Stimulation of matrix metalloproteinase-7 (MMP-7) by Helicobacter pylori in gastric epithelial cells: role in epithelial cell migration

2003 ◽  
Vol 124 (4) ◽  
pp. A6
Author(s):  
Lydia E. Wroblewski ◽  
P.-J. Noble ◽  
Adelina Pagliocca ◽  
D. Mark Pritchard ◽  
C. Tony Hart ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cell Migration ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Matrix Metalloproteinase ◽  
Gastric Epithelial Cells ◽  
Epithelial Cell Migration ◽  
Matrix Metalloproteinase 7 ◽  
Stimulation Of

Effects of corticosteroid-induced apoptosis on airway epithelial wound closure in vitro

2006 ◽  
Vol 291 (4) ◽  
pp. L794-L801 ◽  
Author(s):  
Delbert R. Dorscheid ◽  
Benjamin J. Patchell ◽  
Oscar Estrada ◽  
Bertha Marroquin ◽  
Roberta Tse ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Untreated Control ◽  
Wound Closure ◽  
Airway Epithelial Cell ◽  
Airway Epithelial ◽  
Wound Area ◽  
Epithelial Cell Migration

Damage to the airway epithelium is common in asthma. Corticosteroids induce apoptosis in and suppress proliferation of airway epithelial cells in culture. Whether apoptosis contributes to impaired epithelial cell repair after injury is not known. We examined whether corticosteroids would impair epithelial cell migration in an in vitro model of wound closure. Wounds (∼0.5–1.3 mm2) were created in cultured 1HAEo−human airway epithelial cell monolayers, after which cells were treated with up to 10 μM dexamethasone or budesonide for 24 h. Cultured cells were pretreated for 24 or 48 h with dexamethasone to observe the effect of long-term exposure on wound closure. After 12 h, the remaining wound area in monolayers pretreated for 48 h with 10 μM dexamethasone was 43 ± 18% vs. 10 ± 8% for untreated control monolayers. The addition of either corticosteroid immediately after injury did not slow closure significantly. After 12 h the remaining wound area in monolayers treated with 10 μM budesonide was 39 ± 4% vs. 43 ± 3% for untreated control monolayers. The proportion of apoptotic epithelial cells as measured by terminal deoxynucleotidyltransferase-mediated dUTP biotin nick end labeling both at and away from the wound edge was higher in monolayers treated with budesonide compared with controls. However, wound closure in the apoptosis-resistant 1HAEo−.Bcl-2+cell line was not different after dexamethasone treatment. We demonstrate that corticosteroid treatment before mechanical wounding impairs airway epithelial cell migration. The addition of corticosteroids after injury does not slow migration, despite their ability to induce apoptosis in these cells.

Matrix metalloproteinase 19 processes the laminin 5 gamma 2 chain and induces epithelial cell migration

2005 ◽  
Vol 62 (7-8) ◽  
pp. 870-880 ◽  
Author(s):  
T. Sadowski ◽  
S. Dietrich ◽  
F. Koschinsky ◽  
A. Ludwig ◽  
E. Proksch ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Matrix Metalloproteinase ◽  
Laminin 5 ◽  
Epithelial Cell Migration

scholarly journals Activation of protein kinase A accelerates bovine bronchial epithelial cell migration

2002 ◽  
Vol 282 (5) ◽  
pp. L1108-L1116 ◽  
Author(s):  
John R. Spurzem ◽  
Jitendrakumar Gupta ◽  
Thomas Veys ◽  
Kristen R. Kneifl ◽  
Stephen I. Rennard ◽  
...  
Keyword(s):  
Cell Migration ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Protein Kinase A ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Epithelial Cell Migration ◽  
Kinase A

Bronchial epithelial cell migration is required for the repair of damaged airway epithelium. We hypothesized that bronchial epithelial cell migration during wound repair is influenced by cAMP and the activity of its cyclic nucleotide-dependent protein kinase, protein kinase A (PKA). We found that, when confluent monolayers of bronchial epithelial cells are wounded, an increase in PKA activity occurs. Augmentation of PKA activity with a cell-permeable analog of cAMP, dibutyryl adenosine 3′,5′-cyclic monophosphate, isoproterenol, or a phosphodiesterase inhibitor accelerated migration of normal bronchial epithelial cells in in vitro wound closure assays and Boyden chamber migration assays. A role for PKA activity was also confirmed with a PKA inhibitor, KT-5720, which reduced stimulated migration. Augmentation of PKA activity reduced the levels of active Rho and the formation of focal adhesions. These studies suggest that PKA activation modulates Rho activity, migration mechanisms, and thus bronchial epithelial repair mechanisms.

scholarly journals Epstein-Barr-Virus-Encoded LMP2A Induces Primary Epithelial Cell Migration and Invasion: Possible Role in Nasopharyngeal Carcinoma Metastasis

2005 ◽  
Vol 79 (24) ◽  
pp. 15430-15442 ◽  
Author(s):  
Dirk M. Pegtel ◽  
Aravind Subramanian ◽  
Tzung-Shiahn Sheen ◽  
Ching-Hwa Tsai ◽  
Todd R. Golub ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Epstein Barr Virus ◽  
Cellular Migration ◽  
Migration And Invasion ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epithelial Cell Migration ◽  
Epstein Barr

ABSTRACT Nonkeratinizing nasopharyngeal carcinomas (NPC) are >95% associated with the expression of the Epstein-Barr virus (EBV) LMP2A latent protein. However, the role of EBV, in particular, LMP2A, in tumor progression is not well understood. Using Affymetrix chips and a pattern-matching computational technique (neighborhood analysis), we show that the level of LMP2A expression in NPC biopsy samples correlates with that of a cellular protein, integrin-alpha-6 (ITGα6), that is associated with cellular migration in vitro and metastasis in vivo. We have recently developed a primary epithelial model from tonsil tissue to study EBV infection in epithelial cells. Here we report that LMP2A expression in primary tonsil epithelial cells causes them to become migratory and invasive, that ITGα6 RNA levels are up-regulated in epithelial cells expressing LMP2, and that ITGα6 protein levels are increased in the migrating cells. Blocking antibodies against ITGα6 abrogated LMP2-induced invasion through Matrigel by primary epithelial cells. Our results provide a link between LMP2A expression, ITGα6 expression, epithelial cell migration, and NPC metastasis and suggest that EBV infection may contribute to the high incidence of metastasis in NPC progression.

scholarly journals Cytokine Expression and Production by Purified Helicobacter pylori Urease in Human Gastric Epithelial Cells

2000 ◽  
Vol 68 (2) ◽  
pp. 664-671 ◽  
Author(s):  
Toshihito Tanahashi ◽  
Masakazu Kita ◽  
Tadashi Kodama ◽  
Yoshio Yamaoka ◽  
Naoki Sawai ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Gastric Cancer Cell Line ◽  
Mucosal Inflammation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastric Epithelial Cells ◽  
Cytokine Induction ◽  
H Pylori ◽  
Stimulation Of

ABSTRACT Cytokines have been proposed to play an important role inHelicobacter pylori-associated gastroduodenal diseases, but the exact mechanism of the cytokine induction remains unclear. H. pylori urease, a major component of the soluble proteins extracted from bacterial cells, is considered to be one of the virulence factors for the inflammation in the gastric mucosa that is produced in H. pylori infection. However, the response of human gastric epithelial cells to the stimulation of urease has not been investigated. In the present study, we used human gastric epithelial cells in a primary culture system and examined whetherH. pylori urease stimulates the gastric epithelial cells to induce proinflammatory cytokines by reverse transcription-PCR and enzyme-linked immunosorbent assay. First, by using peripheral blood mononuclear cells (PBMC) and a gastric cancer cell line (MKN-45 cells), we confirmed the ability of purified H. pylori urease to induce the production of proinflammatory cytokines. Furthermore, we demonstrated that the human gastric epithelial cells produced interleukin-6 (IL-6) and tumor necrosis factor alpha, but not IL-8, following stimulation with purified urease. The patterns of cytokine induction differed among human PBMC, MKN-45 cells, and human gastric epithelial cells. These results suggest that the human gastric epithelial cells contribute to the induction of proinflammatory cytokines by the stimulation of H. pylori urease, indicating that the epithelial cells were involved in the mucosal inflammation that accompanied H. pylori infection.

scholarly journals Role of medullary progenitor cells in epithelial cell migration and proliferation

2014 ◽  
Vol 307 (1) ◽  
pp. F64-F74 ◽  
Author(s):  
Dong Chen ◽  
Zhiyong Chen ◽  
Yuning Zhang ◽  
Chanyoung Park ◽  
Ahmed Al-Omari ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Progenitor Cells ◽  
Conditioned Medium ◽  
Side Population ◽  
Collecting Duct ◽  
Tubular Epithelial Cell ◽  
Epithelial Cell Migration ◽  
Cell Migration And Proliferation

This study is aimed at characterizing medullary interstitial progenitor cells and to examine their capacity to induce tubular epithelial cell migration and proliferation. We have isolated a progenitor cell side population from a primary medullary interstitial cell line. We show that the medullary progenitor cells (MPCs) express CD24, CD44, CXCR7, CXCR4, nestin, and PAX7. MPCs are CD34 negative, which indicates that they are not bone marrow-derived stem cells. MPCs survive >50 passages, and when grown in epithelial differentiation medium develop phenotypic characteristics of epithelial cells. Inner medulla collecting duct (IMCD3) cells treated with conditioned medium from MPCs show significantly accelerated cell proliferation and migration. Conditioned medium from PGE2-treated MPCs induce tubule formation in IMCD3 cells grown in 3D Matrigel. Moreover, most of the MPCs express the pericyte marker PDGFR-b. Our study shows that the medullary interstitium harbors a side population of progenitor cells that can differentiate to epithelial cells and can stimulate tubular epithelial cell migration and proliferation. The findings of this study suggest that medullary pericyte/progenitor cells may play a critical role in collecting duct cell injury repair.

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