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Effect of deletion of Impdh2 on gene expression in the forlimbs from E12.5 embryos and osteoclasts (OCs)

ABSTRACT: Effect of deletion of Impdh2 on gene expression in the forlimbs from E12.5 embryos and osteoclasts (OCs)

PROVIDER: PRJNA1021171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26182269_1.fastq.gz	Fastqsanger.gz
	SRR26182269_2.fastq.gz	Fastqsanger.gz
	SRR26182270_1.fastq.gz	Fastqsanger.gz
	SRR26182270_2.fastq.gz	Fastqsanger.gz
	SRR26182271_1.fastq.gz	Fastqsanger.gz

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Effect of deletion of Impdh2 on gene expression in the forlimbs from E12.5 embryos and osteoclasts (OCs)

Project description:Many factors are essential for skeletal development and homeostaisis. Here we report that inosine monophosphate dehydrogenase type II (Impdh2) is a key positive regulator for limb development and bone resorption. Deletion of Impdh2 in limb mesenchymal progenitors impaired the differentiation of mesenchymal cells into chondrocyte. Meanwhile, deletion of Impdh2 in osteoclast precursors results in mice an osteopetrotic phenotype via suppressing osteoclast differentiation. Our results reveal a previously unrecognized role of Impdh2 on skeletal development and homeostasis.

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The gene expression profiles of maturing osteoclasts (OCs) co-cultured with prostate cancer (PCa) cell lines.

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The microRNA profiles of extracellular vesicles (EVs) from osteoclasts (OCs) co-cultured with prostate cancer (PCa) cell lines [OCEVmiRNA-seq]

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IMPDH2 filaments protect from neurodegeneration in AMPD2 deficiency

Project description:Metabolic dysregulation is one of the most common causes of pediatric neurodegenerative disorders. However, how the disruption of ubiquitous and essential metabolic pathways predominantly affect neural tissue remains unclear. Here we use a mouse model of AMPD2 deficiency to study cellular and molecular mechanisms that lead to selective neuronal vulnerability to purine metabolism imbalance. We show that AMPD deficiency in mice primarily leads to hippocampal dentate gyrus degeneration despite causing a generalized reduction of brain GTP levels. Remarkably, we uncover that neurodegeneration resistant regions of the hippocampus accumulate micron sized filaments of IMPDH2, the rate limiting enzyme in GTP synthesis. In contrast, IMPDH2 filaments are barely detectable in the dentate gyrus, which show a progressively neuroinflammation and neurodegeneration. Furthermore, using a human AMPD2 neural cell culture model, we show that blocking IMPDH2 polymerization with a dominant negative IMPDH2 variant impairs AMPD2 deficient neural progenitor growth. Together, our findings suggest that IMPDH2 polymerization prevents detrimental GTP deprivation caused by AMPD2 deficiency, providing resistance to neurodegeneration. This data opens the possibility of exploring the involvement of IMPDH2 assembly as a therapeutic intervention for neurodegeneration.

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Macrophages and osteoclasts stem from a bipotent progenitor that lies downstream of the common macrophage/osteoclast/dendritic cell progenitor

Project description:Macrophages (MΦs), osteoclasts (OCs) and dendritic cells (DCs) are closely related, but the exact steps in their lineage commitment are unclear. We here dissect B220-CD11blow/negc-Kit+c-Fms+ mouse bone marrow (BM) cells into a CD27+Flt3+ progenitor popula

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The gene expression profiles of maturing osteoclasts (OCs) co-cultured with prostate cancer (PCa) cell lines.

Project description:The gene expression profiles of maturing osteoclasts (OCs) co-cultured with prostate cancer (PCa) cell lines.

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Nuclear IMPDH2 controls the DNA damage response by modulating PARP1 activity

Project description:Nuclear metabolism and DNA damage response are intertwined processes, but the precise molecular connections remain elusive. Here, we delve into this crosstalk using as a model triple-negative breast cancer (TNBC), a subtype often prone to DNA damage accumulation. We reveal that the de novo purine synthesis enzyme Inosine monophosphate dehydrogenase 2 (IMPDH2) is enriched on chromatin in TNBC when compared to other subtypes. IMPDH2 chromatin localization is DNA damage dependent and IMPDH2 repression leads to DNA damage accumulation. On chromatin, IMPDH2 interacts and modulates Poly [ADP-ribose] polymerase 1 (PARP1) activity by controlling nuclear availability of nicotinamide adenine dinucleotide (NAD+) -a shared metabolic cofactor- to fine-tune the DNA damage response. However, when IMPDH2 is restricted to the nucleus, it depletes nuclear NAD+, leading to PARP1 cleavage and cell death. Our study identifies a non-canonical nuclear role for IMPDH2 that act as convergence point of nuclear metabolism and DNA damage response. # Contributed equally *Corresponding authors: sara.sdelci@crg.eu; marta.garciacao@crg.eu

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Expression data from osteoclasts before and after co-culture with multiple myeloma plasma cells

Project description:To understand how interactions of myeloma cells with osteoclasts and mesenchymal stem cells in the bone marrow affect the clinical course of myeloma, we used microarrays to study changes in gene expression in freshly isolated myeloma plasma cells following co-cultures with osteoclasts (8 experiments) or with mesenchymal stem cells (13 experiments). Interaction with osteoclasts induced changes in the expression of 675 genes, and interaction with mesenchymal stem cells induced changes in the expression of 296 genes. Expression of only 58 genes commonly and similarly changed in both co-culture systems. Among these, we identified genes associated with overall, progression-free, and post-relapse survival, and developed survival prediction models. Gene expression data from 347 patients treated with total therapy 2 protocol, 433 with total therapy 3, and 98 patients who received various treatments (91 of them high-dose therapy with autologous stem cell support) were used for the analysis. Good predictive models were developed only for post-relapse survival, using genes involved in interaction with osteoclasts or with mesenchymal stem cells. The best predictive model used expression of first relapse of 33 probesets whose expression changed in myeloma cells following interaction with osteoclasts, with hazard ratios of 24, 20, and 12 for patients who relapsed following total therapy 2, total therapy 3 and the various other treatments, respectively. Among the probesets used for prediction, only 10, representing 8 genes, were commonly changed after both co-culture systems. These could present favorable target for therapy. Global gene expression profiling of osteoclasts (OCs) before and after co-culture with primary multiple myeloma plasma cells (MMPCs) was done using Affymetrix microarrays. Eight MMPC and OC co-culture experiments were performed using MMPC isolated from 8 patients and OC prepared from 8 different patients.

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