RESUMO
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.
Assuntos
Coração/crescimento & desenvolvimento , Miocárdio/metabolismo , Fatores de Transcrição/biossíntese , Animais , Diferenciação Celular/genética , Desenvolvimento Embrionário , Regulação da Expressão Gênica no Desenvolvimento , Coração/embriologia , Proteína Homeobox Nanog , RNA Mensageiro/biossíntese , Ratos , Fatores de Transcrição/genéticaRESUMO
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]
RESUMO
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]