Mr Janosch Heller

Interests

I am interested in the molecular changes which occur on the Bruch's membrane in age-related macular degeneration. During the progression of the disease, anti-adhesive molecules such as tenascin-C become upregulated and cause the detachment of the retinal pigment epithelium from Bruch’s membrane. Subsequently, this leads to a degeneration of photoreceptors and to visual loss. Since the retinal pigment epithelium is crucial for the integrity of the retina, a transplantation of these cells into diseased eyes seems to be a promising treatment of age-related macular degeneration. However, transplantions have had limited success due to a lack of adhesion and degeneration of the grafted cells. Therefore, modulating the binding abilities of the retinal pigment epithelium to the pathological Bruch's membrane is key in developing a transplantational cure of the disease. This can be achieved via activation and over-expression of integrins that enhances adhesion and migration of the grafted cells.

TN-C becomes upregulated after laser-induced CNV as an animal model of AMD. Laser-induced CNV was performed in Lister Hooded rats as an animal model of age-related macular degeneration. Only the left eye was lasered and the right eye was used as control (Control, A). The rats were kept for 1, 2, 4 or 8 weeks (B-E) after lasering. Sections were stained for tenascin-C and RPE65. The retinal pigment epithelium was visible as a red monolayer (see arrows). No tenascin-C was detectable in Bruch’s membrane next to the RPE layer in Control (arrows in, A). However, after lasering, tenascin-C became upregulated in Bruch’s membrane (arrows, B-E). In addition, the RPE monolayer was disrupted within the lesion site (arrows, B-E).
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Research Focus

Equipment

Behavioural analysis

Cell culture

Cell transplantation

Confocal microscopy

Fluorescence microscopy

Immunohistochemistry

Microscopy

Recombinant protein expression