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@#AIM: To invesgate the expression of epidermal growth factor-like domain7(EGFL7)protein in several lacrimal gland tumor types and normal lacrimal gland tissues by immunohistochemical staining. And discuss the correlation of EGFL7 expression with tumor cell proliferation activity and the MVD in lacrimal gland epithelial tumors.<p>METHODS: A total of 46 paraffin-embedded specimens of common lacrimal gland epithelial tumors and other lacrimal gland tumor types, including 20 cases of lacrimal gland pleomorphic adenoma, 12 cases of pleomorphic adenocarcinoma, and 14 cases of adenoid cystic carcinoma, as well as ten normal lacrimal glands were analyzed for the expression of EGFL7 protein. For all specimens, the tumor microvascular networks were also labeled with anti-CD34 antibody and the tumor MVD was calculated. The proliferative activity of tumor cells containing Ki67.<p>RESULTS: EGFL7 protein was scored as positive with the presence of brown color in the cytoplasm, and was mainly observed in cells of lacrimal gland pleomorphic adenocarcinomas and adenoid cystic carcinomas. Immunohistochemical staining showed that EGFL7 was not expressed in normal lacrimal gland tissue. The rates of expression of EGFL7 in lacrimal gland pleomorphic adenomas, lacrimal gland pleomorphic adenocarcinomas, and lacrimal adenoid cystic carcinomas were 5%(1/20), 83%(10/12), and 86%(12/14), respectively. The EGFL7 expression in both malignant tumor types was significantly higher than that in pleomorphic adenomas and normal lacrimal gland tissues(<i>P</i><0.001). CD34 staining colored the tumor microvascular network brown-yellow in single cells or clustered cell populations. The expression of CD34 in lacrimal gland pleomorphic adenocarcinomas(32.58±14.46)and adenoid cystic carcinomas(43.43±4.60)was significantly higher than that in pleomorphic adenomas(4.20±1.19)(<i>P</i><0.001). Ki67 staining appeared as a brownish color in cell nuclei, indicating proliferative activity. The expression of Ki67 in lacrimal gland pleomorphic adenocarcinomas(44.83±13.68)and adenoid cystic carcinomas(26.29±8.44)was significantly higher than that in pleomorphic adenomas(2.80±3.14)and normal tissues(0.40±0.70)(<i>P</i><0.001). Furthermore, the expression of EGFL7 protein was positively correlated with high MVD and Ki67 expression in lacrimal epithelial tumors(<i>r</i>s=0.897,<i> P</i><0.001; <i>r</i>s=0.837, <i>P</i><0.001). <p>CONCLUSION: The correlation of EGFL7 expression with high MVD and Ki67 expression suggests that high EGFL7 expression plays an important role in promoting tumor angiogenesis and tumor proliferation.
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OBJECTIVE@#Renal fibrosis is the most common manifestation of chronic kidney disease (CKD). Noting that existing treatments of renal fibrosis only slow disease progression but do not cure it, there is an urgent need to identify novel therapies. Hydrogen sulfide (H2S) is a newly discovered endogenous small gas signaling molecule exerting a wide range of biologic actions in our body. This review illustrates recent experimental findings on the mechanisms underlying the therapeutic effects of H2S against renal fibrosis and highlights its potential in future clinical application.@*DATA SOURCES@#Literature was collected from PubMed until February 2019, using the search terms including "Hydrogen sulfide," "Chronic kidney disease," "Renal interstitial fibrosis," "Kidney disease," "Inflammation factor," "Oxidative stress," "Epithelial-to-mesenchymal transition," "H2S donor," "Hypertensive kidney dysfunction," "Myofibroblasts," "Vascular remodeling," "transforming growth factor (TGF)-beta/Smads signaling," and "Sulfate potassium channels."@*STUDY SELECTION@#Literature was mainly derived from English articles or articles that could be obtained with English abstracts. Article type was not limited. References were also identified from the bibliographies of identified articles and the authors' files.@*RESULTS@#The experimental data confirmed that H2S is widely involved in various renal pathologies by suppressing inflammation and oxidative stress, inhibiting the activation of fibrosis-related cells and their cytokine expression, ameliorating vascular remodeling and high blood pressure, stimulating tubular cell regeneration, as well as reducing apoptosis, autophagy, and hypertrophy. Therefore, H2S represents an alternative or additional therapeutic approach for renal fibrosis.@*CONCLUSIONS@#We postulate that H2S may delay the occurrence and progress of renal fibrosis, thus protecting renal function. Further experiments are required to explore the precise role of H2S in renal fibrosis and its application in clinical treatment.