Thrombin stimulates inositol phosphate formation, intracellular calcium fluxes and DNA synthesis in cultured fetal human non-pigmented ciliary epithelial cells

The interactions that occur between pathogenic micro-organisms and their host cells are complex and intimate. We have used two enteric pathogens, Salmonella typhimurium and enteropathogenic Escherichia coli (EPEC), to examine the interactions that occur between these organisms and epithelial cells. Although these are enteric pathogens, the knowledge and techniques developed from these systems may be applied to the study of dental pathogens. Both S. typhimurium and EPEC disrupt epithelial monolayer integrity, although by different mechanisms. Both pathogens cause loss of microvilli and re-arrangement of the underlying host cytoskeleton. Despite these similarities, both organisms send different signals into the host cell. EPEC signal transduction involves generation of intracellular calcium and inositol phosphate fluxes, and activation of host tyrosine kinases that results in tyrosine phosphorylation of a 90-kDa host protein. Bacterial mutants have been identifed that are deficient in signaling to the host. We propose a sequence of events that occur when EPEC interacts with epithelial cells. Once inside a host cell, S. typhimurium remains within a vacuole. To define some of the parameters of the intracellular environment, we constructed genetic fusions of known genes with lacZ, and used these fusions as reporter probes of the intracellular vacuolar environment. We have also begun to examine the bacterial and host cell factors necessary for S. typhimurium to multiply within epithelial cells. We found that this organism triggers the formation of novel tubular lysosomes, and these structures are linked with intracellular replication.

Download Full-text

Action of hydrocortisone on DNA synthesis in epithelial cells of the biliary tract

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00808722 ◽

1974 ◽

Vol 78 (6) ◽

pp. 1417-1419

Author(s):

P. A. Dyban

Keyword(s):

Epithelial Cells ◽

Dna Synthesis ◽

Biliary Tract

Download Full-text

Mechanosensitive calcium signaling promotes epithelial tight junction remodeling by activating RhoA

10.1101/2021.05.18.444663 ◽

2021 ◽

Author(s):

Saranyaraajan Varadarajan ◽

Rachel E. Stephenson ◽

Eileen R. Misterovich ◽

Jessica L. Wu ◽

Ivan S. Erofeev ◽

...

Keyword(s):

Epithelial Cells ◽

Intracellular Calcium ◽

Tight Junctions ◽

Calcium Influx ◽

Cell Junctions ◽

Mechanical Stimuli ◽

Local Repair ◽

Transient Activation ◽

Epithelial Tight Junction ◽

Sense And Respond

Epithelia maintain an effective barrier by remodeling cell-cell junctions in response to mechanical stimuli. Cells often respond to mechanical stress through activating RhoA and remodeling actomyosin. Previously, we found that local leaks in the barrier are rapidly repaired by localized, transient activation of RhoA – ″Rho flares″ – but how Rho flares are initiated remains unknown. Here, we discovered that intracellular calcium flashes occur in Xenopus laevis epithelial cells undergoing Rho flare-mediated remodeling of tight junctions. Calcium flashes originate at the site of barrier leaks and propagate into the cell. Depletion of intracellular calcium or inhibition of mechanosensitive calcium channels (MSC) reduced the amplitude of calcium flashes and diminished the activation of Rho flares. Furthermore, MSC-dependent calcium influx was necessary to maintain global barrier function by regulating local repair of tight junctions through efficient junction contraction. We propose that MSC-dependent calcium flashes are an important mechanism allowing epithelial cells to sense and respond to local leaks induced by mechanical stimuli.

Download Full-text