This phenomenon, and the sex specificity, was also apparent in bone marrow—derived macrophages stimulated with endotoxin. The extent of gastric erosions was blindly scored. We investigated this using both acute and chronic models of gastric injury. The gastric contents were collected, and the volume and pH of the gastric juice were measured. Acetic acid—induced gastric ulcers were initially similar in size in Muc-2—deficient and wild-type mice of both sexes, but ulcer healing was significantly impaired in male Muc-2—deficient mice. Indomethacin administration caused similar levels of gastric damage in Muc-2—deficient and wild-type mice, but the erosions healed more slowly in the former.
Abstract Mucus is known to contribute significantly to the prevention and repair of mucosal damage throughout the gastrointestinal tract. The stomach was then returned to the abdominal cavity, and the abdominal wall and skin were closed with sutures. Indomethacin was dissolved in 1. This phenomenon, and the sex specificity, was also apparent in bone marrow—derived macrophages stimulated with endotoxin. Images were recorded at identical gain settings, and mean intensity was calculated per image field. The remaining mice were euthanized 10 days after the serosal application of acetic acid, and ulcer areas were measured. Induction of cyclooxygenase-2 in the stomach, in response to indomethacin- or acetic acid—induced ulceration, was significantly reduced in male Muc-2—deficient mice. Primer sequences used were as follows: On the other hand, brief application of acetic acid to the serosal wall of the stomach induces the formation of true ulcers ie, erosions penetrating through the mucosa into the submucosa. During the 43 hours after the initial assessment of damage, however, the erosions progressively healed in the wild-type group more quickly than in the Muc-2—deficient group. Comparisons among groups of data were made using a one-way analysis of variance followed by Dunnett's multiple comparison test. The stomach was removed, with care taken to preserve the gastric contents. Nonadherent cells were removed at day 4 and day 7, and fresh medium was added to the adherent cells. Healing of Acetic Acid-Induced Gastric Ulcers Gastric ulcers were induced in groups of at least 10 mice Muc-2—deficient and wild type; males and females , as described in detail previously. The extent of gastric erosions was blindly scored. A laparotomy was performed and the pylorus was ligated. At least five mice from each of the Muc-2—deficient and wild-type groups were euthanized 5, 12, 24, or 48 hours later. Also, gastric juice was collected from wild-type and Muc-2—deficient mice both sexes in which gastric ulcers had been induced 10 days earlier, and gastric acidity was determined as above. Subsequently, similar experiments were conducted in female mice. The gastric contents were collected, and the volume and pH of the gastric juice were measured. Mucin expression is cell- and tissue-specific. Other tissues, as well as samples of the colon as a positive control , were fixed in neutral-buffered formalin and were processed by routine techniques for immunohistochemical examination of Muc-2 and Muc-5ac expression as described in the next section. This involved measuring the lengths of all hemorrhagic lesions in millimeters , then summing these to give a gastric damage score for each mouse. Published by Elsevier Inc. Acetic acid—induced gastric ulcers were initially similar in size in Muc-2—deficient and wild-type mice of both sexes, but ulcer healing was significantly impaired in male Muc-2—deficient mice. We investigated this using both acute and chronic models of gastric injury.
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