Systemic sclerosis & Raynaud's
Long Noncoding RNA H19 Mediates STAT3 ‐Dependent Activation of Keratinocytes and Fibroblasts in Systemic Sclerosis Skin
Authors' conclusion
This study shows that lncRNA H19 is a key mediator of STAT3-induced changes in fibrotic activation of fibroblast and keratinocytes in SSc skin
Study context
- Population
- Patients with diffuse systemic sclerosis (SSc) and healthy controls; forearm skin biopsies and explanted dermal fibroblasts
- Participants
- 20 vs 8
- Comparison
- Diffuse SSc vs healthy controls
- Diffuse SScn = 20
- Healthy controls (HCs)n = 8reference
- Outcome
- Role of long noncoding RNA (lncRNA) H19 in profibrotic activation of dermal fibroblasts and in their crosstalk with keratinocytes
Methodological detailsin situ hybridization, retroviral transduction and siRNA modulation, gel contraction and Transwell coculture
- In situ hybridization
- Retroviral transduction and siRNA modulation
- Gel contraction and Transwell coculture
Main finding
As reported in the abstract
TGF-β increased H19 expression in HC fibroblasts via STAT3 activation (fold)
2.2
IL-6 increased H19 expression in HC fibroblasts via STAT3 activation (fold)
1.4
IL-11 increased H19 expression in HC fibroblasts via STAT3 activation (fold)
3.5
Original publication
Long Noncoding RNA H19 Mediates STAT3 ‐Dependent Activation of Keratinocytes and Fibroblasts in Systemic Sclerosis Skin. Arthritis Rheumatol. Published 10 April 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →