8 research outputs found
Ion transport in chondrocytes, membrane transporters involved in intracellular ion homeostasis and the regulation of cell volume, free [Ca2+] and pH
Chondrocytes exist in an unusual and
variable ionic and osmotic environment in the extracellular
matrix of cartilage and are responsible for
maintaining the delicate equilibrium between extracellular
matrix synthesis and degradation. The
mechanical performance of cartilage relies on the
biochemical properties of the matrix. Alterations to the
ionic and osmotic extracellular environment of chondrocytes
have been shown to influence the volume,
intracellular pH and ionic content of the cells, which in
turn modify the synthesis and degradation of extracellular
matrix macromolecules. Physiological ion
homeostasis is fundamental to the routine functioning of
cartilage and the factors that control the integrity of this
highly evolved and specialized tissue. Ion transport in
cartilage is relatively unexplored and the biochemical
properties and molecular identity of membrane transport
mechanisms employed by chondrocytes in the control of
intracellular ion concentrations and pH is not fully
defined and this review focuses on these processes.
Chondrocytes have been shown to express voltage and
stretch activated ion channels, passive exchangers and
ATP dependent ion pumps. In addition, recent studies of
transport systems in chondrocytes have demonstrated the
presence of isozyme diversity that includes Na+/H+
exchange (NHE1, NHE3), Na+, K+-ATPase (several
isoforms) and others each of which possess considerably
different kinetic properties and modes of regulation. This
multitude of isozyme diversity indicates the highly specialized handling of ions and protons in order to
accomplish a fine regulation of their transmembrane
fluxes. The complexities of these transport systems and their patterns of isoform expression underscore the
subtlety of ion homeostasis and pH regulation in normal
cartilage. Perturbations in these mechanisms may affect
the physiological turnover of cartilage and thus increase
the susceptibility to degenerative joint disease