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Author Spotlight: Advancing Tendon Research by Developing Mouse Assembloids to Understand Cellular Mechanisms
Published on: March 22, 2024
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Localization of advanced glycation end-products and their receptor in tendinopathic lesions
Eva Asomugha1, Young Cho2, Sharada Paudel3
1OrthoVirginia, Alexandria, VA, USA.
Histology and Histopathology
|February 7, 2024
Summary
Advanced glycation end-products (AGEs) accumulate in tendinopathic tendons, alongside increased receptor of AGEs (RAGE) expression on tenocytes. These findings suggest AGEs and RAGE play a role in tendon injury pathology.
Area of Science:
- Biomedical Science
- Orthopedics
- Pathology
Background:
- Tendinopathy involves pathological changes in tendon tissue.
- Advanced glycation end-products (AGEs) are implicated in various chronic diseases.
- The role of AGEs and their receptor (RAGE) in tendinopathy is not fully understood.
Purpose of the Study:
- To investigate the accumulation of AGEs and expression of RAGE in human tendinopathic posterior tibial tendons (PTT).
- To compare AGEs and RAGE presence in tendinopathic PTT with healthy flexor digitorum longus (FDL) tendon autografts.
Main Methods:
- Histological and immunohistochemical analysis of tendinopathic PTT and control FDL tissues.
- Western blot analysis to confirm protein expression of AGEs and RAGE.
Main Results:
- Tendinopathic PTT showed disorganized collagen, increased cellularity, and vascularity.
- AGEs were heterogeneously accumulated in tendinopathic PTT, particularly around disorganized collagen and in tenocytes.
- RAGE-positive tenocytes were more numerous in tendinopathic PTT compared to controls.
- Western blot confirmed AGEs and RAGE expression in both groups, without significant density differences.
Conclusions:
- The spatial association of AGEs and RAGE-positive tenocytes in tendinopathic lesions suggests their involvement in the molecular pathology of tendinopathy.
- AGEs accumulation and RAGE expression are features of human tendinopathy.
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