Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Am J Physiol Cell Physiol. 2009 Mar;296(3):C414-21. doi: 10.1152/ajpcell.00430.2008. Epub 2008 Dec 10.

Interaction of monocarboxylate transporter 4 with beta1-integrin and its role in cell migration.

Author information

  • 1Dept. of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Thomas Jefferson Univ., 1020 Locust St., Philadelphia, PA 19107, USA.

Abstract

Monocarboxylate transporter (MCT) 4 is a heteromeric proton-coupled lactate transporter that is noncovalently linked to the extracellular matrix metalloproteinase inducer CD147 and is typically expressed in glycolytic tissues. There is increasing evidence to suggest that ion transporters are part of macromolecular complexes involved in regulating beta(1)-integrin adhesion and cell movement. In the present study we examined whether MCTs play a role in cell migration through their interaction with beta(1)-integrin. Using reciprocal coimmunoprecipitation assays, we found that beta(1)-integrin selectively associated with MCT4 in ARPE-19 and MDCK cells, two epithelial cell lines that express both MCT1 and MCT4. In polarized monolayers of ARPE-19 cells, MCT4 and beta(1)-integrin colocalized to the basolateral membrane, while both proteins were found in the leading edge lamellapodia of migrating cells. In scratch-wound assays, MCT4 knockdown slowed migration and increased focal adhesion size. In contrast, silencing MCT1 did not alter the rate of cell migration or focal adhesion size. Taken together, our findings suggest that the specific interaction of MCT4 with beta(1)-integrin may regulate cell migration through modulation of focal adhesions.

PMID:
19073896
[PubMed - indexed for MEDLINE]
PMCID:
PMC2660264
Free PMC Article

Images from this publication.See all images (5)Free text

Fig. 1.
Fig. 2.
Fig. 3.
Fig. 4.
Fig. 5.
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk