Expression of advanced glycation end products and their receptor in skin from patients with systemic sclerosis with and without calcinosis
Davies CA et al. – Findings suggest a possible contribution of advanced glycation (AGE) Nε-carboxymethyl lysine-(CML) deposition on the extracellular matrix (ECM) in the dermis of the lcSScCal subgroup to the pathogenesis of formation of calcinotic deposits. Methods- Study was conducted to:
- To establish which tissue components express AGEs and their receptor (RAGE) in skin from pts with SSc, and
- How their expression relates to the disease subtypes and various clinical parameters
- Skin punch biopsies were taken from the forearms of:
- 61 SSc pts with lcSSc
- 32 with calcinosis (lcSScCal) and
- 29 w/o lcSSc
- 36 with the dcSSc subtype and 22 healthy control subjects
- IHC localization of AGE-CML and RAGE was assessed semi-quantitatively on the microvascular endothelium, dermal fibroblasts and the cutaneous ECM
Results- AGE-CML expression on the papillary dermis ECM of lcSScCal was greater vs control
- The reticular dermis of lcSScCal showed increased AGE- CML expression vs controls, dcSSc, and lcSSc
- Increased immunostaining for RAGE was seen on the reticular dermis ECM of the lcSScCal group vs controls
- lcSScCal subgroup showed correlations for AGE-CML, and to a lesser extent for RAGE, with increased RP duration
- No evidence that the expression of AGE-CML or RAGE related to Ab status, clinical or histological skin score or patient age
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