Mr Janosch Heller

Janosch Heller

University position

PhD student
Supervised by Prof James Fawcett and Prof Keith Martin

Departments

Department of Clinical Neurosciences

Institutes

Cambridge Centre for Brain Repair

Email

jpdh2@cam.ac.uk

Home page

http://www.brc.cam.ac.uk/

Research Themes

Clinical and Veterinary Neuroscience

Cellular and Molecular Neuroscience

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).
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

Keywords

age-related macular degeneration

retinal pigment epithelium

transplantation

Bruch's membrane

integrin

Clinical conditions

Age-related macular degeneration

Equipment

Behavioural analysis

Cell culture

Cell transplantation

Confocal microscopy

Fluorescence microscopy

Immunohistochemistry

Microscopy

Recombinant protein expression

Collaborators

No collaborators listed

Publications

2009

Calamai M, Specht CG, Heller J, Alcor D, Machado P, Vannier C, Triller A (2009), “Gephyrin oligomerization controls GlyR mobility and synaptic clustering.” J Neurosci 29(24):7639-48 Details