Related Experiment Video
Updated: Jul 18, 2025

Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
RBM15-Mediated m6A Modification of K17 Affects Keratinocytes Response to IL-17A Stimulation in Psoriasis
Manni Fu1, Bei Zhou1, Nian Shi1
1Department of Dermatology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China.
Objective:
Psoriasis is characterized by excessive proliferation and abnormal differentiation of epidermal keratinocytes. This study aimed to reveal the function and mechanism of a N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein 15 (RBM15) in IL-17A-induced keratinocytes.
Methods:
A immortalized keratinocyte cell line HaCaT was used to undergo the IL-17A stimulation. The mRNA levels were detected by qRT-PCR, whereas the protein levels were measured by western blotting. The change of keratinocytes proliferation was determined using CCK8 and EdU assays, and the inflammation factors (IL-8 and TNF-α) in keratinocytes were analyzed by qRT-PCR. The m6A modification of Keratin 17 (K17) was confirmed by MeRIP and mRNA stability assays.
Results:
The levels of RBM15 and K17 in skin samples from patients with psoriasis and IL-17A-induced keratinocytes were upregulated, and showed the positive correlation. Silencing RBM15 suppressed viability, proliferation, and inflammation of keratinocytes that were enhanced by IL-17A stimulation. Moreover, RBM15 knockdown reduced the stability of K17 mRNA via m6A modification method. Since K17 is modified by RBM15, its overexpression relieved the effects of RBM15 knockdown on keratinocytes under IL-17A stimulation.
Conclusion:
This study revealed that RBM15 knockdown suppressed proliferation and inflammation by mediating m6A modification of K17 to reduce K17 stability in IL-17A-induced keratinocytes. Our findings may provide novel idea for improving the treatment of psoriasis.
Insights
RNA-binding motif protein 15 (RBM15) regulates psoriasis by controlling keratinocyte proliferation and inflammation. RBM15 knockdown reduces Keratin 17 (K17) mRNA stability via m6A modification, offering new psoriasis treatment insights.
Area of Science:
- Dermatology
- Molecular Biology
- Epigenetics
Background:
- Psoriasis involves keratinocyte hyperproliferation and abnormal differentiation.
- Interleukin-17A (IL-17A) plays a key role in psoriasis pathogenesis.
- N6-methyladenosine (m6A) modification is increasingly recognized in skin diseases.
Purpose of the Study:
- To investigate the function and mechanism of RNA-binding motif protein 15 (RBM15) in IL-17A-induced keratinocytes.
- To explore the role of RBM15 in psoriasis pathogenesis.
Main Methods:
- Utilized HaCaT keratinocyte cell line with IL-17A stimulation.
- Assessed mRNA and protein levels via qRT-PCR and Western blotting.
- Quantified keratinocyte proliferation (CCK8, EdU) and inflammation (IL-8, TNF-α).
- Confirmed m6A modification of Keratin 17 (K17) using MeRIP and mRNA stability assays.
Main Results:
- RBM15 and K17 were upregulated in psoriasis and IL-17A-stimulated keratinocytes.
- RBM15 silencing suppressed keratinocyte viability, proliferation, and inflammation.
- RBM15 knockdown decreased K17 mRNA stability through m6A modification.
- K17 overexpression counteracted the effects of RBM15 knockdown.
Conclusions:
- RBM15 knockdown inhibits keratinocyte proliferation and inflammation by reducing K17 mRNA stability via m6A modification.
- RBM15 acts as a key regulator in IL-17A-induced keratinocyte responses.
- Findings suggest RBM15 as a potential therapeutic target for psoriasis.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Chromatin Modification in iPS Cells
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...
The JAK-STAT Signaling Pathway

