The ocular lens is a transparent epithelial–fibrous organ whose transparency depends,
among other factors, on the regulation of intracellular calcium concentration ([Ca²⁺]ᵢ).
Disruptions in calcium ion (Ca²⁺) signaling are associated with the development of
cataract, the most common cause of vision loss. Among the key regulators of calcium
homeostasis in the lens are TRP family ion channels, particularly TRPV4, which
functions as a mechanosensitive and osmosensitive channel responsible for Ca²⁺ influx
and the maintenance of cellular functionality. This study investigated TRPV4 channel
activity and its role in Ca²⁺ signaling during cataract progression. Postoperative human
lens epithelial samples were obtained from patients at different disease stages at the Eye
Hospital, University Medical Centre Ljubljana. Cells were stained with the fluorescent
calcium indicator Fura-2, and changes in [Ca²⁺]ᵢ were monitored following mechanical
stimulation and after application of the TRPV4 antagonist HC-067047. Quantitative
analysis showed that mechanical stimulation triggered a rapid, transient increase in
[Ca²⁺]ᵢ that propagated intercellularly. Application of the TRPV4 antagonist reduced the
amplitude and slowed the propagation of the Ca²⁺ signal, demonstrating that TRPV4
contributes to maintaining effective Ca²⁺ responses and intercellular communication.
The effect of the TRPV4 antagonist was more pronounced in the earlier stages of the
disease, whereas this effect was less evident in advanced stages of cataract. However,
it should be emphasized that the sample size was limited and the observed differences
were relatively subtle; therefore, the results should be interpreted with caution. The
observed trends may reflect changes in Ca²⁺ signaling associated with cataract
progression, but further studies with a larger number of samples are required to draw
firm conclusions regarding changes in TRPV4 channel functionality.
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