Abstract
BackgroundMuch evidence indicates receptor for advanced glycation end products (RAGE) related inflammation play essential roles during aging. However, the majority of studies have focused on advanced glycation end products (AGEs) and not on other RAGE ligands. In the present study, the authors evaluated whether the accumulation of RAGE ligands and binding intensities between RAGE and its ligands differ in kidney, liver, and skeletal muscle during aging.ResultsIn C57BL/6 N mice aged 12 weeks, 12 months, and 22 months, ligands accumulation, binding intensities between RAGE and its ligands, activated macrophage infiltration, M1/M2 macrophage expression, glyoxalase-1expression, and signal pathways related to inflammation were evaluated. The RAGE ligands age-associated accumulation patterns were found to be organ dependent. Binding intensities between RAGE and its ligands in kidney and liver increased with age, but those in skeletal muscle were unchanged. Infiltration of activated macrophages in kidney and liver increased with age, but infiltration in the skeletal muscle was unchanged. M1 expression increased and M2 and glyoxalase-1 expression decreased with age in kidney and liver, but their expressions in skeletal muscle were not changed.ConclusionThese findings indicate patterns of RAGE ligands accumulation, RAGE/ligands binding intensities, or inflammation markers changes during aging are organs dependent.
Highlights
Much evidence indicates receptor for advanced glycation end products (RAGE) related inflammation play essential roles during aging
The accumulation of high motility group box 1 protein (HMGB1) and S100β in kidney of the three age groups was significantly increased with age (Fig. 1a)
HMGB1 and S100β accumulations in liver were significantly lower in the young group than in the middle-aged group, and HMGB1 and S100β levels in liver were different between the middle-aged and old groups (Fig. 1b)
Summary
Much evidence indicates receptor for advanced glycation end products (RAGE) related inflammation play essential roles during aging. The majority of studies have focused on advanced glycation end products (AGEs) and not on other RAGE ligands. The authors evaluated whether the accumulation of RAGE ligands and binding intensities between RAGE and its ligands differ in kidney, liver, and skeletal muscle during aging. The aging process can be described as a universal, intrinsic, progressive accumulation of deleterious changes in cells and tissues that increase morbidity and lead to death [1]. According to the recent theory of oxidationinflammation, chronic oxidative and inflammatory stress conditions explain the aging process [2]. Several studies have focused on the role played by receptor for advanced glycation end products (RAGE) on aging, because RAGE is known inducer of inflammation and oxidative stress. The extracellular portion of the receptor is followed by a hydrophobic transmembrane-spanning domain and by a highly charged, short cytoplasmic domain that is essential for intracellular RAGE signaling [3, 4].
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