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Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

ABSTRACT: Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

PROVIDER: PRJNA1099896 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28673022_1.fastq.gz	Fastqsanger.gz
	SRR28673022_2.fastq.gz	Fastqsanger.gz
	SRR28673023_1.fastq.gz	Fastqsanger.gz
	SRR28673023_2.fastq.gz	Fastqsanger.gz
	SRR28673024_1.fastq.gz	Fastqsanger.gz

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Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

| PRJNA1100990 | ENA

Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. The supernatants from the co-culture of UV-aged mouse primary keratinocytes with synovial fibroblasts were collected to induce mouse primary articular chondrocytes (CCs) to become aging SNL CCs. On this basis, Spesolimab (100ng/ml) was added to culture aging SNL CCs to study the drug's effect on OA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 groups: control CCs, aging SNL CCs, aging SNL CCs+Spesolimab.

2024-05-01 | GSE264103 | GEO

Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. we generated epidermis keratinocyte conditional knockout mice (IL-36Ra-cKO) with topical administration of capsid-mutant Adeno-associated virus 2 (AAV2) vector23 encoding Cre recombinase (AAV2-Cre) to IL-36Rafl/fl mice. Subsequently, epidermal skin tissues were collected from IL-36Rafl/fl and IL-36Ra-cKO mice for RNA sequencing analysis.

2024-05-31 | GSE263907 | GEO

Enhanced IL-36R signaling promotes barrier impairment and inflammation in skin and intestine

Project description:Deficiency in IL-36R antagonist caused by loss of function mutations in IL-36RN leads to DITRA (1), a rare inflammatory human disease that belongs to a subgroup of Generalized Pustular Psoriasis (GPP). Herein, we report a novel functional genetic mouse model of DITRA with enhanced IL-36R signaling analogous to one observed in DITRA patients which supports and provides new insight in our understanding of IL-36 family of molecules in regulating barrier integrity across multiple tissues. Humanized DITRA-like mice displayed increased skin inflammation in preclinical model of psoriasis, and in vivo blockade of IL-36R pathway using anti-human IL-36R antibody ameliorated IMQ-induced skin pathology at both prophylactic and therapeutic treatments. Deeper characterization of the humanized DITRA-like mice revealed that deregulated IL-36R signaling promoted tissue pathology during intestinal injury and led to impairment in mucosal restoration in the repair phase of chronic DSS-induced colitis. Blockade of IL-36R pathway significantly ameliorated DSS-induced intestinal inflammation and rescued the inability of DITRA-like mice to recover from mucosal damage in vivo. Thus, our results indicate a central role for IL-36 in regulating the pro-inflammatory responses in the skin and epithelial barrier function in the intestine suggesting a new therapeutic potential for IL-36R axis in psoriasis and at the later stages of intestinal pathology.

2020-12-18 | GSE161406 | GEO

Synovial Macrophage Activation Profiles in Experimental Knee Osteoarthritis

Project description:To investigate differences in gene expression of synovial macrophages in experimental rat knee post traumatic osteoarthritis.

2024-03-22 | GSE216932 | GEO

Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading

Project description:Rapgef3 modulates macrophage reprogramming and exacerbates synovitis and osteoarthritis under excessive mechanical loading

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IL-36 receptor deletion aggravates lung injury and mortality in experimental murine sepsis through epithelial

Project description:Inflammation resolution is critical for sepsis induced acute lung injury (ALI) recovery. Interleukin-36 receptor (IL-36R) is a potent anti-inflammatory factor. However, its role in ALI resolution remains unclear. We investigated the effects of IL-36R during the ALI resolution process in a murine cecal ligation and puncture (CLP)-induced ALI model. Knockout IL-36R signaling aggravates CLP-induced lung injury, as manifested by elevated bacterial load and increased neutrophils recruitment to the lung. Thereafter, we used IL-36R knockout mice to discern the source cell of IL-36R during ALI. We found that IL-36R is predominantly generated by epithelial cells during the ALI process. Furthermore, we sorted lung epithelial cells on the ALI process. IL-36R-specific loss in epithelial cells leads to apoptosis through NF-κB pathway. Together, our findings identify molecules that are likely involved in sepsis induced lung injury that may inform biomarker and therapeutic development.

2024-01-02 | GSE240924 | GEO

IL-36R stimulation of colonic mouse fibroblasts

Project description:IL-36R stimulation of colonic mouse fibroblasts

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Upregulation of FOXD1 by YAP alleviates senescence and osteoarthritis

Project description:Cell senescence is a driver of various aging-associated disorders including osteoarthritis. Here, we identified a critical role for Yes-associated protein (YAP), a major effector of Hippo signaling, in maintaining a younger state of human mesenchymal stem cells (MSCs) and ameliorating osteoarthritis in mice. Targeted knockout of YAP in hMSCs resulted in premature cellular senescence. Mechanistically, YAP interacted with TEA domain transcriptional factor (TEAD) to activate forkhead box D1 (FOXD1) expression. YAP deficiency led to the downregulation of FOXD1, a geroprotective protein. In turn, overexpression of YAP or FOXD1 rejuvenated aged hMSCs. Moreover, intra-articular administration of lentiviral vectors encoding YAP or FOXD1 attenuated the development of osteoarthritis in mice. Collectively, our findings reveal YAP-FOXD1, a novel aging-associated regulatory axis, as a potential therapeutic target for gene therapy to alleviate osteoarthritis.

2019-02-17 | GSE110268 | GEO

DDX5-sIL-36R in keratinocytes controls skin inflammation

Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.

2020-09-09 | PXD021379 |

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