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Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

ABSTRACT: Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

PROVIDER: PRJNA967368 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24441100.fastq.gz	Fastqsanger.gz
	SRR24441098.fastq.gz	Fastqsanger.gz
	SRR24441099.fastq.gz	Fastqsanger.gz

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Similar Datasets

Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:Purpose: This study aimed to explore the mechanism of Celastrol in improving psoriasis through single-cell transcriptomics Methods: Supplementation with intragastric administration of celastrol in C57BL/6 mice to observe its effect on IMQ-induced psoriasis. Single-cell RNA sequencing were performed to explore the role of celastrol for IMQ-induced psoriasis. Results: A natural product library was used to screen for a small molecule compound, celastrol, that could interfere with fibroblast-macrophage communication. It was demonstrated that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages, thereby blocking communication between the two cells Conclusion: We report that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages. The use of celastrol maybe a noveltherapeuticoption for psoriasis.

2024-04-20 | GSE231728 | GEO

Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:In the present study, we analyzed single-cell multi-omics data from psoriasis patients and healthy individuals and found that more fibroblast-macrophage communication was present in the dermis of psoriasis lesions, exacerbating psoriasis progression. A natural product library was used to screen for a small molecule compound, celastrol, that could interfere with fibroblast-macrophage communication. It was demonstrated that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages, thereby blocking communication between the two cells. Moreover, conditional knockdown of LRP1 by fibroblasts significantly improved psoriasis in mice, suggesting that LRP1 may be an important target for the treatment of psoriasis.

2024-03-31 | GSE230842 | GEO

Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

| PRJNA962821 | ENA

Celastrol directly targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression.

Project description: Not available

| S-EPMC11959968 | biostudies-literature

Activation of Fibroblast LRP1 by AT2-secreted MDK Affects OTUB1/SLC7A11 Ubiquitination to Inhibit Fibroblast Ferroptosis in Idiopathic Pulmonary Fibrosis.

Project description:Idiopathic pulmonary fibrosis (IPF), a chronic interstitial fibrosing pneumonia of unknown cause, is characterized by an irreversible decrease in alveolar cells and an increase in fibroblasts. In our research, the numbers of AT2 cells and fibroblasts are abnormally regulated, but AT1 cells are significantly reduced in lung tissue sections from patients with IPF and mice. By analyzing the single-cell sequence from GEO database and experimental validation both in vivo and in vitro, it is found that the abnormally regulated AT2 cells secreting a large amount of MDK to activate the CTHRC1+ fibroblasts LRP1 receptor and inhibit the ferroptosis of fibroblasts. Further, by activating the LRP1 receptor in CTHRC1+ fibroblasts, the RNA-seq results reveal that the expression level of OTUB1 increased significantly. The ubiquitination experiment results showed that OTUB1, as a deubiquitinated molecule, can directly bind to the ferroptosis inhibitory protein SLC7A11, removing the ubiquitination modification of SLC7A11 and stabilizing its expression level to inhibit ferroptosis in fibroblasts. Meanwhile, this molecular pathway was verified in mice by dropping adenovirus through the airway, and the same experimental results as in vitro were verified. In conclusion, our study verified that IPF leads to abnormal regulation of AT2 secreting MDK, which activates LRP1 receptor and increases OTUB1 in fibroblasts. Deubiquitylation modification of OTUB1 stabilizes the expression level of SLC7A11, which results in a decrease in fibroblast ferroptosis, leading to an abnormal regulation of its programmed death, ultimately the deterioration of IPF.

2026-05-01 | GSE262882 | GEO

The protective effect of celastrol in ANIT-induced cholestasis

Project description:Purpose: The goals of this study was to (1) evaluate the protective effect of celastrol on alpha-naphthylisothiocyanate (ANIT)-induced cholestasis and (2) which genes were recovered by celastrol. Methods:To investigate the protective effect of celastrol on ANIT-induced cholestasis, the WT mice were randomly assigned into two groups, respectively (n=3): (1) ANIT; (2) ANIT+Celastrol. ANIT+Celastrol group was orally treated with celastrol (10 mg/kg dissolved in 1% DMSO + 2% Tween 80 + 97% water) for 5 consecutive days. After celastrol was treated for 3 days, ANIT and ANIT+Celastrol groups were given a single oral dose of ANIT. All mice were killed 48 h after ANIT administration. Liver samples were harvested and frozen at -80 °C before analysis. Results: A total of 978 DEGs were identified. Large numbers of these DEGs were related to activation of SIRT1, which included increased FXR signaling and inhibition of PPARγ, nuclear factor-kappa B (NF-κB), and P53 signaling. Conclusions: Celastrol could protect ANIT-induced cholestasis by recovering disrupted Sirt1 level.

2018-02-09 | GSE110391 | GEO

Transcription profiling of human LNCaP cells treated with celastrol or vehicle for 6h

Project description:Celastrol is a natural product that affects LNCaP gene expression by 6h; We used microarrays to detail the global programme of gene expression affected by celastrol treatment at 6h Experiment Overall Design: LNCaP cells were grown to 50% confluency and treated with celastrol for 6h prior to direct Trizol lysis and RNA isolation

2008-11-07 | E-GEOD-5505 | biostudies-arrayexpress

Celastrol treatment on mouse embryonic fibroblasts (MEFs)

Project description:Celastrol has been shown to sensitize leptin receptor signaling and reduce ER stress. Current microarray data provide the gene expression profile in mouse embryonic fibroblasts (MEFs) after Celastrol treatment compared with control.

2016-07-08 | GSE84154 | GEO

Hypothalamus of lean mice treated with celastrol or DMSO

Project description:Given that celastrol?s leptin-sensitizing effect requires high levels of circulating leptin, but lean mice have low levels of circulating leptin so that celastrol has no effect on lean mice. Analysis celastrol-induced hypothalamic gene expression profile change in lean mice will also be serving as negative control for DIO mice analysis.

2018-12-27 | GSE124356 | GEO

Adipose-Derived Stem Cell Exosomes Alleviate Psoriasis by Inducing Tregs Differentiation to Inhibit Inflammatory Response

Project description:Psoriasis is an immune-mediated chronic inflammatory skin disease, which is clinically characterized by erythema and scales. The pathogenesis is complex, easy to relapse and difficult to cure. Mesenchymal stem cell exosomes (MSCs) are well known for their potent immunomodulatory properties. However, the possible role and underlying mechanisms of adipose mesenchymal stem cell exosomes (ADSC-EVs) in psoriasis have been rarely studied. Here, we investigate whether ADSC-EVs can alleviate psoriasis-related symptoms. In vivo results indicate that subcutaneous injection of ADSC-EVs can effectively improve imiquimod (IMQ)-induced psoriasis in mice. miRNA sequencing analysis aimed to obtain differentially expressed miRNAs in ADSC-EVs and IL17A-EVs, and found that hsa-miR-21-5p, hsa-miR-10a-5p and hsa-miR-126-5p were up-regulated in ADSC-EVs. For further mechanism research, we used exosomes and miRNA to treat T cells respectively to detect changes in the proportion of Treg cells and inflammation-related factors. The results revealed that ADSC-EVs and hsa-miR-21-5p, hsa-miR-10a-5p and hsa-miR-126-5p can induce Treg differentiation, inhibit the secretion of pro-inflammatory factors and promote the secretion of anti-inflammatory factors. The same conclusion was reached by administering ADSC-EVs in IMQ psoriasis mice. These findings indicated that ADSC-EVs alleviated psoriasis inflammation possibly by promoting Treg differentiation through hsa-miR-21-5p, hsa-miR-10a-5p and hsa-miR-126-5p. This study provides new light on the application of ADSC-EVs as a promising therapeutic method for psoriasis.

2026-09-20 | GSE277657 | GEO

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