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Epoxyeicosatrienoic acids (EETs) have beneficial effects on cardiovascular disease. Soluble epoxide hydrolase (sEH) metabolizes EETs to less active diols, thus diminishing their biological activity. sEH inhibitors can suppress the progression of atherosclerotic lesions in animal models. However, the regulation of sEH in vascular smooth muscle cells (VSMCs) and role of sEH in patients with atherosclerosis have not been evaluated. We hypothesize that sEH in VSMCs plays a pivotal role in atherosclerosis and injury-induced neointima formation. In this study, sEH expression in human autopsy atherosclerotic plaque was determined by immunohistochemistry. In cultured rat and human VSMCs, the phenotypic switching marker and sEH expression induced by plateletderived growth factor-BB (PDGF-BB) were examined by Western blot analysis. Carotid-artery balloon injury was performed after adenovirus- mediated overexpression of sEH or oral administration of a potent sEH inhibitor in Sprague-Dawley rats. sEH was highly expressed in VSMCs of the intima and media within human atherosclerotic plaque. In vitro, PDGF-BB upregulated the expression in VSMCs after transcription and promoted cell proliferation and migration; the latter effect could be largely attenuated by an sEH inhibitor. Adenovirus-mediated overexpression of sEH could mimic the effect of PDGF-BB and induce VSMC proliferation and migration. In vivo, the sEH inhibitor led to a significant decrease in injury-induced neointima formation in a rat carotid-artery injury model. These data establish the effect of sEH expression on atherosclerotic progression and vascular remodeling after injury, thus identifying a novel integrative role for sEH in VSMC phenotypic modulation and migration. Blocking sEH activity may be a potential therapeutic approach for ameliorating vascular occlusive disease. [ABSTRACT FROM AUTHOR]

Increasing evidence has demonstrated that changes in plasma nuclear matrix proteins are specific markers of cancer. Furthermore, proteomic analysis has revealed that calponin-h2 is upregulated in human breast cancer tissue, but is absent in healthy and benign controls. However, the roles of levels of plasma calponin-h2 in the diagnosis of breast cancer and its association with clinicopathological parameters remain to be elucidated. In the present study, the plasma levels of calponin-h2 in patients with breast cancer, benign breast disease and in healthy controls were examined using an enzyme-linked immunosorbent assay. The expression levels of calponin-h2 in invasive breast cancer and normal breast tissues were measured using immunohistochemistry. Statistical analyses examined the association between the levels of plasma calponin-h2 and clinicopathological parameters. The results demonstrated that the plasma level of calponin-h2 in breast cancer was significantly higher than those in the healthy control and benign breast disease groups (P<0.05). The combination of calponin-h2, carcinoembryonic antigen, carbohydrate antigen 15-3 improved the diagnosis of breast cancer. The plasma levels of calponin-h2 PR- breast cancers was significantly higher, compared with PR+ breast cancers (P=0.033), and the plasma levels of calponin-h2 in patients with breast cancer aged >50 years was significantly higher than in patients ≤50 years of age (P=0.001). No association was found between the level of plasma calponin-h2 and other clinicopathological parameters of breast cancer. Taken together, these results indicated that calponin-h2 may be a useful marker of breast cancer. [ABSTRACT FROM AUTHOR]

Background: Human papillomavirus (HPV) infection is a major risk factor for the development of nearly all cases of cervical cancer worldwide. The presence of HPV DNA in cases of esophageal squamous-cell carcinoma (ESCC) has been reported repeatedly from Shantou, China, and other regions with a high incidence of esophageal carcinoma (EC). However, unlike in cervical squamous-cell carcinoma (CSCC), in ESCC, the characteristics of HPV are unclear. Thus, the role of high-risk HPV types in the carcinogenesis of ESCC remains uncertain. Methods: Seventy cases of ESCC with 60 controls and 39 cases of CSCC with 54 controls collected from patients in Shantou region in China were compared for the distributions of HPV-16, -18 and -58; viral load; and viral integration using real-time PCR assay and HPV-16 expression using immunostaining. Results: The detection rates and viral loads of HR-HPV infection were significantly lower in ESCC than in CSCC (50.0% vs. 79.48%, P = 0.005; 2.55 ± 3.19 vs. 361.29 ± 441.75, P = 0.002, respectively). The combined integration level of HPV-16, -18 and -58 was slightly lower in ESCC than in CSCC (P = 0.022). HPV-16 expression was detected in 59.26% of ESCC tissue and significantly associated with tumour grade (P = 0.027). Conclusions: High levels of HR-HPV expression and integration may be an indicator of the risk of ESCC, at least for patients in the Shantou region of China. However, a relatively low HPV copy number and infection rate in ESCC is unlikely to play an essential a role in the carcinogenesis of ESCC as in cervical cancer. Factors other than HR-HPV infection may contribute to the carcinogenesis of ESCC. [ABSTRACT FROM AUTHOR]