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Elevated maxi-K(+) ion channel current in glaucomatous lamina cribrosa cells
Mustapha Irnaten1, Richard C Barry, Deborah M Wallace
1UCD School of Medicine and Medical Science, University College Dublin, Ireland.
Experimental Eye Research
|August 3, 2013
Summary
Glaucoma patients show increased maxi-K(+) channel activity in lamina cribrosa cells, responding more to mechanical stress. This heightened activity, linked to elevated intracellular calcium, may contribute to glaucoma pathogenesis.
Area of Science:
- Ophthalmology
- Cell Physiology
- Biophysics
Background:
- The lamina cribrosa (LC) is a mechanically dynamic region in the eye.
- LC cells are exposed to continuous mechanical forces.
- Glaucoma is associated with changes in ocular biomechanics.
Purpose of the Study:
- To investigate mechano-sensitive maxi-K(+) ion channel activity in lamina cribrosa cells from normal and glaucoma subjects.
- To determine the role of intracellular calcium in regulating maxi-K(+) channel function under mechanical stress.
- To compare channel activity between normal and glaucoma LC cells.
Main Methods:
- Primary cultures of LC cells from normal and glaucoma donors.
- Whole-cell patch-clamp technique to measure maxi-K(+) currents.
- Hypotonic solution-induced cell membrane stretch to simulate mechanical stress.
- Pharmacological inhibition of calcium channels (verapamil) and store re-uptake (2-APB).
Main Results:
- Basal and stretch-induced maxi-K(+) currents were significantly elevated in glaucoma LC cells compared to normal controls.
- Hypotonic stretch markedly increased maxi-K(+) current in both normal and glaucoma LC cells.
- Verapamil and 2-APB reduced basal maxi-K(+) current in glaucoma cells but not normal cells, and reduced stretch-induced currents in both groups.
Conclusions:
- Calcium-dependent maxi-K(+) channel activity is elevated in lamina cribrosa cells of glaucoma patients.
- Increased intracellular calcium levels in glaucoma LC cells may contribute to heightened channel activity.
- These findings suggest a potential role for maxi-K(+) channels in glaucoma pathophysiology.
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