Overexpression of Twist1 in vascular endothelial cells promotes pathological retinal angiogenesis in mice.

Retinal angiogenesis is a critical process for normal retinal function. However, uncontrolled angiogenesis can lead to pathological neovascularization (NV), which is closely related to most irreversible blindness-causing retinal diseases. Understanding the molecular basis behind pathological NV is important for the treatment of related diseases. Twist-related protein 1 (TWIST1) is a well-known transcription factor and principal inducer of epithelial-mesenchymal transition (EMT) in many human cancers. Our previous study showed that Twist1 expression is elevated in pathological retinal NV. To date, however, the role of TWIST1 in retinal pathological angiogenesis remains to be elucidated. To study the role of TWIST1 in pathological retinal NV and identify specific molecular targets for antagonizing pathological NV, we generated an inducible vascular endothelial cell (EC)-specific Twist1 transgenic mouse model ( Tg-Twist1 iEC+ ). Whole-mount retinas from Tg-Twist1 iEC+ mice showed retarded vascular progression and increased vascular density in the front end of the growing retinal vasculature, as well as aneurysm-like pathological retinal NV. Furthermore, overexpression of Twist1 in the ECs promoted cell proliferation but disturbed cell polarity, thus leading to uncontrolled retinal angiogenesis. TWIST1 promoted pathological NV by activating the Wnt/ß-catenin signaling pathway and inducing the expression of NV formation-related genes, thereby acting as a 'valve' in the regulation of pathological angiogenesis. This study identified the critical role of TWIST1 in retinal pathological NV, thus providing a potential therapeutic target for pathological NV.

Exploration and Practice of the Mode of "3+X" in the Cultivation of Scientific Research and Innovation Ability of Medical Students / 中国生物化学与分子生物学报

For a long time, the cultivation of medical students’ scientific research and innovation abilitymainly depends on scattered extracurricular scientific research activities. With limited students, unsystematic teaching and inadequate administrative guarantee, it often results in obvious weakness andinefficiency. Since 2002, the Biochemistry and Molecular Biology teaching team in Shantou UniversityMedical College has been working on a “3+X” model to nurture the scientific research and innovationability of medical students. Guided by the concepts of complementary development of science andeducation, student-centeredness, and Problem-based Learning, a model is established based on the‘HEART” professionalism courses and the academy culture specific to Shantou University. We also takefull advantage of the first-tier disciplines of biology, basic medicine and clinical medicine in ShantouUniversity and collaborate with other professional teaching teams. It is conceptualized in a framework thatembraces the comprehensive connotation of scientific research and innovation ability and adopts a corecurriculum system that runs through the 5-year medical undergraduate education. In this model, " 3" means " whole-person training", " whole-process training" and " omni-directional training" for medicalstudents; " X" refers to several confirmatory dimensions of the operational effectiveness of the " 3+X" model, including organizing medical students to participate in various forms of national college students’ innovative experimental research competitions, international college students’ academic seminars, writingand publishing academic papers by medical undergraduates as the first author, etc. The model proves tobe effective in cultivating the scientific research and innovation ability of medical students, hence settinga good example to solve the current problems in the cultivation of medical students’ scientific researchand innovation ability.

Mechanisms of response to pH shock in microbial fermentation.

The following review highlights pH shock, a novel environmental factor, as a tool for the improvement of fermentation production. The aim of this review is to introduce some recent original studies on the enhancement of microbial fermentation production by pH shock. Another purpose of this review is to improve the understanding of the processes that underlie physiological and genetic differences, which will facilitate future research on the improvement of fermentation production and reveal the associated molecular mechanisms. This understanding will simultaneously promote the application of this strategy to other microbial fermentation systems. Furthermore, improvement of the cellular tolerance of genetically engineered bacteria can also be a new field of research in the future to enhance fermentation production.

Role of transforming growth factor ß1 in the inhibition of gastric cancer cell proliferation by melatonin in vitro and in vivo.

Transforming growth factor ß (TGF­ß) is a polypeptide growth factor with various biological activities, and is widely distributed in various tissues. In mammals, TGF­ß has three isoforms: TGF­ß1, 2, and 3, of which TGF­ß1 is most abundant in the TGF­ß family. TGF­ß1 is closely related to the occurrence and development of tumors. A large number of previous studies have shown that melatonin can inhibit a variety of malignancies. Thus, the aim of the present study was to investigate the role of TGF­ß1 in the melatonin­mediated inhibition of the proliferation of gastric cancer cells in vitro and in vivo. TGF­ß1 cytokine stimulation, anti­TGF­ß1 neutralizing antibody blocking, siRNA TGF­ß1 and other means were utilized to explore the role of TGF­ß1 during the course of anti­gastric cancer by melatonin. The results showed that melatonin upregulated the expression of TGF­ß1 in tumor tissues during the process of inhibiting gastric cancer tumor growth in vivo. Melatonin inhibited the proliferation of gastric cancer cells in vitro, accompanied by increased expression of TGF­ß1 in a time­dependent manner. siRNA­mediated silencing of TGF­ß1 and anti­TGF­ß1 neutralizing antibody completely blocked the TGF­ß1 pathway, which significantly antagonized the melatonin­mediated inhibition of the growth and proliferation of gastric cancer cells, and promoted G1 phase to S phase transformation of MFC cells. Our findings suggest that TGF­ß1 is involved in the regulation of the proliferation of tumor cells. One of the ways in which melatonin inhibits the proliferation of gastric cancer cells is dependent on the TGF­ß1 signaling pathway.