Regulation of Laminin γ2 Expression by CDX2 in Colonic Epithelial Cells Is Impaired During Active Inflammation

Coskun, Mehmet; Soendergaard, Christoffer; Joergensen, Steffen; Dahlgaard, Katja; Riis, Lene; Nielsen, Ole Haagen; Sandelin, Albin; Troelsen, Jesper T.

doi:10.1002/jcb.25636

Cited by 9 publications

(4 citation statements)

References 54 publications

(85 reference statements)

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“…However, we observed a strong induction of LAMB3 and LAMC2 in HUVECs after stimulation with the pro-in ammatory and pro-atherogenic cytokine, TNF-α. This is in line with previous data showing that TNF-α can regulate the expression of LAMC2 in epithelial cells [24,25].…”

Section: Discussionsupporting

confidence: 93%

TNF-a-induced laminin-332 promotes an atherogenic endothelial phenotype

Hayderi,

Zegeye,

Meydan

et al. 2023

Preprint

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Background:Laminins are key components of the basement membranes separating endothelial cells from the underlying tissues. They form complex networks of fibers within the basement membrane to provide structural support and regulate the behavior and function of surrounding cells. In mammals, the products of the five alpha, four beta and three gamma laminin genes are combined to generate 16-18 laminin isoforms, which under physiological circumstances confer some tissue specificity, with alpha 4- and alpha 5-containing isoforms being considered vascular-specific. During inflammation, however, the expression pattern of laminin genes may change, which in turn may affect the behavior of surrounding cells. Objectives: We aimed to investigate the impact of tumor necrosis factor alpha (TNF-a) on laminin gene expression in endothelial cells and examine the impact of TNF-a-induced laminin (laminin-332 or LN332) on endothelial cells’ behavior. Results:TNF-a induces LN332-encoding genes in endothelial cells. Endothelial cells cultured on LN332 display irregular shape and appear loosely connected. These cells acquire lower expression of tight junction protein, claudin-5, elevated expression of leukocyte adhesion molecules and enhanced secretion of chemokines. In addition, cells cultured on LN332 are more adhesive to leukocytes and supernatant from these cells is more attractive for primary monocytes in vitro. Notably, LN332-encoding genes are elevated in human atherosclerotic lesions and correlate with the expression of TNF-a. Conclusions: We demonstrate that TNF-a-induced upregulation of LN332 promotes a pro-atherogenic endothelial phenotype. Elevated levels of LN332-encoding genes in atherosclerotic lesions, correlating with TNF-a, suggest a potential role for LN332 in the pathophysiology of atherosclerosis.

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Section: Discussionsupporting

confidence: 93%

TNF-a-induced laminin-332 promotes an atherogenic endothelial phenotype

Hayderi,

Zegeye,

Meydan

et al. 2023

Preprint

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“…In addition, A . muciniphila can closely bind to laminin 18 , one of the important components of extracellular matrix which can regulate the migration, differentiation and anti-inflammatory responses of IECs 112 – 114 . A GWAS based study showed a strong connection between laminin β1 chain encoding gene and the susceptibility of UC 115 , and showed the laminin γ1 chain encoding gene as a susceptible locus of IBD 116 .…”

Section: A Muciniphila and Intestinal Homeostasis Of Hostmentioning

confidence: 99%

Rational consideration of Akkermansia muciniphila targeting intestinal health: advantages and challenges

Luo

Lan

et al. 2022

npj Biofilms Microbiomes

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As one of the promising next-generation probiotics (NGPs), Akkermansia muciniphila, a well-known mucin-degrading bacterium, has been proven to be closely related to the metabolic diseases of its human host. However, the role of A. muciniphila in the host’s intestinal health remains ambiguous. Here, we comprehensively summarize and discuss the characteristics, the distribution, and the colonization of A. muciniphila in the human gastrointestinal tract (GIT). We propose that the application of A. muciniphila as a biomarker for longevity, for diagnostics and prognostics of intestinal diseases, or for intestinal health should be cautiously considered. Precise dietary regulation can mediate the treatment of intestinal diseases by altering the abundance of A. muciniphila. Although the beneficial role of A. muciniphila and its component in intestinal inflammation has been discovered, in gnotobiotic mice with specific gut microbiota, certain genotype, and colorectal cancer, or in animal models infected with a specific pathogen, A. muciniphila may be related to the occurrence and development of intestinal diseases. Genomic analysis, emphasizing the strain-level phylogenetic differences of A. muciniphila, indicates that a clear description and discussion of each strain is critical before its practical application. Our review provides much needed insight for the precise application of A. muciniphila.

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“…It has been well established that TLR4-mediated activation of NF-κB, a vital transcript factor involved in inflammation, is crucial in regulating intestinal inflammation. [27][28][29] Activation of the NF-κB signaling pathway in macrophages is associated with increased production of proinflammatory cytokines. 30 We have previously found that TLR4 is one of the important regulators of the NF-κB pathway in macrophages.…”

Section: Conflict Of Interestsmentioning

confidence: 99%

PTPRO exaggerates inflammation in ulcerative colitis through TLR4/NF‐κB pathway

Zhao

Yan

Zhu

et al. 2019

J of Cellular Biochemistry

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Previous studies have implicated protein tyrosine phosphatase receptor type O (PTPRO) as a key regulator in inflammation‐associated diseases; however, its role in ulcerative colitis (UC) remains largely unknown. Thus, we aim to elucidate the potential role and underlying mechanism of PTPRO in UC. In this study, increased expression of PTPRO, toll‐like receptor (TLR4) and inflammatory cytokines were observed in mucosal tissues (MTs) from inflamed areas and lamina propria mononuclear cells (LPMCs) of patients with UC compared with those from healthy controls. Then, it was manifested that PTPRO promoted the expression of TLR4 and proinflammatory cytokines in lipopolysaccharide‐induced (LPS‐induced) inflammatory macrophage model. Besides, PTPRO inhibited the proliferation of intestinal epithelial cells (IECs) but enhanced the apoptosis of IECs in macrophages. Moreover, levels of phosphorylated nuclear factor κB (NF‐κB)/p65 and inhibitor of NF‐κB α (IκBα) were more significantly increased in PTPRO overexpressed macrophages. In addition, the area under receiver operating characteristic curve was 0.807 (95%CI = 0.686‐0.958, P < .001) suggesting PTPRO as an ideal diagnostic marker for UC. Taken these, the present study shows strong evidence that PTPRO exaggerates inflammation in UC via TLR4/NF‐κB signaling pathway.

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Regulation of Laminin γ2 Expression by CDX2 in Colonic Epithelial Cells Is Impaired During Active Inflammation

Cited by 9 publications

References 54 publications

TNF-a-induced laminin-332 promotes an atherogenic endothelial phenotype

TNF-a-induced laminin-332 promotes an atherogenic endothelial phenotype

Rational consideration of Akkermansia muciniphila targeting intestinal health: advantages and challenges

PTPRO exaggerates inflammation in ulcerative colitis through TLR4/NF‐κB pathway

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