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KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease

ABSTRACT: KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease

PROVIDER: PRJNA603350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10971369.fastq.gz	Fastqsanger.gz
	SRR10971370.fastq.gz	Fastqsanger.gz
	SRR10971371.fastq.gz	Fastqsanger.gz
	SRR10971372.fastq.gz	Fastqsanger.gz
	SRR10971373.fastq.gz	Fastqsanger.gz

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KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease

Project description:Kallikrein-related peptidase 6 (KLK6) is a secreted serine protease hypothesized to promote inflammation via cleavage of protease-activated receptors (PAR)1 and PAR2. KLK6 levels are elevated in multiple inflammatory and autoimmune conditions, but no definitive role in pathogenesis has been established. Here, we show that skin-targeted overexpression of KLK6 causes generalized, severe psoriasiform dermatitis with spontaneous development of debilitating psoriatic arthritis-like joint disease. The psoriatic skin and joint phenotypes are reversed by normalization of skin KLK6 levels and attenuated following genetic elimination of PAR1 but not PAR2. Conservation of this regulatory pathway was confirmed in human psoriasis using vorapaxar, an FDA-approved PAR1 antagonist, on explanted lesional skin from psoriasis patients. Beyond defining a critical role for KLK6-PAR1 signaling in promoting psoriasis, our results demonstrate that KLK6-PAR1-mediated inflammation in the skin alone is sufficient to drive inflammatory joint disease. Further, we identify PAR1 as a promising cytokine-independent target in therapy of psoriasis and psoriatic arthritis.

2020-03-25 | GSE144312 | GEO

KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease.

Project description:Kallikrein-related peptidase 6 (KLK6) is a secreted serine protease hypothesized to promote inflammation via cleavage of protease-activated receptor 1 (PAR1) and PAR2. KLK6 levels are elevated in multiple inflammatory and autoimmune conditions, but no definitive role in pathogenesis has been established. Here, we show that skin-targeted overexpression of KLK6 causes generalized, severe psoriasiform dermatitis with spontaneous development of debilitating psoriatic arthritis-like joint disease. The psoriatic skin and joint phenotypes are reversed by normalization of skin KLK6 levels and attenuated following genetic elimination of PAR1 but not PAR2. Conservation of this regulatory pathway was confirmed in human psoriasis using vorapaxar, an FDA-approved PAR1 antagonist, on explanted lesional skin from patients with psoriasis. Beyond defining a critical role for KLK6/PAR1 signaling in promoting psoriasis, our results demonstrate that KLK6/PAR1-mediated inflammation in the skin alone is sufficient to drive inflammatory joint disease. Further, we identify PAR1 as a promising cytokine-independent target in therapy of psoriasis and psoriatic arthritis.

| S-EPMC7260032 | biostudies-literature

RNA-seq of dorsal root ganglion from IMQ-induced psoriasiform dermatitis mice.

Project description:We divided the male C57BL/6 mice into two groups: a non-treatment group and an IMQ-induced psoriasiform dermatitis group. We isolated the C3-C5 ganglia from male mice, then preserved them in RNA stabilization solution. RNA was extracted using Trizol, followed by transcriptome sequencing.

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Single-cell sequencing of dorsal root ganglion from IMQ-induced psoriasiform dermatitis mice.

Project description:We divided the e male C57BL/6 mice into two groups: a non-treatment group and an IMQ-induced psoriasiform dermatitis group. The dorsal root ganglia of the mice were extracted, enzymatically digested, and then enriched using Percoll. Subsequently, single-cell RNA sequencing was performed.

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RNA-seq of dorsal root ganglion from IMQ-induced psoriasiform dermatitis mice.

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Project description:Single-cell sequencing of dorsal root ganglion from IMQ-induced psoriasiform dermatitis mice.

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Complement C3 Exacerbates Imiquimod-Induced Skin Inflammation and Psoriasiform Dermatitis.

Project description: Not available

| S-EPMC5319416 | biostudies-literature

Immunity to commensal skin fungi promotes psoriasiform skin inflammation

Project description:Immunity to commensal skin fungi promotes psoriasiform skin inflammation

| PRJNA605153 | ENA

Transcription profiling of wild type and transgenic 35S:PAR1-GG Arabidopsis seedlings

Project description:Transcription profiling of wild type and transgenic 35S:PAR1-GG seedlings. To characterize the transcriptional networks altered by constitutive overexpression of PAR1 in seedlings, using two-color long-oligonucleotide microarrays.

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