signals. Disabling LINC impacts tendon mechanics and collagen structure differently in energy-storing versus positional tendons.

Keywords:
KASH‐domainLINCSUN‐domaindevelopmentmechanobiologymechanotransductionnesprinnuclear mechanosensingtendontenogenesis

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Area of Science:

  • Cellular mechanobiology
  • Skeletal biology
  • Connective tissue development

Background:

  • Mechanical signals are crucial for tendon development, but their regulation remains poorly understood.
  • The nucleus, through the linker of nucleoskeleton and cytoskeleton (LINC) complex, is a key regulator of cellular mechanosensation.
  • The specific role of LINC in tenogenesis (tendon formation) has not been previously investigated.

Purpose of the Study:

  • To investigate the role of the LINC complex in regulating tendon development and tenogenesis.
  • To determine how disabling LINC-mediated mechanosensing affects tendon mechanical properties and structural organization.
  • To compare the effects of LINC disruption on an energy-storing tendon (Achilles tendon) versus a positional tendon (tail tendon).

Main Methods:

  • Utilized a mouse model with dominant-negative KASH (dnKASH) domain overexpression to disable LINC complex function.
  • Performed mechanical testing on Achilles tendons (AT) and tail tendons (TT) at postnatal day 10.
  • Analyzed changes in tendon mechanical properties, cross-sectional area, and collagen crimp distance.

Main Results:

  • Disabling the LINC complex significantly altered tendon mechanical properties and cross-sectional area in dnKASH mice.
  • The impact of LINC disruption on mechanical properties and structure differed between ATs and TTs.
  • Collagen crimp distance was significantly decreased in ATs and increased in TTs of dnKASH mice compared to controls.

Conclusions:

  • Nuclear mechanotransduction via the LINC complex plays a significant role in regulating neonatal tendon formation.
  • Disruption of the LINC complex specifically impacts tendon mechanics and collagen crimp structure.
  • Tendon responses to LINC complex disruption vary between energy-storing and positional tendons, highlighting distinct developmental mechanisms.