scholarly journals The Critical Role of 15-Lipoxygenase-1 in Colorectal Epithelial Cell Terminal Differentiation and Tumorigenesis

2005 ◽  
Vol 65 (24) ◽  
pp. 11486-11492 ◽  
Author(s):  
Imad Shureiqi ◽  
Yuanqing Wu ◽  
Dongning Chen ◽  
Xiu L. Yang ◽  
Baoxiang Guan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Critical Role ◽  
Terminal Differentiation

scholarly journals Prostacyclin as a potent effector of adipose-cell differentiation

1989 ◽  
Vol 257 (2) ◽  
pp. 399-405 ◽  
Author(s):  
R Négrel ◽  
D Gaillard ◽  
G Ailhaud
Keyword(s):  
Arachidonic Acid ◽  
Cyclic Amp ◽  
Critical Role ◽  
Terminal Differentiation ◽  
Prostaglandin F2 Alpha ◽  
Adipogenic Effect ◽  
Adipose Cells

The terminal differentiation of Ob1771 pre-adipose cells induced by arachidonic acid in serum-free hormone-supplemented medium containing insulin, transferrin, growth hormone, tri-iodothyronine and fetuin (5F medium) was strongly diminished in the presence of inhibitors of prostaglandin synthesis, namely aspirin or indomethacin. Carbaprostacyclin, a stable analogue of prostacyclin (prostaglandin I2) known to be synthesized by pre-adipocytes and adipocytes, behaved as an efficient activator of cyclic AMP production and was able, when added to 5F medium, to mimic the adipogenic effect of arachidonic acid. Prostaglandins E2, F2 alpha and D2, unable to affect the cyclic AMP production, failed to substitute for carbaprostacyclin. However, prostaglandin F2 alpha, which is another metabolite of arachidonic acid in pre-adipose and adipose cells, able to promote inositol phospholipid breakdown and protein kinase C activation, potentiated the adipogenic effect of carbaprostacyclin. In addition, carbaprostacyclin enhanced both a limited proliferation and terminal differentiation of adipose precursor cells isolated from rodent and human adipose tissues maintained in primary culture. These results demonstrate the critical role of prostacyclin and prostaglandin F2 alpha on adipose conversion in vitro and suggest a paracrine/autocrine role of both prostanoids in the development of adipose tissue in vivo.

197 Critical Role of Epithelial Cell-Derived IL-25 in Nematode Infection-Induced Changes in Intestinal Function in Mice

2010 ◽  
Vol 138 (5) ◽  
pp. S-36
Author(s):  
Aiping Zhao ◽  
Joseph F. Urban ◽  
Rex Sun ◽  
Jennifer A. Stiltz ◽  
Motoko Morimoto ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Critical Role ◽  
Nematode Infection ◽  
Intestinal Function ◽  
Induced Changes

scholarly journals Critical Role of Constitutive Type I Interferon Response in Bronchial Epithelial Cell to Influenza Infection

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e32947 ◽  
Author(s):  
Alan C-Y. Hsu ◽  
Kristy Parsons ◽  
Ian Barr ◽  
Sue Lowther ◽  
Deborah Middleton ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Type I Interferon ◽  
Influenza Infection ◽  
Critical Role ◽  
Bronchial Epithelial Cell ◽  
Interferon Response ◽  
Type I ◽  
Bronchial Epithelial

Critical Role of Tet3 in Neural Progenitor Cell Maintenance and Terminal Differentiation

2014 ◽  
Vol 51 (1) ◽  
pp. 142-154 ◽  
Author(s):  
Ting Li ◽  
Dehua Yang ◽  
Jia Li ◽  
Yu Tang ◽  
Juan Yang ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Critical Role ◽  
Terminal Differentiation ◽  
Neural Progenitor Cell ◽  
Neural Progenitor ◽  
Cell Maintenance

scholarly journals Contributions of Nitric Oxide to AHR-Ligand-Mediated Keratinocyte Differentiation

2020 ◽  
Vol 21 (16) ◽  
pp. 5680
Author(s):  
Carrie Hayes Sutter ◽  
Haley M. Rainwater ◽  
Thomas R. Sutter
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cell ◽  
Cell Fate ◽  
Terminal Differentiation ◽  
Metabolic Reprogramming ◽  
Keratinocyte Differentiation ◽  
Epidermal Keratinocytes ◽  
Nitric Oxide Signaling ◽  
Selective Ligand

Activation of the aryl hydrocarbon receptor (AHR) in normal human epidermal keratinocytes (NHEKs) accelerates keratinocyte terminal differentiation through metabolic reprogramming and reactive oxygen species (ROS) production. Of the three NOS isoforms, NOS3 is significantly increased at both the RNA and protein levels by exposure to the very potent and selective ligand of the AHR, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Inhibition of NOS with the chemical N-nitro-l-arginine methyl ester (l-NAME) reversed TCDD-induced cornified envelope formation, an endpoint of terminal differentiation, as well as the expression of filaggrin (FLG), a marker of differentiation. Conversely, exposure to the NO-donor, S-nitroso-N-acetyl-DL-penicillamine (SNAP), increased the number of cornified envelopes above control levels and augmented the levels of cornified envelopes formed in response to TCDD treatment and increased the expression of FLG. This indicates that nitric oxide signaling can increase keratinocyte differentiation and that it is involved in the AHR-mediated acceleration of differentiation. As the nitrosylation of cysteines is a mechanism by which NO affects the structure and functions of proteins, the S-nitrosylation biotin switch technique was used to measure protein S-nitrosylation. Activation of the AHR increased the S-nitrosylation of two detected proteins of about 72 and 20 kD in size. These results provide new insights into the role of NO and protein nitrosylation in the process of epithelial cell differentiation, suggesting a role of NOS in metabolic reprogramming and the regulation of epithelial cell fate.

scholarly journals Role of the Intestinal Epithelium and Its Interaction With the Microbiota in Food Allergy

2020 ◽  
Vol 11 ◽  
Author(s):  
Ayesha Ali ◽  
HuiYing Tan ◽  
Gerard E. Kaiko
Keyword(s):  
Food Allergy ◽  
Epithelial Cell ◽  
Nutrient Uptake ◽  
Intestinal Epithelium ◽  
Digestive System ◽  
Critical Role ◽  
Innate Immune ◽  
Intestinal Epithelial ◽  
Physical Barrier

The intestinal epithelial tract forms a dynamic lining of the digestive system consisting of a range of epithelial cell sub-types with diverse functions fulfilling specific niches. The intestinal epithelium is more than just a physical barrier regulating nutrient uptake, rather it plays a critical role in homeostasis through its intrinsic innate immune function, pivotal regulation of antigen sensitization, and a bi-directional interplay with the microbiota that evolves with age. In this review we will discuss these functions of the epithelium in the context of food allergy.

scholarly journals G-protein-coupled receptor kinase-2 is a critical regulator of TNFα signaling in colon epithelial cells

2017 ◽  
Vol 474 (14) ◽  
pp. 2301-2313 ◽  
Author(s):  
Michael D. Steury ◽  
Peter C. Lucas ◽  
Laura R. McCabe ◽  
Narayanan Parameswaran
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
G Protein ◽  
Critical Role ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

G-protein-coupled receptor kinase-2 (GRK2) belongs to the GRK family of serine/threonine protein kinases critical in the regulation of G-protein-coupled receptors. Apart from this canonical role, GRK2 is also involved in several signaling pathways via distinct intracellular interactomes. In the present study, we examined the role of GRK2 in TNFα signaling in colon epithelial cell–biological processes including wound healing, proliferation, apoptosis, and gene expression. Knockdown of GRK2 in the SW480 human colonic cells significantly enhanced TNFα-induced epithelial cell wound healing without any effect on apoptosis/proliferation. Consistent with wound-healing effects, GRK2 knockdown augmented TNFα-induced matrix metalloproteinases (MMPs) 7 and 9, as well as urokinase plasminogen activator (uPA; factors involved in cell migration and wound healing). To assess the mechanism by which GRK2 affects these physiological processes, we examined the role of GRK2 in TNFα-induced MAPK and NF-κB pathways. Our results demonstrate that while GRK2 knockdown inhibited TNFα-induced IκBα phosphorylation, activation of ERK was significantly enhanced in GRK2 knockdown cells. Our results further demonstrate that GRK2 inhibits TNFα-induced ERK activation by inhibiting generation of reactive oxygen species (ROS). Together, these data suggest that GRK2 plays a critical role in TNFα-induced wound healing by modulating MMP7 and 9 and uPA levels via the ROS–ERK pathway. Consistent with in vitro findings, GRK2 heterozygous mice exhibited enhanced intestinal wound healing. Together, our results identify a novel role for GRK2 in TNFα signaling in intestinal epithelial cells.

scholarly journals ILC3s control splenic cDC homeostasis via lymphotoxin signaling

2021 ◽  
Vol 218 (5) ◽  
Author(s):  
Matthias Vanderkerken ◽  
Antonio P. Baptista ◽  
Marco De Giovanni ◽  
Satoshi Fukuyama ◽  
Robin Browaeys ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cell ◽  
Adaptive Immunity ◽  
Lymphoid Tissue ◽  
Critical Role ◽  
Terminal Differentiation ◽  
Time Frame ◽  
Tissue Homeostasis ◽  
Pharmacological Interventions

The spleen contains a myriad of conventional dendritic cell (cDC) subsets that protect against systemic pathogen dissemination by bridging antigen detection to the induction of adaptive immunity. How cDC subsets differentiate in the splenic environment is poorly understood. Here, we report that LTα1β2-expressing Rorgt+ ILC3s, together with B cells, control the splenic cDC niche size and the terminal differentiation of Sirpα+CD4+Esam+ cDC2s, independently of the microbiota and of bone marrow pre-cDC output. Whereas the size of the splenic cDC niche depended on lymphotoxin signaling only during a restricted time frame, the homeostasis of Sirpα+CD4+Esam+ cDC2s required continuous lymphotoxin input. This latter property made Sirpα+CD4+Esam+ cDC2s uniquely susceptible to pharmacological interventions with LTβR agonists and antagonists and to ILC reconstitution strategies. Together, our findings demonstrate that LTα1β2-expressing Rorgt+ ILC3s drive splenic cDC differentiation and highlight the critical role of ILC3s as perpetual regulators of lymphoid tissue homeostasis.

scholarly journals IL-13 deficiency exacerbates lung damage and impairs epithelial-derived type 2 molecules during nematode infection

2020 ◽  
Author(s):  
AL Chenery ◽  
S Rosini ◽  
JE Parkinson ◽  
JA Herrera ◽  
Craig Lawless ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Stress Responses ◽  
Tissue Injury ◽  
Critical Role ◽  
Lung Damage ◽  
Surfactant Protein D ◽  
Nippostrongylus Brasiliensis ◽  
Tissue Remodelling

AbstractIL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of atopic and fibrotic diseases such as allergic asthma. Matrix remodelling is an important component of repair processes in the lung but also a hallmark of chronic conditions involving fibrosis. Hence, understanding the role of IL-13 in tissue remodelling has important clinical implications. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 following acute tissue injury. In this study, we used Nippostrongylus brasiliensis infection as a model of acute lung tissue damage comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact. Importantly, we found that IL-13 played a critical role in limiting tissue injury and haemorrhaging in the lung following infection. Through proteomic and transcriptomic profiling, we identified IL-13-dependent changes in matrix and associated regulators. We further showed that IL-13 is required for the induction of epithelial-derived type 2 effector molecules such as RELM-α and surfactant protein D. Pathway analyses predicted that IL-13 was heavily involved in the induction of cellular stress responses and regulation of lung epithelial cell differentiation by suppression of Foxa2 pathways. Thus, we propose that IL-13 has tissue-protective functions during lung injury and regulates epithelial cell responses during type 2 immunity in this acute setting.

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