Bcl-xl and Bak protein expression in human optic nerve axons in ...

Abstract The aim of our study was an evaluation of Bcl-xl and Bak protein expressions in optic nerve axons in eyeballs after severe
injury and absolute glaucoma. We examined a series of 41 eye-
balls, which were enucleated, following extensive injury and a
series of 19 eyeballs from patients with absolute glaucoma. The
immunohistochemical reaction was performed, using antibodies
against human Bcl-xl and Bak protein with LSAB and DAB. In
the injured eyeballs in Group I, Bcl-xl protein expression was
observed in 53.8%, Bak in 38.5%, in Group II, Bcl-xl in 40%,
Bak 55%; in Group III, Bcl-xl in 62.5%, Bak in 62.5%. Nine (9),
out of 19 (47.4%) cases showed Bcl-xl protein positivity, Bak
15, out of 19 (78.9%). The percentage of cases with Bak protein
positivity was statistically higher than that for Bcl-xl (Bak/Bcl-
xl p=0.0356). The results showed that there may be a dominance
expression of proapoptotic proteins in optic nerve axons in glau-
coma. Introduction Perforative or obtuse severe trauma of the eyeball frequent- ly leads to complete and permanent loss of vision, which is usu-
ally caused by a direct mechanical damage to photoreceptors
and nerve cells, as well as in result of necrosis and apoptosis.
Retinal detachment can also be caused by trauma. In animal
experimental models, apoptosis - the programmed death of cells
- has been implicated as the major factor in the mechanism, leading to death of photoreceptors in this condition [1, 2]. It is
known, that the death of retinal ganglion cells, the axons of
which form the optic nerve, can be caused by experimental axo-
tomy. It has been demonstrated that retinal ganglion cell degen-
eration, due to trauma of this kind, is caused by apoptosis [1, 2,
3, 4]. However, to date, there have been no reports concerning
the mechanism of axon damage of ganglion cells, due to severe
trauma of the eyeball. Glaucoma is an optic neuropathy, charac-
terized by retinal ganglion cell death, axon loss, and an exca-
vated appearance of the optic nerve head. Retinal ganglion cell
mechanisms in experimental animal models of glaucoma and in
human glaucoma have been shown to involve apoptosis [5, 6, 7,
8]. The apoptotic cascade invokes a series of cellular events
which lead to cell death. Proteins from the Bcl-2 family play a
major role in apoptosis regulation at its decisive stage [9, 10].
Bcl-2 protein family may inhibit apoptosis - anti-apoptotic: Bcl-
2, Bcl-xl, Bcl-w and protein enhancing apoptosis -proapoptotic:
Bcl-xs, Bak and Bax [9, 11, 12]. There are no reports on apop-
totic protein expression in human retinal ganglion cells and their
axons under physiological conditions. It is not known how pro-
tein expression in the Bcl-2 subgroup changes in posttraumatic
conditions, the opportunity to assess the expression of these pro-
teins in the unique material provided in the form of eyeballs
enucleated as a result of severe trauma is interesting and useful
in attempting to explain the process of apoptosis in retinal gan-
glion cells. The aim of our study was an evaluation of Bcl-xl and
Bak expression in optic nerve axons in eyeballs after severe
trauma and absolute glaucoma. Material and Methods We examined a series of 41 eyeballs, which were enucleated after an extensive injury at the Department of Ophthalmology of
the Medical University of Bialystok over the period from 1991 to
2003, and a series of 19 eyeballs from patients with absolute glau-
coma, suffering from severe ophthalmalgia and treated, of neces- Bcl-xl and Bak protein expression in human optic nerve axons in eyeballs post- trauma and in the eyes with absolute glaucoma Resze

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