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. 1999 Oct;83(10):1178–1182. doi: 10.1136/bjo.83.10.1178

Apolipoproteins J and E co-localise with amyloid in gelatinous drop-like and lattice type I corneal dystrophies

K Nishida 1, A Quantock 1, A Dota 1, N Choi-Miura 1, S Kinoshita 1
PMCID: PMC1722813  PMID: 10502582

Abstract

AIMS—Apolipoprotein J (apoJ) and apolipoprotein E (apoE) are thought to contribute to amyloid formation in patients with Alzheimer's disease. The aim of this investigation was to discover whether or not these apolipoproteins associate with corneal amyloid in gelatinous drop-like corneal dystrophy (GDCD) and lattice corneal dystrophy type I (LCD-I).
METHODS—Corneas from three eyes of three patients with GDCD and one eye of one patient with LCD-I were examined immunohistochemically using antibodies against apoJ and apoE. Two normal corneas were similarly examined. Tissue sections of brain from a patient with Alzheimer's disease were used as positive controls for the antibodies. For all negative controls, mouse IgG was used instead of the primary antibody.
RESULTS—Intense apoJ and apoE immunoreactivities were found in congophilic amyloid deposits in GDCD and LCD-I. These deposits were located subepithelially in GDCD, and subepithelially and intrastromally in LCD-I. In GDCD, immunostaining of subepithelial amyloid with anti-apoJ was noticeably stronger than with anti-apoE.
CONCLUSIONS—As in senile plaques in brain from a patient with Alzheimer's disease, apoJ and apoE co-localise with amyloid in corneas with GDCD and LCD-I.



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Figure 1  .

Figure 1  

(A-C) Immunostaining of brain from a patient who had died of Alzheimer's disease with antibodies to (A) anti-apolipoprotein J and (B) anti-apolipoprotein E. Positive immunostaining is seen in senile plaques. (C) Control section incubated with normal mouse serum IgG shows no discernible immunolabelling. (D-F) Immunostaining of normal cornea with anti-apolipoprotein J and anti-apolipoprotein E antibodies. The epithelium is delineated by arrowheads, and the endothelium identified by an arrow; s = stroma. (D) The antibodies to apolipoprotein J stain the superficial epithelium (as was found previously21), whereas (E) the antibody to apolipoprotein E antibody does not stain epithelium. (E) Anti-apolipoprotein E appears to stain the endothelial/Descemet's membrane region, although at this time we cannot totally rule out the possibility that this might represent an edge artefact. (D, E) Diffuse staining for apolipoprotein J and apolipoprotein E was found in stroma. (F) Control section incubated with normal mouse serum IgG shows no discernible immunolabelling. Bar=50 µm (A-C) and 100 µm (D-F).

Figure 2  .

Figure 2  

Immunostaining of gelatinous drop-like corneal dystrophy cornea with anti-apolipoprotein J and anti-apolipoprotein E antibodies. The epithelium (delineated by arrowheads in (B)) varies greatly in thickness. (A) When viewed under polarised light, congo red staining is seen in epithelial and subepithelial regions, showing a birefringent polarisation typical of amyloid. The posterior cornea is not visible here because tissue was obtained by a lamellar keratoplasty. (B) The antibodies to apolipoprotein J stain the subepithelial amyloid deposit (a) fairly intensely, and the stroma (s) more diffusely. (C) The anti-apolipoprotein E antibody also stains amyloid, but much less strongly than the anti-apolipoprotein J antibodies. (D) Control section incubated with normal mouse serum IgG shows no discernible immunolabelling. Bar=100 µm.

Figure 3  .

Figure 3  

Immunostaining of a lattice corneal dystrophy type I cornea with anti-apolipoprotein J and anti-apolipoprotein E antibodies. The epithelium is delineated by arrowheads, and the endothelium identified by an arrow. (A) When viewed under polarised light, congo red staining is seen subepithelially and in corneal stroma, showing birefringent polarisation typical of amyloid. (B) Immunostaining for apolipoprotein J clearly mirrors the distribution of subepithelial and intrastromal amyloid deposits. (C) Apolipoprotein E immunoreactivity also co-exists with amyloid, but appears to stain the section less strongly than the apolipoprotein J antibodies. (D) Control section incubated with normal mouse serum IgG shows no discernible immunolabelling. Bar=100 µm.

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