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RNA seq data of B cells from naïve, OPN knockout (Spp1-/-), ONKOSCID (SCID Spp1-/-) BALB/c mice

ABSTRACT: RNA seq data of B cells from naïve, OPN knockout (Spp1-/-), ONKOSCID (SCID Spp1-/-) BALB/c mice

PROVIDER: PRJNA486913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7725710.fastq.gz	Fastqsanger.gz
	SRR7725705.fastq.gz	Fastqsanger.gz
	SRR7725706.fastq.gz	Fastqsanger.gz
	SRR7725707.fastq.gz	Fastqsanger.gz
	SRR7725708.fastq.gz	Fastqsanger.gz

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RNA seq data of B cells from naïve, OPN knockout (Spp1-/-), ONKOSCID (SCID Spp1-/-) BALB/c mice

Project description:Marginal zone (IgM[hi] CD23[lo]MZ) and Follicular B (IgM[lo] CD23[hi]FB) cells in SCID Spp1-/- mice have different profile from naïve and Spp1-/- B cells. In addition, OPN mutation on the SCID background induced upregulation of genes involved in DNA replication and class switching of B cells

2021-08-20 | GSE118826 | GEO

Rab37-mediated OPN secretion enriches SPP1+ macrophages through autocrine–paracrine signaling to drive lung tumor progression

Project description:Tumor-associated Macrophages (TAMs) are highly plastic immune cells that shape the tumor microenvironment (TME) and influence cancer progression. However, the molecular determinants governing their functional heterogeneity remain incompletely understood. In this study, we identify Rab37 as a key regulator that remodels the states of macrophages within the lung TME. Single-cell RNA sequencing revealed that Rab37 wild-type (WT) tumors were enriched in immunosuppressive Spp1+ TAMs, whereas Rab37 knockout (KO) tumors contained a higher proportion of Thbs1+ TAMs, suggesting Rab37-dependent shifts in macrophage programming. Mechanistically, Rab37 promoted osteopontin (OPN) secretion, which activated STAT3 signaling to establish an autocrine feedback loop that sustained Spp1 expression and induced M2-like polarization. Paracrine OPN signaling further enhanced lung cancer cell proliferation, migration, and invasion. In clinical lung cancer specimens, CD163+/Rab37+/OPN+ TAMs correlated with recurrence and poor survival, and multivariate analysis confirmed their independent prognostic value. Together, these findings demonstrate that Rab37 governs macrophage phenotype and function by orchestrating OPN/STAT3 signaling, thereby reinforcing an immunosuppressive TME and promoting lung cancer progression. Targeting the Rab37–OPN axis may thus represent a promising therapeutic strategy.

2026-01-28 | GSE311076 | GEO

Cryptococcus exploits delayed microglial activation, and microglial osteopontin (OPN/Spp1) impairs peripheral host control

Project description:Cryptococcus, a neurotropic fungus and the World Health Organization (WHO) critical-priority pathogen, causes cryptococcal meningoencephalitis (CM), the second leading cause of death in HIV/AIDS patients. Despite the significance, host brain responses during CM remain underexplored. In a non-acute systemic mouse model, Cryptococcus infiltrates the brain within one day from circulation, yet full activation of microglia is delayed until 14 days post-infection. Microglia, regarded as sentinels of the central nervous system (CNS), exhibit slow responses, partly due to limited direct fungal recognition and reliance on T cells as a source of IFNg. Once activated, microglia upregulate Spp1, encoding osteopontin (OPN), a factor highly expressed in neurodegenerative diseases. Our findings demonstrate that microglia-derived OPN negatively impacts the host by altering peripheral immune responses. Thus, Cryptococcus exploits the delayed host response to establish brain infection, with activated microglia producing OPN in a host-detrimental manner.

2025-11-06 | GSE284662 | GEO

Gene expression profile of B cells from OPN-competent and deficient Faslpr autoimmune mice

Project description:We performed gene expression profile on splenic CD19+ cells from autoimmune Faslpr/lpr and OPN-/-Faslpr/lpr mice to investigate the dynamics at the basis of the more incident transformation characterizing OPN-deficient animals. GEP on splenic CD19+ from BALB/c and OPN-/- mice was performed as control.

2022-12-21 | GSE193790 | GEO

Comparative microRNA expression profiles of Schistosoma japonicum from SCID mouse and BALB/c mouse

Project description:Background: In immunodeficient mice, the growth and reproduction of schistosome were significantly retarded, and their virulence on the host was also weakened. Some studies have suggested that host factors including endocrine and immune signals can modulate the parasite’s development and maturation. However, it is still not clear for the molecular mechanisms underlying the growth and maturation regulation of schistosome. Methods: We isolated the total RNAs of female and male schistosome from immunodeficient SCID mice and immunocompetent BALB/c mice (labeled as S_F, S_M, B_F and B_M) obtained at five weeks post infection with cercariae, and constructed cDNA libraries of small RNAs using small RNA sample pre kit for small RNA deep sequencing on an Illumina (Solexa) platform. Results: Of the 122 (75 known and 47 novel) identified S. japonicum-specific miRNAs, statistical analysis revealed that 33 miRNAs (17 miRNAs were up-regulated and 16 were down-regulated, P<0.05) in female schistosome and 33 miRNAs (13 miRNAs were up-regulated and 20 were down-regulated, P<0.05) in male schistosome from SCID mice were differentially expressed when compared with those from BALB/c mice. The Venn diagram of the differentially expressed miRNAs shows 21 miRNAs were common between S_F vs B_ F and S_M vs B_M, 12 miRNAs were specific in female comparison, and other 12 were specific in male comparison. Conclusions: This study provides a comparative microRNAs expression profiles of schistosomes derived from SCID mice and immunocompetent BALB/c mice. A number of microRNAs were identified to potentially participate in regulating the development of schistosomes. These findings lay the foundation for schistosomiasis research in regulation of the development of schistosomes and provide a valuable resource for screening antischistosomal intervention targets or vaccine candidates.

2020-11-06 | GSE122318 | GEO

Cryptococcus exploits delayed microglial activation, and microglial osteopontin (OPN/Spp1) impairs peripheral host control

Project description:Cryptococcus exploits delayed microglial activation, and microglial osteopontin (OPN/Spp1) impairs peripheral host control

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Rab37-mediated OPN secretion enriches SPP1+ macrophages through autocrine–paracrine signaling to drive lung tumor progression

Project description:Rab37-mediated OPN secretion enriches SPP1+ macrophages through autocrine–paracrine signaling to drive lung tumor progression

| PRJNA1368629 | ENA

Comparative microRNA expression profiles of Schistosoma japonicum from SCID mouse and BALB/c mouse

Project description:Comparative microRNA expression profiles of Schistosoma japonicum from SCID mouse and BALB/c mouse

| PRJNA504624 | ENA

Comparative analysis of transcriptional profiles of Schistosoma japonicum from SCID mouse and BALB/c mouse

Project description:Comparative analysis of transcriptional profiles of Schistosoma japonicum from SCID mouse and BALB/c mouse

| PRJNA504625 | ENA

Characterization of Spp1-TAP and Mer2-TAP interactomes

Project description:Histone H3K4 methylation is a feature of meiotic recombination hotspots shared by many organisms including plants and mammals. Meiotic recombination is initiated by programmed double strand break (DSB) formation that in budding yeast is directed in gene promoters by histone H3K4 di/trimethylation. This histone modification is indeed recognized by Spp1, a PHD-finger containing protein that belongs to the conserved histone H3K4 methyltransferase Set1 complex. During meiosis, Spp1 binds H3K4me and recruits a DSB protein, Mer2, to promote DSB formation close to gene promoters. How Set1C and Mer2 related functions of Spp1 are connected is not clear.

2018-01-30 | PXD007590 | Pride

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