|
|
|
|
|
|
|
||
Article |
Early Ca2+-related Tight Junction Events
The molecular mechanisms by which Ca2+ and metal ions interact with the binding sites that modulate the tight junctions (TJs) have not been fully described. Metal ions were used as probes of these sites in the frog urinary bladder. Basolateral Ca2+ withdrawal induces the opening of the TJs, a process that is abruptly terminated when Ca2+ is readmitted, and is followed by a complete recovery of the TJ seal. Mg2+ and Ba2+ were incapable of keeping the TJ sealed or of inducing TJ recovery. In addition, Mg2+ causes a reversible concentration-dependent inhibition of the Ca2+-induced TJ recovery. The effects of extracellular Ca2+ manipulation on the TJs apparently is not mediated by changes of cytosolic Ca2+ concentration. The transition elements, Mn2+ and Cd2+, act as Ca2+ agonists. In the absence of Ca2+, they prevent TJ opening and almost immediately halt the process of TJ opening caused by Ca2+ withdrawal. In addition, Mn2+ promotes an almost complete recovery of the TJ seal. Cd2+, in spite of stabilizing the TJs in the closed state and halting TJ opening, does not promote TJ recovery, an effect that apparently results from a superimposed toxic effect that is markedly attenuated by the presence of Ca2+. The interruption of TJ opening caused by Ca2+, Cd2+, or Mn2+, and the stability they confer to the closed TJs, might result from the interaction of these ions with E-cadherin. Addition of La3+ (2 µM) to the basolateral Ca2+-containing solution causes an increase of TJ permeability that fully reverses when La3+ is removed. This effect of La3+, observed in the presence of Ca2+ (1 mM), indicates a high La3+ affinity for the Ca2+-binding sites. This ability of La3+ to open TJs in the presence of Ca2+ is a relevant aspect that must be considered when using La3+ in the evaluation of TJ permeability of epithelial and endothelial membranes, particularly when used during in vivo perfusion or in the absence of fixatives.
Key Words: tight junction • calcium • cadmium • lanthanum • E-cadherin
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  M. G. Price, C. F. Davis, F. Deng, and D. L. Burgess The {alpha}-Amino-3-hydroxyl-5-methyl-4-isoxazolepropionate Receptor Trafficking Regulator "Stargazin" Is Related to the Claudin Family of Proteins by Its Ability to Mediate Cell-Cell Adhesion J. Biol. Chem., May 20, 2005; 280(20): 19711 - 19720. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Jans, J. Simaels, E. Lariviere, P. Steels, and W. Van Driessche Extracellular Ca2+ regulates the stimulation of Na+ transport in A6 renal epithelia Am J Physiol Renal Physiol, October 1, 2004; 287(4): F840 - F849. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Kassab Jr., R. P. Marques, and F. Lacaz-Vieira Modeling Tight Junction Dynamics and Oscillations J. Gen. Physiol., July 30, 2002; 120(2): 237 - 247. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-C. Lacherade, A. Van De Louw, E. Planus, E. Escudier, M.-P. D'Ortho, C. Lafuma, A. Harf, and C. Delclaux Evaluation of basement membrane degradation during TNF-{alpha}-induced increase in epithelial permeability Am J Physiol Lung Cell Mol Physiol, July 1, 2001; 281(1): L134 - L143. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. D. CRANDALL and M. A. MATTHAY Alveolar Epithelial Transport . Basic Science to Clinical Medicine Am. J. Respir. Crit. Care Med., March 15, 2001; 163(4): 1021 - 1029. [Full Text]
|
|
|
|
 |
|
 P. De Smet, J. Li, and W. Van Driessche Hypotonicity activates a lanthanide-sensitive pathway for K+ release in A6 epithelia Am J Physiol Cell Physiol, July 1, 1998; 275(1): C189 - C199. [Abstract] [Full Text] [PDF]
|
|
|
|
