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Salivary ZG16B expression loss marks onset of oral Chronic Graft-Versus-Host Disease and exocrine gland dysfunction

ABSTRACT: Salivary ZG16B expression loss marks onset of oral Chronic Graft-Versus-Host Disease and exocrine gland dysfunction

PROVIDER: PRJNA748669 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15207440.fastq.gz	Fastqsanger.gz
	SRR15207441.fastq.gz	Fastqsanger.gz
	SRR15207442.fastq.gz	Fastqsanger.gz
	SRR15207443.fastq.gz	Fastqsanger.gz
	SRR15207444.fastq.gz	Fastqsanger.gz

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Salivary ZG16B expression loss marks onset of oral Chronic Graft-Versus-Host Disease and exocrine gland dysfunction

Project description:Chronic graft-versus-host disease (cGVHD) targets include the oral mucosa and salivary glands after allogeneic hematopoietic stem cell transplant (HSCT). Without incisional biopsy, no diagnostic test exists to confirm oral cGVHD. Consequently, therapy is often withheld until severe manifestations develop. This proteomic study examined saliva and human salivary gland for a biomarker profile at first onset of oral cGVHD prior to initiation of topical steroid therapy. Whole saliva collected at onset of biopsy-proven oral GVHD was assessed using liquid chromatography coupled tandem mass spectrometry with identification of 569 proteins, of which 77 significantly changed in abundance. ZG16B, a secretory lectin protein, was reduced 2-fold in oral cGVHD saliva (p < 0.05), and significantly decreased in salivary gland secretory cells affected by cGVHD. Single-cell RNAseq analysis of healthy MSG localized ZG16B expression to two discreet acinar cell populations. Reduced expression of ZG16B may indicate specific cGVHD activity, general salivary gland dysfunction.

2022-01-05 | GSE180544 | GEO

Salivary ZG16B expression loss follows exocrine gland dysfunction related to oral chronic graft-versus-host disease.

Project description: Not available

| S-EPMC8718990 | biostudies-literature

Swip-1 promotes exocytosis of glue granules in the exocrine Drosophila salivary gland.

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Salivary gland during development and onset of xerostomia in murine model of Sjögren's syndrome-like disease

Project description:Differential gene expression in the salivary gland during development and onset of xerostomia in Sjögren’s syndrome-like disease of the C57BL/6.NOD-Aec1Aec2 mouse. Recently, we reported the development of the C57BL/6.NOD-Aec1Aec2 mouse that carries two genetic intervals derived from the NOD mouse capable of conferring Sjögren’s syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice. In an attempt to define the molecular bases underlying onset of stomatitis sicca (xerostomia) in this C57BL/6.NOD-Aec1Aec2 mouse model, we have carried out a study utilizing microarray technology.

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Changes in nuclear lamin-B stability marks the onset of aging in Drosophila

Project description:Changes in nuclear lamin-B stability marks the onset of aging in Drosophila

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Changes in nuclear lamin-B stability marks the onset of aging in Drosophila

Project description:In this study, we showed that reduced nuclear lamin-B marks the onset of physiological decline in young adult Drosophila and its ectopic expression in dopaminergic neurons is sufficient to improve their locomotor activity during aging. Furthermore, the decline in lamin-B protein appeared to be unrelated to its mRNA level. Instead, we found drastic changes to its protein solubility during aging. Given the importance of nuclear lamin-B in genome organization and the advancement of single-cell epigenome profiling technology, our findings provide the community the basis to further study how altered level of lamin-B protein may elicit changes in gene expression that can contribute to the onset of physiological decline in animals.

2021-11-30 | GSE155357 | GEO

Aggregation of respiratory complex subunits marks the onset of proteotoxicity in proteasome inhibited cells

Project description:Proteostasis is maintained by optimum expression, folding, transport, and clearance of proteins. Deregulation of any of these processes triggers protein aggregation and is implicated in many age-related pathologies. Here, using quantitative proteomics and microscopy we show that aggregation of many nuclear-encoded mitochondrial proteins is an early protein-destabilization event during short-term proteasome inhibition. Among these, Respiratory Chain Complex (RCC) subunits represent a group of functionally related proteins consistently forming aggregates under multiple proteostasis-stresses with varying aggregation-propensities. Sequence analysis reveals that several RCC subunits, irrespective of cleavable mitochondrial targeting sequence (MTS), contain low complexity regions (LCR) at N-terminus. Using different chimeric and mutant constructs we show that these low complexity regions partially contribute to intrinsic instability of multiple RCC subunits. Taken together, we propose that physicochemically driven aggregation of unassembled RCC subunits destabilizes their functional assembly inside mitochondria. This deregulates the biogenesis of respiratory complexes and marks the onset of mitochondrial dysfunction.

2019-01-28 | PXD012204 | Pride

Salivary gland during development and onset of xerostomia in murine model of SjM-CM-6gren's syndrome-like disease

Project description:Differential gene expression in the salivary gland during development and onset of xerostomia in SjM-CM-6grenM-bM-^@M-^Ys syndrome-like disease of the C57BL/6.NOD-Aec1Aec2 mouse. Recently, we reported the development of the C57BL/6.NOD-Aec1Aec2 mouse that carries two genetic intervals derived from the NOD mouse capable of conferring SjM-CM-6grenM-bM-^@M-^Ys syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice. In an attempt to define the molecular bases underlying onset of stomatitis sicca (xerostomia) in this C57BL/6.NOD-Aec1Aec2 mouse model, we have carried out a study utilizing microarray technology. The present study was designed to define the changing gene expression profiles within the salivary glands of C57BL/6.NOD-Aec1Aec2 mice at five time points representing a pre-disease stage (4 weeks), the early pre-clinical stage (8 weeks), the initial influx of leukocytes into the salivary glands (12 weeks), the early clinical phase of autoimmunity (16 weeks), and the early onset of clinical SjSlike disease characterized by secretory dysfunction (20 weeks). The C57BL/6.NOD-Aec1Aec2 mouse is a model of primary SjS in which the Idd3 region of chromosome 3 and the Idd5 region of chromosome 1 derived from the NOD mouse were bred into the non-autoimmune C57BL/6 mouse, resulting in a SjS-like disease susceptibility that mimics both the pathophysiological characteristics and reduced secretory responses observed with NOD mice during development and onset of disease. This SjS-susceptible strain was designated C57BL/6.NOD-Aec1Aec2, where Aec1 corresponds to Idd3 (of chromosome 3) and Aec2 corresponds to Idd5 (of chromosome 1).

2009-04-11 | E-GEOD-15640 | biostudies-arrayexpress

Single-cell transcriptome analysis reveals atypical monocytes circulating ahead of acute graft-versus-host disease clinical onset

Project description:Acute graft-versus-host disease (aGVHD) represents the rejection of the skin, gut and liver tissues of the recipient of an allogenic hematopoietic stem cell transplantation (HSCT) by the donor T-cells. The onset of aGVHD is often rapid and its evolution unpredictable. We undertook the single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) collected before aGVHD clinical onset in three patients and at aGVHD diagnosis in one, using four HSCT recipients who remained free of aGVHD as controls. This analysis unveiled the presence in the circulation of particular subpopulations of monocytes and cytotoxic T cells (CTLs) in pre-aGVHD samples up to 18 days before clinical disease. These pre-aGVHD monocytes were characterized by an upregulation of the M2 polarity marker CD163, and the transmembrane protein SIGLEC1/CD169, while their CTL counterparts stood out for the upregulation of the CXCL10 receptor CXCR3 and the antigenic stimulation marker CD70. The occurrence of CD163/CD169-co-expressing monocytes upstream of aGVHD onset was validated using RNAseq data from an independent cohort and by flow cytometry of blood samples. These findings point to potential early diagnostic tools and preventive therapeutic strategies for aGVHD.

2025-07-07 | GSE269338 | GEO

Graft Source-dependent Biomarkers for Risk of Chronic Graft-Versus-Host Disease and Death

Project description:We identify risk markers and graft specific markers at day 90 post-HCT (hematopoietic cell transplant). For this, we developed a 4-plex TMT plasma proteomic approach comparing day-90 samples from PB (peripheral-blood stem cells) graft recipients who developed cGVHD by day 180, PB graft recipients who did not develop cGVHD, BM (bone marrow) graft recipients who developed cGVHD by day 180, BM graft recipients who did not developed cGVHD. Five markers were candidate risk markers and selected to move to the validation phase. Using ELISA assays these 5 markers were measured along with nine previously identified cGVHD proteomic biomarkers (ST2, CXCL9, MMP3, OPN, CXCL10, soluble CD163, IL17, B-cell activating factor (BAFF), and C-C-motif-chemokine-15 (CCL15)16,23-29 in 335 recipients (from CTN0201 to test if they were markers of risk and graft-specific markers). Finally, we measured the six significant candidate risk markers in CTN0201 in 653 patients from the CTN1202 study, an independent contemporary cohort.

2021-12-17 | MSV000088585 | MassIVE

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