Original communicationAcidic conditions ameliorate both adenosine triphosphate depletion and the development of hyperpermeability in cultured Caco-2BBe enterocytic monolayers subjected to metabolic inhibition☆
References (53)
- et al.
Rapid development of vasopressin-induced hydroosmosis in kidney collecting tubules measured by a new fluorescent technique
Biophys J
(1988) - et al.
Spectral and photophysical studies of benzo[c]xanthene dyes: dual emission pH sensors
Anal Biochem
(1991) - et al.
A new generation of Ca2+ indicators with greatly improved fluorescence properties
J Biol Chem
(1985) - et al.
Effect of pH on the kinetics of frog muscle phosphofructokinase
J Biol Chem
(1966) - et al.
Regulation of (Na+ + K+)-ATPase by inorganic phosphate: pH dependence and physiologic implications
Biochem Biophys Res Commun
(1984) Cellular and subcellular calcium signalling in gastrointestinal epithelium
Gastroenterology
(1994)Calcium signalling
Cell
(1995)The Ca2+ pump of the plasma membrane
J Biol Chem
(1992)Approaches to the study of mammalian phospholipases
J Lipid Res
(1985)- et al.
Inhibition of nonlysozomal calcium-dependent proteolysis by glycin during anoxic injury of rat hepatocytes
Gastroenterology
(1994)
A pH-dependent phospholipase A2 contributes to loss of plasma membrane integrity during chemical hypoxia in rat hepatocytes
Biochem Biophys Res Commun
Interferon-y directly affects barrier function of cultured intestinal epithelial monolayers
J Clin Invest
IFN-y modulation of epithelial barrier function: time course, reversibility, and site of cytokine binding
J Immunol
Nitric oxide mediates interferon-gamma-induced hyperpermeability in cultured human intestinal epithelial monolayers
Crit Care Med
IL-4 directly modulates function of a model human intestinal epithelium
J Immunol
Insulin regulates the paracellular permeability of cultured intestinal epithelial cell monolayers
J Clin Invest
Regulation of T84 cell monolayer permeability by insulin-like growth factors
Am J Physiol
Regulation of paracellular permeability in Caco-2 cell monolayers by protein kinase C
Am J Physiol
Nitric oxide dilates tight junctions and depletes ATP in cultured Caco-2BBe intestinal epithelial monolayers
Am J Physiol
Effect of reversible ATP depletion on tight-junction integrity in LLC-PK1 cells
Am J Physiol
“Chemical hypoxia” increases junctional permeability and activates chloride transport in human intestinal epithelial monolayers
Surgery
Uncoupling of the molecular ‘fence’ and paracellular ‘gate’ functions in epithelial tight junctions
Nature
Hyperpermeability and ATP depletion induced by chronic hypoxia or glycolytic inhibition in Caco-2BBe monolayers
Am J Physiol
Endotoxin-induced ileal mucosal hyperpermeability in pigs: role of tissue acidosis
Am J Physiol
The conductance of cultured epithelial cell monolayers: oxidants, adenosine triphosphate, and phorbol dibutyrate
Am J Respir Cell Mol Biol
Cited by (11)
Cytopathic hypoxia: Mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis
2001, Critical Care ClinicsCitation Excerpt :Endogenous production of ONOO− secondary to iNOS induction plus O2−⋅ generation has been implicated as the major factor leading to impaired mitochondrial respiration in some tissues, such as rat diaphragm, following in vivo challenge with LPS.7 The author's laboratory has obtained indirect evidence that endogenous production of ONOO− is responsible for ATP depletion in cultured enterocytes incubated with the proinflammatory cytokine interferon-γ.85 The author's laboratory has shown that inhibiting iNOS enzymatic activity preserves mitochondrial function in a rat model of sublethal endotoxemia.
Cell response to metabolic acidosis
1999, Reanimation UrgencesIntestinal epithelial hyperpermeability
1998, Gastroenterology Clinics of North AmericaBicarbonate for acute acidosis
2021, Cochrane Database of Systematic Reviews
- ☆
Supported in part by grant GM37631 from the National Institutes of Health (NIH). Dr. Unno was supported by Uehara Memorial Foundation (Japan). Dr. Hagen was supported in part by grant DK 15081 from the NIH and in part by the morphology core of the Harvard Digestive Disease Center (NIH grant DK 34854).