Related Experiment Video

Updated: Jul 16, 2026

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration
10:43

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration

Published on: May 19, 2016

Osteopontin stimulates vascular smooth muscle cell migration by inducing FAK phosphorylation and ILK

Jing-Jing Li1, Mei Han, Jin-Kun Wen

  • 1Department of Biochemistry and Molecular Biology, Hebei Medical University, Shijiazhuang 050017, China.

Biochemical and Biophysical Research Communications
|March 6, 2007
PubMed

Insights

Osteopontin (OPN) triggers vascular smooth muscle cell (VSMC) migration by altering focal adhesion kinase (FAK) and integrin-linked kinase (ILK) activity. OPN induces FAK phosphorylation and ILK dephosphorylation, revealing a key signaling pathway.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Integrin-mediated cell migration is crucial for vascular smooth muscle cell (VSMC) function.
  • Focal adhesion kinase (FAK) and integrin-linked kinase (ILK) are key regulators of cell migration.
  • The specific roles of FAK and ILK in osteopontin (OPN)-induced VSMC migration are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms and signaling pathways governing OPN-induced VSMC migration.
  • To investigate the relationship between FAK and ILK activity during OPN-stimulated VSMC migration.

Main Methods:

  • VSMCs were treated with OPN.
  • Phosphorylation and dephosphorylation status of FAK and ILK were assessed.
  • The interaction and signaling cascade between FAK and ILK were analyzed.

Main Results:

  • OPN treatment induced FAK phosphorylation and ILK dephosphorylation in VSMCs.
  • OPN treatment led to the dissociation of FAK and ILK.
  • Evidence suggests ILK functions downstream of FAK in the OPN-induced VSMC migration pathway.

Conclusions:

  • FAK phosphorylation and ILK dephosphorylation are critical events in OPN-induced VSMC migration.
  • The interplay between FAK and ILK represents a significant signaling axis in VSMC motility.

More Related Videos

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Quantitative Measurement of Invadopodia-mediated Extracellular Matrix Proteolysis in Single and Multicellular Contexts14:23

Quantitative Measurement of Invadopodia-mediated Extracellular Matrix Proteolysis in Single and Multicellular Contexts

Published on: August 27, 2012

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Cancer Cell Migration through Invadopodia01:35

Cancer Cell Migration through Invadopodia

Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However, invadopodia can...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...