Localization of advanced glycation end-products and their receptor in tendinopathic lesions

• Eva Asomugha ^[5] ; Young Cho ^[1] ; Sharada Paudel ^[2] ; Yi Guo ^[3] ; Lew Schon ^[4] ; Zijun Zhang ^[4]
  1. [1] Rowan University

     Rowan University

     Borough of Glassboro, Estados Unidos

     
  2. [2] Frederick National Laboratory for Cancer Research

     Frederick National Laboratory for Cancer Research

     Estados Unidos

     
  3. [3] Montefiore Medical Center

     Montefiore Medical Center

     Estados Unidos

     
  4. [4] Mercy Medical Center

     Mercy Medical Center

     City of Springfield, Estados Unidos

     
  5. [5] OrthoVirginia, Alexandria, VA, USA

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• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 39, Nº. 9, 2024, págs. 1209-1215
• Idioma: inglés
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• Resumen

  • This study was designed to investigate the accumulation of advanced glycation end-products (AGEs) and the expression of the receptor of AGEs (RAGE) in tendinopathic tissues. In this study, tendinopathic posterior tibial tendons (PTT) were collected from patients (n=6). Redundant autografts of flexor digitorum longus tendon (FDL; n=3) were used for controls. The control and tendinopathic tendon tissues were used for extraction of proteins for western blot and sectioned for histology and immunohistochemistry. Tendinopathy of the PTT was confirmed histologically by the presentation of disorderly collagen fibers, high cellularity and increased vascularity. By immunohistochemistry, heterogeneous accumulation of AGEs was detected on the PTT sections and concentrated in areas, where collagen fibers were disorderly and tangled. In the PTT, roundish tenocytes were also AGEs-positive. In contrast, AGEs were diffuse, lightly stained in the FDL. A greater number of tenocytes within the tendinopathic lesions in the PTT were RAGE positive, compared to the tenocytes in the FDL. Western blot confirmed the presence of AGEs and RAGE in both tendinopathic PTT and control FDL but their band densities were not significantly different. The spatial relation of the accumulated AGEs and RAGEpositive tenocytes within the tendinopathic lesions indicates their involvement in the molecular pathology of tendinopathy.