Expression of Signal Transducer and Activator of Transcription-3 in Androgenetic Alopecia: A Case-Control Study

Abstract

Background: Signal transducer and activator of transcription (STAT)-3 belongs to a group of latent transcription factors phosphorylated and activated by several protein tyrosine kinases, including members of Janus-kinases (JAKs) family. It is has been implicated that the JAK-STAT pathway activation could promote quiescence in the hair cycle, and topical treatment of mouse and human skin with JAK-inhibitors was shown to result in rapid hair growth. Objective: Our aim was to assess the tissue expression of STAT3 in patients with androgenetic alopecia and correlate it with disease severity and clinical parameters. Methods: Twenty five androgenetic alopecia patients who served as both cases and controls were included in this study. Full clinical examination was done and tissue STAT3 gene expression was then measured by real-time polymerase chain reaction. Results: Scalp tissue affected by androgenetic alopecia show significantly higher STAT3 gene expression levels compared to unaffected (androgen independent) areas. (P<0.001), but no statistically significant relation was found between tissue STAT3 expression level and severity of hair loss (P=0.660) Limitations: Limited sample size Conclusion: This study demonstrated an upregulation in STAT3 gene expression in androgenetic alopecia. Further studies are needed to assess the possible role of the JAK-STAT pathway in the pathogenesis of androgenetic alopecia.

Targeted immunotherapy for hair regrowth and regeneration

“…Pharmacological, immunological and genetic inhibition of these macrophages sufficiently induced anagen in mice. Whether a similar mechanism is present in the human HF niche is unknown, but STAT3 is upregulated in AGA scalps ( 35 ).…”

“…Topical JAK inhibition not only reverses hair loss in AA mice, but also induces the telogen-to-anagen transition in disease-free C56Bl/6 mice (33). This suggests that the JAK-STAT pathway is also involved in normal hair cycles (34), leading to the discovery of a distinct subset of TREM2+ macrophages that maintain HFSC quiescence by secreting oncostatin M (1). Pharmacological, immunological and genetic inhibition of these macrophages sufficiently induced anagen in mice.…”