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Calprotectin in Murine Oral Microbiome

ABSTRACT: Calprotectin (S100A8/A9) is an innate immune effector in experimental periodontitis

PROVIDER: PRJEB48266 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7162320.fastq.gz	Fastqsanger.gz
	ERR7162330.fastq.gz	Fastqsanger.gz
	ERR7162340.fastq.gz	Fastqsanger.gz
	ERR7162350.fastq.gz	Fastqsanger.gz
	ERR7162360.fastq.gz	Fastqsanger.gz

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Transcriptomic Characterization of Human Choroidal Neovascular Membranes Identifies Calprotectin as a Novel Biomarker for Patients with Age-related Macular Degeneration

Project description:Although genome-wide association studies, animal models, and cell culture systems have yielded important insights into the pathogenesis of neovascular age-related macular degeneration (nAMD), the underlying molecular pathways remain ill defined. Recent studies have deciphered the transcriptional profile of choroidal neovascularisation (CNV) of body donor eyes and were thus limited by the time span from death to preservation and the associated rapid 5'-RNA degradation. In this study, CNVs were therefore formalin-fixed immediately after surgical extraction from patients with nAMD and analyzed using a 3’ RNA sequencing approach called Massive Analysis of cDNA Ends (MACE). Age-matched formalin-fixed paraffin-embedded (FFPE) RPE-choroidal specimens obtained from the macular region of enucleated eyes with ciliary body melanoma served as controls. Transcriptome profiles were generated and disease-associated gene signatures were identified using statistical and bioinformatic methods. Calprotectin (S100A8/A9) protein expression was investigated by immunohistochemistry and ELISA.We identified 158 differentially-expressed genes (DEG) that were significantly increased in CNV compared to control tissue. Gene ontology enrichment analysis demonstrated that these DEG contributed to biological processes, such as Blood Vessel Development, Extracellular Structure Organization, Response to Wounding and several immune-related terms. The S100 calcium-binding protein A8 (S100A8) and S100A9 emerged among the top DEG, as confirmed by immunohistochemistry on CNV tissue and protein analysis of vitreous samples from nAMD patients and controls. This study provides a high-resolution RNA-sequencing-based transcriptional signature of choroidal neovascular membranes in AMD patients and reveals S100A8/A9 as a novel biomarker and promising target for AMD-directed therapeutics and diagnostics.

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Characterization of Calprotectin treated medium

Project description:The goal of this study is to correlate the transcriptional response of S. aureus cells grown in Calprotectin treated medium with that of cells grown in Mn or Zn depletion conditions. Keywords: RNA sample Staphylcoccus aureus strain Newman was grown to mid-log phase in Calprotectin treated medium or medium lacking either Zn or Mn. RNA was isolated, labeled and hybridized to an S. aureus Affymetrix GeneChip. Biological replicates are indicated as A, B, or C.

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S100A8/A9 activate key genes and pathways in colon tumor progression

Project description:Studies using bone marrow chimeric mice revealed that S100A8/A9 expression on myeloid cells is essential for development of colon tumors. Our results thus reveal a novel role for myeloid-derived S100A8/A9 in activating specific downstream genes associated with tumorigenesis and in promoting tumor growth and metastasis. Subconfluent cultures of MC38 cells were serum-starved for 16 hrs and activated with 10ug/mL S100A8/A9 for 6 hrs. Total RNA was extracted from unactivated or activated cells. 2 replicates each per stimulated cells, unstimulated cells, and control cells.

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S100A8/A9 induced by interaction with macrophages in esophageal squamous cell carcinoma promotes the migration and invasion of cancer cells via Akt and p38 MAPK pathways

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Reawakening of Dormant Tumor Cells by Modified Lipids derived from Stress Activated Neutrophils

Project description:Tumor recurrence years after seemingly successful treatment of primary tumors is one of the major causes of mortality in cancer patients. Reactivation of dormant tumor cells is largely responsible for this phenomenon. Using models of lung and ovarian cancer, we found a specific mechanism that may govern this process mediated by stress and neutrophils. Stress hormones cause rapid release of S100A8/A9 proteins by neutrophils. S100A8/A9 induce activation of myeloperoxidase resulting in accumulation of oxidized lipids. These lipids up-regulate fibroblast growth factor pathway in tumor cells causing tumor cell exit from the dormancy and formation of tumor lesions. Higher serum levels of S100A8/A9 were associated with shorter time to recurrence in patients with lung cancer after complete tumor resection. Targeting of S100A8/A9 or β2 adrenergic receptors abrogated stress induced reactivation of dormant tumor cells. These observations demonstrate a mechanism linking stress, and specific neutrophils activation with early recurrence in cancer.

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