The expression analysis of nanog in the developing rat myocardial tissues.

OBJECTIVES: To investigate the expression dynamic of nanog gene in the development of rat myocardial tissues. METHODS: SD rats were studied at 5 time points before and after birth. The techniques of immunohistochemistry, immunofluorescence, western blotting and RT-PCR were used to investigate the expression of nanog gene in the rat myocardial tissues at different embryonic (E) and postnatal (P) stages, and image analysis system was used for the quantitative analysis. RESULTS: The immunohistochemistry, immunofluorescence and western blotting analyses have shown that expression of nanog protein was highest in the rat myocardial tissues at E18, then it gradually declined at postnatal stages (P<0.05), and became nearly undetectable in most myocardial tissues at P30 with very few remaining nanog-positive cells. RT-PCR result indicated that the expression of nanog gene was strong at E18, but gradually decreased from E18 to P30. CONCLUSION: The mRNA transcription and protein translation of nanog gene in the rat heart gradually decreased with every consecutive growth stage. This indicates that nanog gene has potential regulatory functions in the differentiation of myocardial cells during rat development.

[Corrigendum] Overexpression of the chimeric plasmin-resistant VEGF165/VEGF183 (132-158) protein in murine breast cancer induces distinct vascular patterning adjacent to tumors and retarded tumor growth.

After the publication of the article, the authors noted that they had made an error regarding certain facts in their manuscript: In the abstract VEGF192 (132-158) should be changed to VEGF183 (132-158) (Page 1, Line 2). In addition, width should be changed to width2 (Page 3, Line 50). The authors regret these errors. [the original article was published in the Molecular Medicine Reports 11: 1483-1489, 2015 DOI: 10.3892/mmr.2014.2866]

Overexpression of the chimeric plasmin-resistant VEGF165/VEGF183 (132-158) protein in murine breast cancer induces distinct vascular patterning adjacent to tumors and retarded tumor growth.

A chimeric plasmin­resistant vascular endothelial growth factor (VEGF)165/VEGF183 (132-158) protein, named as VEGF183 (according to the nomenclature of VEGF), designed by a previous study, was demonstrated to have an enhanced affinity for the extracellular matrix (ECM) amongst other bioactivities. However, it is now accepted that mutant VEGFs frequently demonstrate different angiogenic activities and produce different vascular patterning from the parental molecule. The present study hypothesized that VEGF183, due to its enhanced binding affinity to the ECM, would exhibit a different angiogenic activity and produce a different vascular patterning compared to those of VEGF165. Murine breast cancer EMT­6 cells were manipulated to stably overexpress VEGF165 or VEGF183. These cells were then inoculated intradermally into BALB/c mice in order to monitor the formation of vascular patterning in skin proximal to tumors. In vivo angiogenesis experiments revealed that overexpression of VEGF183 in murine breast cancer cells resulted in irregular, disorganized and dense vascular patterning as well as induced a significant inhibition of tumor growth compared with that of VEGF165. In addition, allograft tumor immunochemical assays of VEGF183­overexpressing tumors demonstrated significantly lower vascular densities than those of VEGF165­overexpressing tumors; however, VEGF183 tumors had a significantly enlarged vascular caliber. Conversely, cell wound healing experiments revealed that VEGF183­overexpressing EMT­6 cells had significantly decreased migration rates compared with those of VEGF165­overexpressing EMT­6 cells. In conclusion, the results of the present study supported the hypothesis that the altered ECM affinity of VEGF induced structural alterations to vasculature. In addition, these results provided a novel insight into VEGF design and indirect evidence for the function of exon 8 in VEGF. [Corrected]

Effect of 1-octyl-3-methylimidazolium chloride on cell replication and membrane permeability of Escherichia coli DH5α.

Ionic liquids (ILs) have elicited attention due to their unique properties. ILs may pose environmental risks to aquatic ecosystems once released into water during generation and application. Therefore, the toxic and antimicrobial properties of ILs should be analysed. This study aims to evaluate the cytotoxicity of 1-octyl-3-methylimidazolium chloride ([C8mim] [Cl]) on Escherichia coli DH5α by MTT (3-[4,5-dimethylthiazol-2yl]-2,5 diphenyl tetrazolium bromide) assay, and to determine the effect of [C8mim] [Cl] on the replication and membrane permeability of E. coli DH5α. The results showed that [C8mim] [Cl] decreased cell viability and inhibited bacterial cell replication. [C8mim] [Cl] increased protein and nucleic acid contents in the extracellular fluid, damaged the cell membrane, and increased membrane permeability. The increase of cell membrane permeability induced by [C8mim] [Cl] could be the cause of decreased cell viability and replication.

Expression of N-cadherin proteins in myocardial hypertrophy in rats.

The aim of the present study was to examine the expression of N-cadherin in the myocardial tissues of isoproterenol-induced myocardial hypertrophy in rats. In addition, the present study provided morphological data to investigate the signal transduction mechanisms of myocardial hypertrophy and reverse myocardial hypertrophy. A myocardial hypertrophy model was established by subcutaneously injecting isoprenaline into healthy adult Sprague-Dawley rats. The myocardial tissue was collected, embedded in conventional paraffin, sectioned and stained with hematoxylin and the pathological changes were observed. The expression and distribution of N-cadherin were detected by immunohistochemistry (IHC) and the changes in mRNA expression of N-cadherin in the myocardial tissues of rats were detected by reverse transcription polymerase chain reaction. Image analysis software was used to quantitatively analyze the expression of N-cadherin. The IHC and immunofluorescence results showed that there was no statistically significant difference between the experimental and control groups in the positive expression of N-cadherin. Furthermore, mRNA expression of N-cadherin, in the myocardial tissues of rats, was consistent with the IHC and immunofluorescence results. Thus, N-cadherin may have a significant function in the occurrence and development of myocardial hypertrophy.

Expressions of CD11a, CD11b, and CD11c integrin proteins in rats with myocardial hypertrophy.

OBJECTIVES: To examine the expressions of CD11a, CD11b, and CD11c integrins in the myocardial tissues of rats with isoproterenol-induced myocardial hypertrophy. This study also provided morphological data to investigate the signal transduction mechanisms of myocardial hypertrophy and reverse it. MATERIALS AND METHODS: A myocardial hypertrophy model was established by subcutaneously injecting isoprenaline in healthy adult Sprague-Dawley rats. Myocardial tissues were obtained, embedded in conventional paraffin, sectioned, and stained with hematoxylin. Pathological changes in myocardial tissues were then observed. The expressions and distributions of CD11a, CD11b, and CD11c integrins were detected by immunohistochemistry. Changes in the mRNA expressions of CD11a, CD11b, and CD11c in the myocardial tissues of rats were detected by RT-PCR. Image analysis software was used to determine the expressions of CD11a, CD11b, and CD11c integrins quantitatively. RESULTS: Immunohistochemical results showed that the positive expressions of CD11a, CD11b, and CD11c integrins increased significantly in the experimental group compared with those in the control group. The mRNA expressions of CD11a, CD11b, and CD11c in the myocardial tissues of rats were consistent with the immunohistochemical results. CONCLUSION: The increase in the protein expressions of CD11a, CD11b, and CD11c integrins may have an important role in the occurrence and development of myocardial hypertrophy.

Implantation with new three-dimensional porous titanium web for treatment of parietal bone defect in rabbit.

Titanium net (meshes) with excellent mechanical properties can promote bone compatibility and has been used as a repairing material for bone defects in clinical settings. In the present study, using spiral computed tomography (CT) and histomorphological techniques, we investigated the effect of a novel kind of titanium web with a three-dimensional (3D) porous structure on bone formation in rabbit skull (os parietal) defect. The images from the spiral CT scan demonstrate that the titanium web is completely fused with the surrounding bone tissue, even at the first month after implantation. The histomorphological findings show that different cells and tissues, including osseous tissue, connective tissue, and adipose cells, can easily grow into the 3D scaffold meshes of the titanium web, even in the center of the web and combine together as a whole body, suggesting that the titanium web possesses a very good biocompatibility, which is beneficial to the growth of bone tissue and promotes healing of the defected rabbit skull.