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Abstract
Background and aim: Patients with dysplasia in Barrett’s esophagus (BE) have a considerable risk of developing esophageal adenocarcinoma (EAC). The mucosal expression of the pro-inflammatory angiotensin II receptor type 1 (AT1R) is elevated in these patients, suggesting a role in carcinogenesis. The purpose of this study was to determine whether interference with the renin–angiotensin system (RAS) would influence downstream markers of carcinogenesis.
Methods: Endoscopic mucosal biopsies from BE patients with low-grade dysplasia (LGD) were sampled before and after a three-week period of RAS-interfering treatment. Thirty patients were randomly allocated to enalapril (ACE inhibitor, 5 mg od), candesartan (AT1R antagonist, 8 mg od), or no drug. The expression of 12 proteins known to be associated with RAS and carcinogenesis was assessed using western blot.
Results: We found altered expression of several proteins after enalapril treatment (decreased: NFκB, p = .043; NLRP3, p = .050; AMACR, p = .017; and caspase 3, p = .025; increased: p53, p = .050). Candesartan treatment was associated with increased iNOS expression (p = .033). No significant changes were seen in the no-drug group.
Conclusion: Interference with angiotensin II formation was associated with altered expression of inflammation- and carcinogenesis-related proteins. The present results speak in favor of involvement of angiotensin II in BE dysplasia, but the role of AT1R should be investigated further.
Acknowledgements
The technical assistance of Christina Ek, My Engström and Niclas Björnfot is gratefully appreciated, and we thank Sören Lundberg for reviewing the statistics. We thank the participating patients especially, for their loyalty and generosity.
Disclosure atatement
We declare that there are no conflicts of interests.
Funding
This study was supported through the ALF agreement, and by grants from the Swedish Research Council, the Gothenburg Medical Society, the Health and Medical Care Committee of the Western Region of Sweden, the Capio Research Fund.
