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Endothelial LATS2 is a suppressor of bone marrow fibrosis

ABSTRACT: Endothelial LATS2 is a suppressor of bone marrow fibrosis

PROVIDER: PRJNA935694 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23497664_1.fastq.gz	Fastqsanger.gz
	SRR23497664_2.fastq.gz	Fastqsanger.gz
	SRR23497665_1.fastq.gz	Fastqsanger.gz
	SRR23497665_2.fastq.gz	Fastqsanger.gz
	SRR23497666_1.fastq.gz	Fastqsanger.gz

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Endothelial LATS2 is a suppressor of bone marrow fibrosis

Project description:The skeletal system vasculature and specialized capillary subtypes regulate crucial elements of bone growth and regeneration. However, little is known about endothelial cell (EC) activation and plasticity during bone remodeling. Here, we demonstrate that the inactivation of the gene encoding Hippo kinase large tumor suppressor kinase 2 (Lats2) in ECs results in the development of a vascular defect in the metaphysis, which favours accumulation of hypertrophic chondrocytes and induces bone marrow fibrosis in the bone.

2024-06-03 | GSE225429 | GEO

Endothelial LATS2 is a suppressor of bone marrow fibrosis.

Project description:Myelofibrosis and osteosclerosis are fibrotic diseases disrupting bone marrow function that occur in various leukemias but also in response to non-malignant alterations in hematopoietic cells. Here we show that endothelial cell-specific inactivation of the Lats2 gene, encoding Hippo kinase large tumor suppressor kinase 2, or overexpression of the downstream effector YAP1 induce myofibroblast formation and lead to extensive fibrosis and osteosclerosis, which impair bone marrow function and cause extramedullary hematopoiesis in the spleen. Mechanistically, loss of LATS2 induces endothelial-to-mesenchymal transition, resulting in increased expression of extracellular matrix and secreted signaling molecules. Changes in endothelial cells involve increased expression of serum response factor target genes, and, strikingly, major aspects of the LATS2 mutant phenotype are rescued by inactivation of the Srf gene. These findings identify the endothelium as a driver of bone marrow fibrosis, which improves understanding of myelofibrotic and osteosclerotic diseases, for which drug therapies are currently lacking.

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Expression profiling in primary embryonic fibroblasts deficient for the lats2 locus

Project description:We previously reported LATS2 null mice (Yabuta et al., 2007). LATS2 known as a tumor suppressor protein. However, the LATS2 mediated transcriptional regulation remains largely unknown. To investigate potential signaling pathways, we performed the expression profiling by using primary MEFs derived from wild type and LATS2 null mice.

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