RESUMO
The formation of new blood vessels and homeostasis are important to ensure the normal physiological activities of cells. The blood vessel formation is strictly regulated by many factors for the stabilities and functions of internal environment and immune systems. Endoglin (ENG), a type I transmembrane glycoprotein mainly expressed on endothelial cells, plays an important role in angiogenesis and homeostasis by acting as a co⁃receptor of transforming growth factor β family. With more and more proteins interacting with ENG have been uncovered, such as matrix metalloproteinase 14 (MMP14), integrin, leucine⁃rich alpha⁃2⁃glycoprotein⁃1 (LRG1) and GAIP interacting protein C⁃terminus (GIPC), many new research progresses in molecular mechanism of ENG have been developing recently. However, the exquisite regulatory network between these proteins remains to be explored and combed. Understanding the characteristics of these proteins, their influences in signal transduction and their contribution to angiogenesis under patho⁃physiological conditions will be helpful for the development of novel therapeutics. This review summarized the interactions between ENG and TGF⁃β or non⁃TGF⁃β family associated proteins in regulating angiogenesis. We also proposed some suggestions for future study on ENG allowing us to better understand the mechanisms of ENG⁃associated diseases.
RESUMO
Objective To observe the expression changes of nuclear factor-erythroid derived 2-related factors （Nrf2） in different cells at different time points after human cerebral cortex contusion, and to discuss its application in brain wound age estimation. Methods Thirty-six human brain tissues were selected, of which 6 were for control and 30 were cortical contusion at different time points post-injury, which were divided into 0-1 h, 3-6 h, 1-3 d, 5-7 d, and 10-14 d post-injury groups, with 6 cases in each group. Based on paraffin embedded sections, HE staining was used to observe the morphological changes post-injury, and double immunofluorescence staining was used to detect the expression of Nrf2 in neurons, astrocytes, and microglia. The number of positive cells was counted and statistical analysis was made. Results The number of neurons decreased 1-3 d post-injury. The expression of Nrf2 cells in neurons increased after injury, and the rate of positive cells peaked at 1-3 d post-injury. Glial cells were activated 1-3 d post-injury, and the activation peaked at 5-7 d post-injury. The cerebromalacia began to form at 10-14 d post-injury. Glial fibrillary acidic protein （GFAP） positive cells in mice increased gradually after injury and peaked at 5-7 d post-injury, while the proportion of Nrf2 in GFAP positive cells was relatively stable. After injury, ionized calcium-binding adapter molecule 1 （IBA1） positive cells increased and activated gradually. The expression proportion of Nrf2 in IBA1 positive cells increased gradually, reached its peak at 5-7 d post-injury, and then decreased. Conclusion The expression of Nrf2 in different cells involves in the biological function of different cells post-injury, and the dynamic expression of single cells has a time-dependent pattern. This may provide a new reference index for the wound age estimation of brain contusion in human.