795 Senescent adipocytes accumulate in the dermis of obese mice deficient in leptin signaling

The hair follicle is a complex mini-organ that undergoes continuous cycles of growth and regeneration. Hair cycling depends on tightly coordinated crosstalk between epithelial cells, fibroblasts, immune adipocytes. Recent studies demonstrated in addition to metabolic dysregulation neurocognitive impairment, mice are genetically deficient leptin (ob/ob) or its receptor (db/db) exhibit prolonged telogen, suggesting role for obesity and/or signaling the control cycling. Cellular senescence state irreversible cell cycle arrest which cells also secrete pro-inflammatory cytokines (known as senescence-associated secretory phenotype; SASP) promote aging age-related disorders. Previous showed adipocytes obese ob/ob db/db senescent, their SASP drives pathology by recruiting macrophages. Our laboratory previously established Trem2+ macrophages stem quiescence (HFSC) during telogen. However, whether these responsible telogen phenotype observed signaling-deficient mice, recruitment presence senescent dermal remain unknown. Here, we show adipocyte layer expanded characterized an accumulation upregulated expression. Furthermore, skin was defined increased infiltration We postulate driven adipocytes, turn recruit HFSC quiescence-promoting via SASP. suggest physiological biology, further underscore importance control.