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Gene expression of leptin receptor (LEPR)+ bone marrow (BM) mesenchymal stem cells after lymphotoxin 훽 receptor (LT훽R) inhibition [LTbR]

ABSTRACT: Gene expression of leptin receptor (LEPR)+ bone marrow (BM) mesenchymal stem cells after lymphotoxin 훽 receptor (LT훽R) inhibition [LTbR]

PROVIDER: PRJNA785162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17085066_1.fastq.gz	Fastqsanger.gz
	SRR17085066_2.fastq.gz	Fastqsanger.gz
	SRR17085067_1.fastq.gz	Fastqsanger.gz
	SRR17085067_2.fastq.gz	Fastqsanger.gz
	SRR17085068_1.fastq.gz	Fastqsanger.gz

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Gene expression of leptin receptor (LEPR)+ bone marrow (BM) mesenchymal stem cells after lymphotoxin receptor (LT R) inhibition [LTbR]

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Project description:To study the effect of LTbR induction on spleen and duodenum transcriptome, we performed RNA sequencing of the spleen and intestine after Intravenous LTbR agonist AC H6 or isotype treatment. We analyzed differential gene expression.

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Comprehensive understanding the molecular components of LTBR signalling complex in cancers

Project description:Lymphotoxin beta receptor (LTBR), a member of TNFRSF, was identified as a key regulator in the development, organization, and homeostasis of lymphoid tissues (Wolf, Seleznik, Zeller, & Heikenwalder, 2010). Recently, LTBR has been shown to play a role in tumor biology, both in solid tumors and in hematological cancers (Fernandes et al., 2016; Haybaeck et al., 2009; Lo et al., 2007). However, the role of LTBR in cancer biology is still controversial. From the perspective of tumor eradication, the combination of LIGHT and IFN-g can induce apoptotic cell death in HT29 cells and some other cell lines via the increase of intracellular reactive oxygen species (ROS) (Chang, Chao, Hsieh, & Lin, 2004; Zhang, Liu, Demchik, Zhai, & Yang, 2004). Artificial LTBR agonist was shown to induce tumor necrosis and decrease tumor burden in vivo in colon cancer or melanoma. (Hu et al., 2013), while recent studies revealed that LTBR mediated tumor progression, triggered by either LTα1b2 or LIGHT stimulation, leads to the recruitment of more infiltrating immune cells and the secretion of pro-survival inflammatory cyto-/chemokines (Ware, 2005). From this, the aim of the project is to compare the signalling changes between WT cells and HOIP absent Hep3B cells using a moTAP tagged LIGHT ligand. This ligand was pulled down by Flag IP, followed by Strep-tactin IP to explore the LTBR signalling complex with and without LUBAC. The result from this experiment would provide an unbiased picture of components of the LTBR-SC, also pointing out the differences between canonical NF-kB pathway and noncanonical Nf-kB pathway.

2025-04-01 | PXD034142 | Pride

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ANGPTL4 binds to leptin receptor to regulate ectopic bone formation and fat metabolism

Project description:Leptin protein was thought to be unique to leptin receptor (LepR), but the phenotypes of mice with mutation in LepR (db/db) and leptin (ob/ob) are not identical, and the cause remains unclear. Here, we show that db/db, but not ob/ob mice had defect in tenotomy-induced heterotopic ossification (HO), implicating alternative ligand(s) for LepR might be involved. Ligand screening revealed that ANGPTL4, a stress and fasting-induced factor, was elicited from brown adipose tissue after tenotomy, bound to LepR on PRRX1+ mesenchymal cells at the HO cite, thus promotes chondrogenesis and HO development. Disruption of LepR in PRRX1+ cells, or lineage ablation of LepR+ cells, or deletion of ANGPTL4 impeded chondrogenesis and HO in mice. Surprisingly, exogenous ANGPTL4 treatment not only promoted HO, but facilitated the transformation from white to brown adipose tissue in mice. These findings identify ANGPTL4 as a novel ligand for LepR to stimulate HO and regulate fat metabolism.

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