Cell swelling is the main feature of lens osmotic expansion; several proteins such as AR, P-gp, and Clcn3 are proposed to participate in this pathological mechanism.
Despite a matter of debate existed, most investigators thought that modulation of cell volume mainly depended on the coordination of P-gp and Clcn3 [15, 16].
P-gp has already been approved to have bimodal functions; it not only serves as the transmembrane transporter being responsible for the efflux of multidrugs in isotonic condition but also switches to a modulator of Clcn3 in hyperosmotic environment [20, 21].
On the basis of the previous theories and results, we hypothesize that lens osmotic expansion, imposed by AR overactivation, would stimulate Clcn3 and its modulator P-gp to delay the lenticular swelling.
mRNA Expressions of AR, P-Gp, and Clcn3 in LECs and Lenses.
Protein Detection of AR, P-Gp, and Clcn3 by Western Blot.
mRNA Expressions and Protein Levels of AR, P-g, and Clcn3 in LECs Induced by Galactose.
Protein levels of AR, P-gp, and Clcn3 were summarized in Figure 2(b).
mRNA Expressions and Protein Levels of AR, P-Gp, and Clcn3 in Rat Lenses.
Since elevation of gene transcription was not always coincident with gene translation, we further examined the protein levels of target genes including AR, P-gp, and Clcn3 by Western blot (Figure 4(b)).
The related proteins involved in osmotic expansion are AR, Clcn3, and its modulator P-gp.
In animals with binocular vision, fluoxetine promoted an increase in the expression of CLCN3
(20% increased), KCNV1 (20% increased), and KCNQ3 (30% increased), which encode ion channels that mediate chloride and potassium conductance (P < 0.05), and in animals with monocular deprivation fluoxetine produced also an increase in the expression of CLCN3
(50% increased expression; P = 0.01).