Thyroid cell spreading and focal adhesion formation depend upon protein tyrosine phosphorylation and actin

A S Yap1, J R Keast, S W Manley

  • 1Department of Physiology and Pharmacology, University of Queensland St. Lucia, Brisbane, Australia.

Insights

Thyroid cells use protein tyrosine phosphorylation and microfilament dynamics for spreading on collagen. Thyrotropin (TSH) and cell contact regulate this adhesion, preserving thyroid follicular differentiation in culture.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Biochemistry

Background:

  • Cellular adhesion to the extracellular matrix influences cell function and behavior.
  • Thyroid cell spreading on substrates is mediated by adhesive interactions.
  • Thyrotropin (TSH) and intercellular contact were previously found to inhibit thyroid cell spreading, not initial attachment, preserving differentiation.

Purpose of the Study:

  • To investigate the role of cytoplasmic components in mediating thyroid cell adhesion to collagen.
  • To understand the intracellular mechanisms regulated by TSH and cell contact in thyroid cell adhesion.

Main Methods:

  • Observed changes in focal adhesions, stress fibers, and microtubules during cell spreading.
  • Utilized genistein (tyrosine kinase inhibitor) and cytochalasin B (microfilament disruption).
  • Used colchicine to disrupt microtubules.

Main Results:

  • Cell spreading involved accumulation of vinculin and phosphotyrosine in focal adhesions, followed by cytoskeletal assembly.
  • Genistein and cytochalasin B inhibited cell spreading and focal adhesion formation but not initial attachment.
  • Microtubule disruption with colchicine did not affect thyroid cell-substrate adhesion parameters.

Conclusions:

  • Protein tyrosine phosphorylation and microfilament integrity are crucial for thyroid cell spreading on substrates.
  • These cytoplasmic components are potential targets for TSH and intercellular contact to regulate cell adhesion and thyroid cell behavior.

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