Premium
Acidification of damaged cells is a consequence of damage to the gastric epithelium, and may contribute to surface pH increases after damage
Author(s) -
Demitrack Elise Susan,
Montrose Marshall H
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.980.1
Subject(s) - extracellular , cell damage , chemistry , epithelium , intracellular ph , intracellular , biophysics , cell , gastric mucosa , gastric glands , foveolar cell , stomach , pathology , biochemistry , biology , medicine
Focal damage of the gastric surface epithelium causes a transient rise in extracellular pH (pH o ) over the damage site, prior to epithelial repair. To identify sources of the pH o rise we measured intracellular pH (pH i ) of cells in and around the damaged area. The exposed gastric mucosa of anesthetized mice was loaded with 5 μM SNARF‐5F‐AM, and tissue imaged on a two‐photon microscope stage, during tissue superfusion with buffered pH 3 saline. A 2‐3 cell region of the gastric epithelium was photodamaged (710 nm, 350 mW for 5‐10 sec). Damage was monitored as loss of NAD(P)H autofluorescence and disrupted cell structure (confocal reflectance). pH i was measured near the damage (5‐10 μm), far from the damage (100‐150 μm), or in the actual damaged area. Before damage, initial pH i values were similar in all cell groups (~pH 7.1). After damage, pH i values were similar in near and far cells (7.17 ± 0.06 and 7.15 ± 0.04), but decreased to 6.45 ± 0.08 in damaged cells (n=4). Adding 20 μM iv EIPA or 100 μM luminal SITS did not significantly change initial pH i values in any cell type. After damage, EIPA selectively acidified damaged cells vs control (6.00 ± 0.09 vs. 6.45 ± 0.08, n=4), but SITS did not affect damaged cell acidification (6.59 ± 0.3, n=4). We conclude that damaged gastric epithelial cells may activate basolateral Na/H exchange as part of transepithelial alkali secretion that causes the luminal pH o increase seen after epithelial damage.