Esophageal Injury with External Esophageal Perfusion1

Li, Yan; Wo, John M.; Su, Ruifeng; Ray, Mukunda B.; Jones, Warren T.; Martin, Robert C.G.

doi:10.1016/j.jss.2005.04.018

Cited by 17 publications

(12 citation statements)

References 29 publications

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“…This may explain why duodenoesophageal reflux induces EAC without an exogenous carcinogen in surgical animal models of BE and EAC (42). Another study showed that the typical injuries and cellular changes seen in severe reflux esophagitis that may lead to the development of BE, are induced in rats by continuous perfusion with bovine bile after treatment for only 4 weeks (43). These results underscore the importance of bile acids in BE as a premalignant lesion.…”

Section: Discussionmentioning

confidence: 99%

Expression of Bile Acid Transporting Proteins in Barrett's Esophagus and Esophageal Adenocarcinoma

Dvorak

Watts²,

Ramsey³

et al. 2009

Am J Gastroenterol

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OBJECTIVES Barrett’s esophagus (BE) is a metaplastic lesion characterized by replacement of the normal squamous epithelium by columnar intestinal epithelium containing goblet cells. It is speculated that this process is an adaptation to protect cells from components of refluxate, such as gastric acid and bile acids. In contrast to the normal squamous epithelium, enterocytes of the distal ileum are adapted to transport bile acids from the intestinal lumen. Several bile acid transporters are utilized for effective removal of bile acids, including the apical sodium-dependent bile acid transporter (ASBT), the ileal bile acid-binding protein (IBABP), and the multidrug-resistant protein 3 (MRP3). We hypothesized that one of the possible functions of newly arising metaplastic epithelium, in the esophagus, is to transport bile acids. Our major goal was to evaluate the expression of bile acid transporters in normal squamous epithelium, BE with different grades of dysplasia, and esophageal adenocarcinoma (EAC). METHODS A total of 101 patients were included in this study. Immunohistochemistry (IHC) and reverse transcriptase (RT)–PCR were used to detect the expression of these transporters at the mRNA and protein levels. RESULTS Our immunohistochemical studies showed that all three bile acid transporters are expressed in BE glands, but not in squamous epithelium. ASBT was found in the apical border in BE biopsies. The highest frequency of ASBT expression was in patients with nondysplastic BE (9 of 15, 60%), and a progressive loss of ASBT was observed through the stages of dysplasia. ASBT was not detected in EAC (0 of 15). IBABP staining was observed in the cytoplasm of BE epithelial surface cells. Expression of IBABP was found in 100% of nondysplastic BE (14 of 14), in 93% of low-grade dysplasia (LGD, 15 of 16), in 73% of high-grade dysplasia (HGD, 10 of 14), and in 33% of EAC (5 of 15). MRP3 was expressed in the basolateral membrane in 93% of nondysplastic BE (13 of 14), in 60% of LGD (10 of 16), and in 86% of HGD (11 of 13). Only weak MRP3 staining was detected in EAC biopsies (5 of 15, 33%). In addition, RT–PCR studies showed increased expression of mRNA coding for ASBT (6.1×), IBABP (9.1×), and MRP3 (2.4×) in BE (N = 13) compared with normal squamous epithelium (N = 15). Significantly increased mRNA levels of IBABP (10.1×) and MRP3 (2.5×) were also detected in EAC (N = 21) compared with normal squamous epithelium. CONCLUSIONS We found that bile acid transporters expression is increased in BE tissue at the mRNA and protein levels and that expression of bile acid transporter proteins decreased with progression to cancer.

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Section: Discussionmentioning

confidence: 99%

Expression of Bile Acid Transporting Proteins in Barrett's Esophagus and Esophageal Adenocarcinoma

Dvorak

Watts²,

Ramsey³

et al. 2009

Am J Gastroenterol

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“…ApopTag In situ Apoptosis Detection kit (Intergen Co.) was used to detect the apoptotic cells according to a procedure reported previously (10,12). Briefly, after endogenous peroxidase was blocked with H 2 O 2 in methanol for 20 min, the sections underwent proteinase K digestion for 15 min.…”

Section: Methodsmentioning

confidence: 99%

Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Martin¹,

Liu²,

Wo³

et al. 2007

Clinical Cancer Research

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Purpose: Oxidative stress is related to the carcinogenic pathway of reflux esophagitis to Barrett's metaplasia to esophageal adenocarcinoma (EAC). Recent studies have shown that a decreased manganese superoxide dismutase (MnSOD) level is associated with the increased incidences of Barrett's esophagus (BE) and EAC. The aim of this study was to investigate MnSOD supplementation as a chemopreventive agent to prevent oxidative injury and subsequent BE and EAC formation. Experimental Design: Our esophagoduodenal anastomotic (EDA) model was done on rats according to our established procedure and treated with Mn(III)tetrakis(4-benzoic acid) porphyrin (MnTBAP; 10 mg/kg, i.p. every 3 days). Histologic changes were determined after the EDA model at 1, 3, and 6 months. Lipid peroxidation and 8-hydroxy-deoxyguanosine for DNA oxidative damage were determined by thiobarbituric acid^reactive substance assay and immunohistochemical staining. Enzymatic activities of MnSOD and Cu/ZnSOD were evaluated, and the rate of proliferation was determined by proliferating cell nuclear antigen staining. Results: Severe esophagitis was seen in 100% of the EDA rats, and morphologic transformation within the esophageal epithelium was observed with intestinal metaplasia (40% of animals) and cancer (40% of animals) identified after 3 months. Decreased oxidative damage, along with the decreased degree of esophagitis and incidence of BE (20%) and EAC (0%), was found in MnTBAP-treated EDA rats comparing with the saline-treated EDA control. Decreased proliferation (46%) and increased SOD enzymatic activities (25%) were also found in the EDA rats treated with MnTBAP. Conclusion: MnTBAP protected rat esophageal epithelium from oxidative injury induced by EDA, and it could prevent the transformation of esophageal epithelial cell to BE to EAC by preservation of antioxidants.Esophageal adenocarcinoma (EAC) has received considerable attention because of the dramatically increased incidence in the past 2 decades and the poor prognoses with a 5-year survival rate of 10% to 20% (1 -5). Currently, it is widely accepted that a cause-effect relationship exists between gastroesophageal reflux disease and EAC. Oxidative stress has been proposed to be closely related to the carcinogenic progression of reflux esophagitis, Barrett's metaplasia, and EAC. It has been shown that reactive oxygen species increase with the grade of reflux esophagitis and are highest in Barrett's esophagus (BE) in clinical patients (6). Several studies have also shown that reactive oxygen species cause DNA injury, such as strand breakage, alterations in guanine and thymine bases, and DNA cross-linkage (7,8). Therefore, oxidative DNA damage may contribute to the accumulation of genetic damage, and the accumulation of genetic and epigenetic aberrations produces one or more clones with metaplastic and/or malignant potential (9).In our previous studies using an external esophageal perfusion rat model (10 -13), we have shown significant increased levels of lipid peroxidation and 8-hydr...

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“…An ApopTag ® in situ apoptosis detection kit (Intergen Company, Purchase, NY, USA) was used to detect apoptotic cells following a method reported previously. 34,35 In vitro testing Three esophageal cell lines were used to analyze further the response of the esophageal cells to the CS-GGS nanoparticles and near infrared light. The cells used were a human squamous esophageal epithelium cell line (Het-1A), a Barrett's epithelium cell line (BAR-T), and an esophageal adenocarcinoma cell line (OE-19).…”

Section: Tunel Assay Of Ex Vivo Samplesmentioning

confidence: 99%

Infrared light-absorbing gold/gold sulfide nanoparticles induce cell death in esophageal adenocarcinoma

Li¹,

Gobin²,

Dryden³

et al. 2013

IJN

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Gold nanoparticles and near infrared-absorbing light are each innocuous to tissue but when combined can destroy malignant tissue while leaving healthy tissue unharmed. This study investigated the feasibility of photothermal ablation therapy for esophageal adenocarcinoma using chitosan-coated gold/gold sulfide (CS-GGS) nanoparticles. A rat esophagoduodenal anastomosis model was used for the in vivo ablation study, and three human esophageal cell lines were used to study the response of cancer cells and benign cells to near infrared light after treatment with CS-GGS. The results indicate that both cancerous tissue and cancer cells took up more gold nanoparticles and were completely ablated after exposure to near infrared light. The benign tissue and noncancerous cells showed less uptake of these nanoparticles, and remained viable after exposure to near infrared light. CS-GGS nanoparticles could provide an optimal endoluminal therapeutic option for near infrared light ablation of esophageal cancer.

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Esophageal Injury with External Esophageal Perfusion1

Cited by 17 publications

References 29 publications

Expression of Bile Acid Transporting Proteins in Barrett's Esophagus and Esophageal Adenocarcinoma

Expression of Bile Acid Transporting Proteins in Barrett's Esophagus and Esophageal Adenocarcinoma

Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Infrared light-absorbing gold/gold sulfide nanoparticles induce cell death in esophageal adenocarcinoma

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