Silenced DMBT1 promotes nasal mucosa epithelial cell growth

Lu, Xin; Xu, Yuping; Zhao, Yan; Tao, Qilei; Wu, Jian

doi:10.1111/ahg.12230

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…26,27 DBMT1 has been demonstrated to be a regulator of nasal epithelial proliferation through apoptosis, where reduced levels of DBMT1 in nasal polyp tissue is associated with reduced apoptosis. 28 The findings from this study support these findings with a 2.5-increased fold change in the levels of DBMT1 in mucus from healthy patients compared with in the levels in mucus from patients with CRSwNP.…”

Section: Tissue Remodelingsupporting

confidence: 82%

Proteomic analysis of nasal mucus samples of healthy patients and patients with chronic rhinosinusitis

Kao

Bassiouni

Ramezanpour

et al. 2021

Journal of Allergy and Clinical Immunology

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Section: Tissue Remodelingsupporting

confidence: 82%

Proteomic analysis of nasal mucus samples of healthy patients and patients with chronic rhinosinusitis

Kao

Bassiouni

Ramezanpour

et al. 2021

Journal of Allergy and Clinical Immunology

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“…The top 10 DEGs are listed in Table 1. The functions of these DEGs were determined by Gene Ontology analysis and a comprehensive literature review [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. All DEGs (fold changes of > 1.5, p < 0.05) in PG and SMG were listed in Supplementary Figures 1 and 2.…”

Section: Differentially Expressed Genes (Degs) In Young and Old Sg Ti...mentioning

confidence: 99%

Adiponectin is associated with inflammaging and age-related salivary gland lipid accumulation

Kim

Choi

et al. 2023

Aging

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Dry mouth is frequently observed in the elderly, and enhanced lipid accumulation plays a critical role in cellular senescence in the salivary gland (SG). We investigated the mechanisms that mediate lipogenesis-associated SG senescence. Adult (28.6 ± 6.6 y.o. and 43.3 ± 1.5 y.o.) and aged (82.0 ± 4.3 y.o. and 88.0 ± 4.3 y.o.) human parotid and submandibular glands were compared with respect to histologic findings, 8-OHdG (8-hydroxy 2 deoxyguanosine) expression patterns, TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) and SA-β-gal (senescence-associated β-galactosidase) assay results. Also, microarray analysis was performed on RNA extracted from adult and aged SG to identify DEGs (differentially expressed genes). The effects of silencing ADIPOQ (Adiponectin) were evaluated by quantifying cell proliferation, immunohistochemical staining for cellular senescence and inflammation-associated proteins, SA-β-gal assays, RT-PCR, and western blot. Histological findings demonstrated the presence of more lipocytes, chronic inflammation, fibrosis, and lymphocytic infiltration in old SG. In addition, old tissues demonstrated higher expressions of SA-β-gal, more apoptotic cells in TUNEL assays, and higher oxidative stress by 8-OHdG immunostaining. Microarray analysis showed lipogenesis was significantly upregulated in old tissues. Silencing of ADIPOQ (a lipogenesis-related gene) reduced inflammation and SA-β-gal levels and increased cell proliferation and the expressions of amylase and aquaporin 5 in human SG epithelial cells. The study shows ADIPOQ is a potential target molecule for the modulation of lipogenesis associated with SG senescence.

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“…Like all the other measures in the small intestine, such effects induced by prenatal LPS exposure disappeared after 5 days. This could be related to DMBT1, which negatively affects epithelial cell growth (35) and is associated with a change from proliferation to differentiation in the epithelium and thereby epithelial regeneration following mucosal damage (36).…”

Section: Discussionmentioning

confidence: 99%

Postnatal Gut Immunity and Microbiota Development Is Minimally Affected by Prenatal Inflammation in Preterm Pigs

et al. 2020

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Chorioamnionitis (CA), resulting from intra-amniotic inflammation, is a frequent cause of preterm birth and exposes the immature intestine to bacterial toxins and/or inflammatory mediators before birth via fetal swallowing. This may affect intestinal immune development, interacting with the effects of enteral feeding and gut microbiota colonization just after birth. Using preterm pigs as model for preterm infants, we hypothesized that prenatal exposure to gram-negative endotoxin influences postnatal bacterial colonization and gut immune development. Pig fetuses were given intra-amniotic lipopolysaccharide (LPS) 3 days before preterm delivery by cesarean section and were compared with littermate controls (CON) at birth and after 5 days of formula feeding and spontaneous bacterial colonization. Amniotic fluid was collected for analysis of leukocyte counts and cytokines, and the distal small intestine was analyzed for endotoxin level, morphology, and immune cell counts. Intestinal gene expression and microbiota were analyzed by transcriptomics and metagenomics, respectively. At birth, LPS-exposed pigs showed higher intestinal endotoxin, neutrophil/macrophage density, and shorter villi. About 1.0% of intestinal genes were affected at birth, and DMBT1, a regulator of mucosal immune defense, was identified as the hub gene in the co-expression network. Genes related to innate immune response (TLR2, LBP, CD14, C3, SFTPD), neutrophil chemotaxis (C5AR1, CSF3R, CCL5), and antigen processing (MHC II genes and CD4) were also affected, and expression levels correlated with intestinal neutrophil/macrophage density and amniotic fluid cytokine levels. On day 5, LPS and CON pigs showed similar sensitivity to necrotizing enterocolitis, endotoxin levels, morphology, immune cell counts, gene expressions, and microbiota composition (except for difference in some low-abundant species). Our results show that CA markedly affects intestinal genes at preterm birth, including genes related to immune cell infiltration. However, a few days later, following the physiological adaptations to Pan et al.Gut Development After Prenatal Inflammation preterm birth, CA had limited effects on intestinal structure, function, gene expression, bacterial colonization, and necrotizing enterocolitis sensitivity. We conclude that short-term, prenatal intra-amniotic inflammation is unlikely to exert marked effects on intestinal immune development in preterm neonates beyond the immediate neonatal period.

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Silenced DMBT1 promotes nasal mucosa epithelial cell growth

Abstract: DMBT1 plays an important role in the growth and division of nasal epithelial cells. The possible mechanism might involve DMBT1 regulating the AKT-p53 pathway to promote cell viability and reduce apoptosis of nasal epithelial cells.

Cited by 7 publications

References 23 publications

Proteomic analysis of nasal mucus samples of healthy patients and patients with chronic rhinosinusitis

Proteomic analysis of nasal mucus samples of healthy patients and patients with chronic rhinosinusitis

Adiponectin is associated with inflammaging and age-related salivary gland lipid accumulation

Postnatal Gut Immunity and Microbiota Development Is Minimally Affected by Prenatal Inflammation in Preterm Pigs

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