Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2018-06-15 Cooperative journals: 《南方医科大学学报》
Abstract： Objective To investigate the correlation between tumor-associated macrophages (TAMs) and the development of high risk human papilloma virus (hr-HPV)-related cervical cancer. Methods A total of 112 cases of cervical tissue were collected, including 16 normal cervical tissues, 55 cervical intraepithelial neoplasia (CIN) tissues and 41 squamous cervical cancer (SCC) tissues. The expression of CD163 + macrophages in the cervical tissues was detected by immunohistochemical method, and the results were analyzed in relation with the clinical data of the patients. Results Immunohistochemical analysis showed that the cell density of CD163+ macrophages increased progressively with the increase in the tissue malignancy, in the order of normal cervical tissue, CIN I, CIN II-III, and SCC. Correlation analysis revealed a positive relationship between CD163 + macrophage density and tissue malignancy (P=0.000). The density of CD163 + macrophages was significantly upregulated in HR-HPV-positive SCC tissue (P<0.05). CD163 + macrophages were positively correlated with cervical lymph node metastasis (P=0.005) and FIGO stage (P=0.004) of SCC. Conclusion The expression of CD163+ macrophages is positively correlated with malignant transformation of cervical tissues, and hr-HPV infection is significantly correlated with CD163 expression level in the macrophages. CD163 + macrophages can be used as predictors of the occurrence and progression of cervical cancer caused by hr-HPV infection.
Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2017-12-27 Cooperative journals: 《南方医科大学学报》
Abstract： Objective To investigate the effect of prostaglandins E2 (PGE2) in enhancing vascular endothelial growth factor (VEGF) expression in a rat macrophage cell line and the effect of the media from PGE2-inuced rat macrophages on angiogenetic ability of human umbilical vein endothelial cells (HUVECs) in vitro. Methods Western blotting and qPCR were employed to investigate the expressions of VEGF protein and mRNAs in rat macrophage cell line NR8383 stimulated by PGE2 in the presence or absence of EP2 receptor inhibitor (AH6809) and EP4 receptor inhibitor (AH23848). Conditioned supernatants were obtained from different NR8383 subsets to stimulate HUVECs, and the tube formation ability and migration of the HUVECs were assessed with Transwell assay. Results PGE2 stimulation significantly enhanced the expression of VEGF protein and mRNAs in NR8383 cells in a dose-dependent manner. The supernatants from NR8383 cells stimulated by PGE2 significantly enhanced tube formation ability of HUVECs (P<0.05) and promoted the cell migration. Such effects of PGE2 were blocked by the application of AH6809 and AH23848. Conclusion PGE2 can dose-dependently increase VEGF expression in NR8383 cells, and the supernatants derived from PGE2-stimulated NR8383 cells can induce HUVEC migration and accelerate the growth of tube like structures. PGE2 are essential to corpus luteum formation by stimulating macrophages to induce angiogenesis through EP2/EP4.
Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2017-12-07 Cooperative journals: 《南方医科大学学报》
Abstract： Objective To investigate the mechanism of miR-133a in reversing neonatal rat cardiomyocyte hypertrophy induced by phenylephrine. Methods A miR-133a precursor cDNA was used to construct an adenovirus vector, which was transfected into 293 cells to harvest miR-133a-containing virus. Neonatal rat cardiac myocytes treated by phenylephrine were exposed to miR-133a adenovirus, and the changes in cell area was measured; the expression levels of miR-133a and Acta1, Actc1, Actb, Myh6, Myh7, and BNP mRNAs were detected by quantitative RT-PCR. Results Phenylephrine treatment increased the area of cardiomyocytes by more than 3 folds and significantly enhanced the expression levels of Acta1, Actc1, Actb, Myh6, Myh7 and BNP mRNAs. All these changes were obviously reverse by miR-133a treatment. Conclusion miR-133a is an important regulator of phenylephrine-induced cardiomyocyte hypertrophy and negatively regulates this process.
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