Sodium transport systems in human chondrocytes II. Expression of ENaC, Na+/K+/2Cl- cotransporter and Na+/H+ exchangers in healthy and arthritic chondrocytes

• Trujillo, E. ^[1] ; Alvarez de la Rosa, D. ^[1] ; Mobasheri, A. ^[2] ; Gonzalez, T. ^[4] ; Canessa, C.M. ^[3] ; Martín Vasallo, P. ^[1]
  1. [1] Universidad de La Laguna

     Universidad de La Laguna

     San Cristóbal de La Laguna, España

     
  2. [2] University of Westminster

     University of Westminster

     Reino Unido

     
  3. [3] Yale University

     Yale University

     Town of New Haven, Estados Unidos

     
  4. [4] Rheumatology Service, Universitary Hospital of Canarias, La Cuesta, Tenerife, Spain

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• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 14, Nº. 4, 1999, págs. 1023-1031
• Idioma: inglés
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  • In this article, the second of two, we continue our studies of sodium-dependent transport systems in human cartilage from healthy individuals and with osteoarthritis (OA) and rheumatoid arthritis (RA). We demonstrate the presence of the epithelia1 sodium channel (ENaC), previously undescribed in chondrocytes. This system is composed of three subunits, a, 13 and y. We have shown that the human chondrocytes express at least the a and the l3 subunit of ENaC. The expression of these subunits is altered in arthritic chondrocytes. In RA samples the quantity of a and B is significantly higher than in control samples. On the other hand, ENaC a and B subunits are absent in the chondrocytes of OA cartilage. Human chondrocytes also possess three isoforms of the Na+/H+ exchanger (NHE), NHE1, NHE2 and NHE3. The NHE system is composed of a single protein and is believed to participate in intracellular pH regulation. Furthermore, our studies indicate that at least one isoform of the electroneutral Naf/K+/2C1- cotransporter (NKCC) is present in human chondrocytes. There are no obvious variations in the relative expression of NHE isoforms or NKCC between healthy and arthritic cartilage. Our data suggests that chondrocytes from arthritic cartilage may adapt to changes in their environmental sodium concentration through variations in ENaC protein levels. ENaC is also likely to serve as a major sodium entry mechanism, a process that, along with cytoskeletal proteins, may be part of mechanotransduction in cartilage.