Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2004 Oct:(427 Suppl):S152-62.

Hyaluronan and CD44: modulators of chondrocyte metabolism

Cheryl B Knudson  1 , Warren Knudson
Affiliations
  • PMID: 15480059
Review

Hyaluronan and CD44: modulators of chondrocyte metabolism

Cheryl B Knudson et al. Clin Orthop Relat Res. 2004 Oct.

Abstract

Stability of cell-matrix interactions promotes tissue homeostasis, and matrix receptors provide for the assembly and retention of matrix as well as the linkage to the signal transduction pathways activated in response to changes within the extracellular matrix. Therefore, changes in cell-matrix interactions may influence cell responses to cytokines and cell survival and may facilitate tissue remodeling. Matrix components sequester or present soluble morphogens to their signaling receptors. Another layer of complexity would be the establishment of new or uncoupling of cell-matrix interactions, leading to altered cellular response to morphogens. The hyaluronan receptor CD44 serves as the critical link for the retention of hyaluronan-proteoglycan aggregates to the chondrocyte cell surface. As we continue to define functional chondrocyte CD44, future studies will need to include analysis of the variant CD44 isoform expression, phosphorylation, cytoskeletal interactions, occupancy, and turnover. Disruption of chondrocyte CD44:hyaluronan interaction will induce a cascade of events resulting in the activation of both catabolic as well as anabolic gene products. Fragments of hyaluronan produced in free radical processes have the potential to augment the production of nitric oxide in a CD44-dependent mechanism. Data also support an emerging paradigm that CD44-mediated signaling affects both chondrocyte survival pathways as well as apoptotic pathways.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

LinkOut - more resources