Photodynamic therapy: basic principles and potential uses for the veterinary ophthalmologist

Giuliano, Elizabeth A.; Ota, Juri; Tucker, Sheryl A.

doi:10.1111/j.1463-5224.2007.00578.x

Cited by 30 publications

(35 citation statements)

References 60 publications

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“…The wavelength for excitation in photodynamic therapy is determined by the selection of photosensitizing agents. Furthermore, the depth for which the laser penetrates tissue depends on the wavelength of the light (26). For example, a long-wavelength light (from 600 to 700 nm) penetrates 50 -200% further than a short-wavelength light (from 400 to 500 nm).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of destruction is thought to be similar to that for photodynamic therapy, a cancer treatment, which involves the use of photochemical reactions mediated through the interaction of light, photosensitizing agents, and molecular oxygen (26,27). The reactions in the present study require ThT, indicating that laser-excited ThT plays an important role.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, photodynamic therapy has been considered to be a promising treatment for cancer, even though the cancer tissues are usually not directly accessible to the laser beams (26,27). For the same reason, by pursuing the methodology of applying the laser beams to various types of amyloid deposits, the laser beam-dependent destruction can become a general therapeutic approach against amyloidoses.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Destruction of Amyloid Fibrils of Keratoepithelin Peptides by Laser Irradiation Coupled with Amyloid-specific Thioflavin T

Ozawa

Kaji

Yagi

et al. 2011

Journal of Biological Chemistry

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Mutations in keratoepithelin are associated with blinding ocular diseases, including lattice corneal dystrophy type 1 and granular corneal dystrophy type 2. These diseases are characterized by deposits of amyloid fibrils and/or granular non-amyloid aggregates in the cornea. Removing the deposits in the cornea is important for treatment. Previously, we reported the destruction of amyloid fibrils of ␤ 2 -microglobulin K3 fragments and amyloid ␤ by laser irradiation coupled with the binding of an amyloid-specific thioflavin T. Here, we studied the effects of this combination on the amyloid fibrils of two 22-residue fragments of keratoepithelin. The direct observation of individual amyloid fibrils was performed in real time using total internal reflection fluorescence microscopy. Both types of amyloid fibrils were broken up by the laser irradiation, dependent on the laser power. The results suggest the laser-induced destruction of amyloid fibrils to be a useful strategy for the treatment of these corneal dystrophies.A number of proteins and peptides have been found to aggregate into insoluble amyloid fibrils that are involved in various diseases, including Alzheimer's disease, Parkinson's disease, and dialysis-related amyloidosis (1-5). Keratoepithelin is one of the amyloidogenic proteins responsible for blinding corneal dystrophies (6 -9). Although precursor proteins range from native globular proteins to unstructured peptides, the resultant amyloid fibrils have many characteristics in common (1-4). Amyloid fibrils are typically long, unbranched, and often twisted, consisting of several protofilaments. X-ray fiber diffraction experiments have shown that they are commonly constructed from ordered ␤-strands. The basic structure has been considered a cross-␤ structure in which the ␤-strands are located perpendicular to the fibril axis. In addition, amyloid fibrils exhibit specific optical behavior such as green birefringence when bound to the dye Congo red. They also bind to the fluorescence dye thioflavin T (ThT) 3 , resulting in a characteristic fluorescence emission at 482-490 nm with an excitation maximum at 446 -455 nm (10, 11).Hereditary corneal dystrophies are characterized by the abnormal deposition of amyloid fibrils and/or granular aggregation in the cornea (6 -9). Mutations of keratoepithelin, an extracellular matrix protein composed of 683 amino acids, also known as transforming growth factor ␤-induced (TGF␤I), are responsible for the dystrophies. Population analyses have revealed two hot spots of mutation, Arg-124 and Arg-555, associated with corneal dystrophies (7, 12). Regarding Arg-124, four different mutations are associated with four different phenotypes. The R124C mutation has been linked with lattice corneal dystrophy type 1, R124H with granular corneal dystrophy type 2, R124L with granular corneal dystrophy type 3, and R124S with a variant of granular corneal dystrophy type 1. Despite numerous studies, an effective therapeutic approach for these corneal dystrophies has yet to be established (9).Re...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Destruction of Amyloid Fibrils of Keratoepithelin Peptides by Laser Irradiation Coupled with Amyloid-specific Thioflavin T

Ozawa

Kaji

Yagi

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

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“…Photodynamic therapy involves the use of photochemical reactions of light with photosensitizing agents, inducing the generation of various types of active oxygen (27,28). The substrate can further react with oxygen molecules to produce superoxide anions, which can then create hydroxyl radicals.…”

Section: Laser-induced Inhibition and Destruction Of A␤(1-40)mentioning

confidence: 99%

Laser-induced Propagation and Destruction of Amyloid β Fibrils

Yagi

Ozawa

Sakurai

et al. 2010

Journal of Biological Chemistry

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The amyloid deposition of amyloid ␤ (A␤) peptides is a critical pathological event in Alzheimer disease (AD). Preventing the formation of amyloid deposits and removing preformed fibrils in tissues are important therapeutic strategies against AD. Previously, we reported the destruction of amyloid fibrils of ␤ 2 -microglobulin K3 fragments by laser irradiation coupled with the binding of amyloid-specific thioflavin T. Here, we studied the effects of a laser beam on A␤ fibrils. As was the case for K3 fibrils, extensive irradiation destroyed the preformed A␤ fibrils. However, irradiation during spontaneous fibril formation resulted in only the partial destruction of growing fibrils and a subsequent explosive propagation of fibrils. The explosive propagation was caused by an increase in the number of active ends due to breakage. The results not only reveal a case of fragmentation-induced propagation of fibrils but also provide insights into therapeutic strategies for AD.

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“…From its triplet state in the presence of oxygen, reactive free radicals and singlet oxygen species ensue. These, in turn, react with cell membranes, causing direct damage to the mitochondria, endoplasmic reticulum, and/or plasma membranes [3].…”

Section: Introductionmentioning

confidence: 99%

Spatial Laser Induced Fluorescence Imaging (SLIFIMG) Analysis to Assess Tissue Photosensitizer Uptake

Ahmed¹

2013

IOSR-JPBS

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Photodynamic therapy: basic principles and potential uses for the veterinary ophthalmologist

Cited by 30 publications

References 60 publications

Destruction of Amyloid Fibrils of Keratoepithelin Peptides by Laser Irradiation Coupled with Amyloid-specific Thioflavin T

Destruction of Amyloid Fibrils of Keratoepithelin Peptides by Laser Irradiation Coupled with Amyloid-specific Thioflavin T

Laser-induced Propagation and Destruction of Amyloid β Fibrils

Spatial Laser Induced Fluorescence Imaging (SLIFIMG) Analysis to Assess Tissue Photosensitizer Uptake

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