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J Thorac Cardiovasc Surg 2008;135:1226-1227
© 2008 The American Association for Thoracic Surgery

Invited Commentary

Discussion

The first 20% of the full text of this article appears below.

Dr Steven DeMeester (Los Angeles, Calif). I would like to congratulate Dr Weyant and his colleagues both for an excellent presentation and a very clearly written manuscript.

In this study the authors evaluated the role of sPLA2 in a mouse model of surgically induced gastroduodenoesophageal reflux. By using an inbred mouse strain deficient in the gene for phospholipase A2, they were able to ascertain the role of this enzyme in early esophageal mucosal changes associated with reflux. Compared with normal mice, the knockout mice showed significantly less increase in epithelial thickness and in Ki67 activity, with levels in the knockout mice equivalent to those in control animals. They conclude that phospholipase A2 is involved in the early squamous mucosal changes associated with gastroduodenoesophageal reflux.

The authors are to be congratulated for several things. First, they successfully developed this mouse model of surgically induced reflux, which has been a hurdle for many investigators in the past. Second, they demonstrate that the phospholipase A2 protein can be found in esophageal tissue in the mouse. Third, they designed an elegant first experiment by using a mouse knockout model for this gene to demonstrate the role of phospholipase A2 in early squamous esophageal mucosal injury associated with reflux. I have 3 questions for you.

First, changes in esophageal mucosal thickness or the old (Ishmael . . . [Full Text of this Article]


Related Article

Secretory phospholipase A2 is required to produce histologic changes associated with gastroduodenal reflux in a murine model
Ashok Babu, Xianzhong Meng, Anirban M. Banerjee, Fabia Gamboni-Robertson, Joseph C. Cleveland, Sagar Damle, David A. Fullerton, and Michael J. Weyant
J. Thorac. Cardiovasc. Surg. 2008 135: 1220-1227. [Abstract] [Full Text] [PDF]





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