Advanced glycation end products (AGE) and the receptor for AGE are present in gastrointestinal tract of familial amyloidotic polyneuropathy patients but do not induce NF-κB activation

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1970
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Abstract
Familial amyloidotic polyneuropathy (FAP), Portuguese type, is a hereditary amyloidosis caused by mutated transthyretin (ATTR) in which an exchange of valine for methionine at position 30 has taken place (ATTR Val30Met). Gastrointestinal complications, such as nausea, diarrhoea and malabsorption, have a significant impact on survival since the cause of death in the majority of cases is a consequence of extreme malnutrition due to dysmotility of the gastrointestinal tract. Recently, a role of the receptor for advanced glycation end products (RAGE) has been implicated in amyloid toxicity. Transthyretin (TTR) amyloid fibrils have been shown to have affinity for RAGE and subsequently induce NF-κB activation and apoptosis. Since gastrointestinal dysfunction plays an important role in FAP, we wanted to investigate if amyloid toxicity in the gastrointestinal tract is related to RAGE, NF-κB activation and apoptosis. Gastrointestinal tract autopsy samples were studied for the distribution of amyloid, RAGE, advanced glycation end products (AGE) and NF-κB. Furthermore, we examined the immunoreactivity of an apoptotic marker to investigate if an apoptotic pathway contributes to amyloid toxicity. The distribution of RAGE and AGE strongly correlated to that of amyloid deposits. Sequential immunofluorescence staining revealed a clear relationship between TTR, AGE and RAGE. No correlation between NF-κB, apoptotic marker and amyloid deposits was found. We conclude that RAGE-AGE or RAGE-TTR interaction might play important roles for gastrointestinal dysfunction and amyloid toxicity, although not through NF-κB activation and apoptosis.
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matsunaga1970actaadvanced Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Noriko Matsunaga;Intissar Anan;Sture Forsgren;Ryoji Nagai;Peter Rosenberg;Seikoh Horiuchi;Yukio Ando;Ole B. Suhr;Noriko Matsunaga;Intissar Anan;Sture Forsgren;Ryoji Nagai;Peter Rosenberg;Seikoh Horiuchi;Yukio Ando;Ole B. Suhr;
Journal acta neuropathologica
Year 1970
DOI
doi:10.1007/s00401-002-0574-0
URL
https://link.springer.com/article/10.1007/s00401-002-0574-0
Keywords
pathology neurosciences

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