scholarly journals Cucurbitacin E Inhibits Proliferation and Migration of Intestinal Epithelial Cells via Activating Cofilin

2018 ◽  
Vol 9 ◽  
Author(s):  
Huapei Song ◽  
Yu Wang ◽  
Li Li ◽  
Hehuan Sui ◽  
Pei Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
And Migration ◽  
Cucurbitacin E ◽  
Proliferation And Migration

scholarly journals IL-22–induced cell extrusion and IL-18–induced cell death prevent and cure rotavirus infection

2020 ◽  
Vol 5 (52) ◽  
pp. eabd2876
Author(s):  
Zhan Zhang ◽  
Jun Zou ◽  
Zhenda Shi ◽  
Benyue Zhang ◽  
Lucie Etienne-Mesmin ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Viral Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
And Migration ◽  
Rapid Drop ◽  
Cell Extrusion ◽  
Proliferation And Migration

Bacterial flagellin can elicit production of TLR5-mediated IL-22 and NLRC4-mediated IL-18 cytokines that act in concert to cure and prevent rotavirus (RV) infection. This study investigated the mechanism by which these cytokines act to impede RV. Although IL-18 and IL-22 induce each other’s expression, we found that IL-18 and IL-22 both impeded RV independently of one another and did so by distinct mechanisms that involved activation of their cognate receptors in intestinal epithelial cells (IEC). IL-22 drove IEC proliferation and migration toward villus tips, which resulted in increased extrusion of highly differentiated IEC that serve as the site of RV replication. In contrast, IL-18 induced cell death of RV-infected IEC thus directly interrupting the RV replication cycle, resulting in spewing of incompetent virus into the intestinal lumen and causing a rapid drop in the number of RV-infected IEC. Together, these actions resulted in rapid and complete expulsion of RV, even in hosts with severely compromised immune systems. These results suggest that a cocktail of IL-18 and IL-22 might be a means of treating viral infections that preferentially target short-lived epithelial cells.

Effects of spermine on the proliferation and migration of porcine intestinal epithelial cells

2021 ◽  
pp. 1-8
Author(s):  
Xiaomei Xu ◽  
Guangmang Liu ◽  
Gang Jia ◽  
Hua Zhao ◽  
Xiaoling Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals IL-22 induced cell extrusion and IL-18-induced pyroptosis prevent and cure rotavirus infection

2019 ◽  
Author(s):  
Zhan Zhang ◽  
Jun Zou ◽  
Zhenda Shi ◽  
Benyue Zhang ◽  
Lucie Etienne-Mesmin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Immune Systems ◽  
And Migration ◽  
Rapid Drop ◽  
Cell Extrusion ◽  
Proliferation And Migration

SummaryAdministration of bacterial flagellin elicits production of TLR5-mediated IL-22 and NLRC4-mediated IL-18 that act in concert to cure and prevent rotavirus (RV) infection. This study investigated the mechanism by which these cytokines act to impede this virus. Although IL-18 and IL-22 induce each other’s expression, we found that IL-18 and IL-22 both impeded RV independently of each other and did so by distinct mechanisms, in both cases via activation of their cognate receptors in intestinal epithelial cells (IEC). IL-22 drove IEC proliferation and migration toward villus tips, which resulted in increased extrusion of highly differentiated IEC that serve as the site of RV replication. In contrast, IL-18 induced pyroptotic death of RV-infected IEC thus directly interrupting the RV replication cycle, resulting in spewing of incompetent virus into the intestinal lumen and causing a rapid drop in levels of RV-infected IEC. Together, these actions resulted in rapid and complete expulsion of RV, even in hosts with severely compromised immune systems. These results suggest that IL-18/22 might be a means of treating viral infections that preferentially target short-lived epithelial cells.

A thermal injury-induced circulating factor(s) compromises intestinal cell morphology, proliferation, and migration

1999 ◽  
Vol 277 (1) ◽  
pp. G175-G182 ◽  
Author(s):  
Maryam Varedi ◽  
George H. Greeley ◽  
David N. Herndon ◽  
Ella W. Englander
Keyword(s):  
Epithelial Cells ◽  
Thermal Injury ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Rat Serum ◽  
In Vitro Effects ◽  
Mucosal Morphology ◽  
And Migration

The effects of a 60% body surface area thermal injury in rats on the morphology and proliferation of the epithelium of the small intestine and the in vitro effects of serum collected from scalded rats on intestinal epithelial cells were investigated. Scald injury caused significant reductions in duodenal villus width and crypt dimensions, villus enterocytes changed in shape from columnar to cuboidal, and the number of goblet cells decreased. The proportion of bromodeoxyuridine-labeled S phase cells in crypts was also diminished. In vitro, incubation of intestinal epithelial cells (IEC-6) with scalded rat serum (SRS) collected at either 12 or 24 h after injury caused a disruption in the integrity of the confluent culture and induced the appearance of large denuded areas. SRS also decreased DNA synthesis and delayed wound closure in an in vitro wound-healing model. The thermal injury-induced changes in intestinal mucosal morphology and epithelial cell growth characteristics described in this study may underlie, in part, the mechanism(s) involved in the diminished absorption of nutrients, increased intestinal permeability, and sepsis in patients with thermal injury.

scholarly journals Redox control of Cas phosphorylation requires Abl kinase in regulation of intestinal epithelial cell spreading and migration

2016 ◽  
Vol 311 (3) ◽  
pp. G458-G465 ◽  
Author(s):  
Jason D. Matthews ◽  
Ronen Sumagin ◽  
Benjamin Hinrichs ◽  
Asma Nusrat ◽  
Charles A. Parkos ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Focal Adhesion ◽  
Intestinal Epithelial Cells ◽  
Cell Spreading ◽  
Intestinal Epithelial ◽  
Protein Signaling ◽  
Abl Kinase ◽  
Cytoskeletal Dynamics ◽  
And Migration ◽  
Signaling Modules

Intestinal wounds often occur during inflammatory and ischemic disorders of the gut. To repair damage, intestinal epithelial cells must rapidly spread and migrate to cover exposed lamina propria, events that involve redox signaling. Wounds are subject to extensive redox alterations, particularly resulting from H2O2 produced in the adjacent tissue by both the epithelium and emigrating leukocytes. The mechanisms governing these processes are not fully understood, particularly at the level of protein signaling. Crk-associated substrate, or Cas, is an important signaling protein known to modulate focal adhesion and actin cytoskeletal dynamics, whose association with Crk is regulated by Abl kinase, a ubiquitously expressed tyrosine kinase. We sought to evaluate the role of Abl regulation of Cas at the level of cell spreading and migration during wound closure. As a model, we used intestinal epithelial cells exposed to H2O2 or scratch wounded to assess the Abl-Cas signaling pathway. We characterized the localization of phosphorylated Cas in mouse colonic epithelium under baseline conditions and after biopsy wounding the mucosa. Analysis of actin and focal adhesion dynamics by microscopy or biochemical analysis after manipulating Abl kinase revealed that Abl controls redox-dependent Cas phosphorylation and localization to influence cell spreading and migration. Collectively, our data shed new light on redox-sensitive protein signaling modules controlling intestinal wound healing.

scholarly journals Cucurbitacin E Induces Autophagy-Involved Apoptosis in Intestinal Epithelial Cells

2020 ◽  
Vol 11 ◽  
Author(s):  
Huapei Song ◽  
Hehuan Sui ◽  
Qiong Zhang ◽  
Pei Wang ◽  
Fengjun Wang
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Cucurbitacin E

Substance P stimulates Ca2+ release and migration in intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. A610-A611
Author(s):  
Douglas J. Turner ◽  
Bernard S. Marasa ◽  
Jaladanki N. Rao ◽  
Xin Guo ◽  
Jian-Ying Wang ◽  
...  
Keyword(s):  
Substance P ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
And Migration

Chemokine receptor CCR6 transduces signals that activate p130Casand alter cAMP-stimulated ion transport in human intestinal epithelial cells

2005 ◽  
Vol 288 (2) ◽  
pp. C321-C328 ◽  
Author(s):  
Charles C. Yang ◽  
Hiroyuki Ogawa ◽  
Michael B. Dwinell ◽  
Declan F. McCole ◽  
Lars Eckmann ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Chemokine Receptor ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Human Colon ◽  
Scaffolding Protein ◽  
Intestinal Epithelial ◽  
Cell Functions ◽  
And Migration

Human colon epithelial cells express the G protein-coupled receptor CCR6, the sole receptor for the chemokine CCL20 (also termed MIP-3α). CCL20 produced by intestinal epithelial cells is upregulated in response to proinflammatory stimuli and microbial infection, and it chemoattracts leukocytes, including CCR6-expressing immature myeloid dendritic cells, into sites of inflammation. The aim of this study was to determine whether CCR6 expressed by intestinal epithelial cells acts as a functional receptor for CCL20 and whether stimulation with CCL20 alters intestinal epithelial cell functions. The human colon epithelial cell lines T84, Caco-2, HT-29, and HCA-7 were used to model colonic epithelium. Polarized intestinal epithelial cells constitutively expressed CCR6, predominantly on the apical side. Consistent with this, apical stimulation of polarized intestinal epithelial cells resulted in tyrosine phosphorylation of the p130 Crk-associated substrate (Cas), an adaptor/scaffolding protein that localizes in focal adhesions and has a role in regulating cytoskeletal elements important for cell attachment and migration. In addition, CCL20 stimulation inhibited agonist-stimulated production of the second messenger cAMP and cAMP-mediated chloride secretory responses by intestinal epithelial cells. Inhibition was abrogated by pertussis toxin, consistent with signaling through Gαiproteins that negatively regulate adenylyl cyclases and cAMP production. These data indicate that signaling events, occurring via the activation of the apically expressed chemokine receptor CCR6 on polarized intestinal epithelial cells, alter specialized intestinal epithelial cell functions, including electrogenic ion secretion and possibly epithelial cell adhesion and migration.

scholarly journals Wnt11 Signaling Promotes Proliferation, Transformation, and Migration of IEC6 Intestinal Epithelial Cells

2004 ◽  
Vol 279 (25) ◽  
pp. 26707-26715 ◽  
Author(s):  
Lillian Ouko ◽  
Thomas R. Ziegler ◽  
Li H. Gu ◽  
Leonard M. Eisenberg ◽  
Vincent W. Yang
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
And Migration
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