The role of yeast-derived β-glucan in angiogenesis has not been elucidated because there have been few specific studies on its clinical and physiological significance. Therefore, this study investigated the correlation between β-glucan and histone deacetylase 5 (HDAC5) in human umbilical vein endothelial cells (HUVECs), revealing the role of β-glucan in angiogenesis. We confirmed that HDAC5 was phosphorylated by β-glucan stimulation and released from the nucleus to the cytoplasm. Furthermore, we found that β-glucan-stimulated HDAC5 translocation mediates the transcriptional activation of MEF2. As a result, the expression of KLF2, EGR2, and NR4A2, whose expression is MEF2-dependent and involved in angiogenesis, increased. Thus, we showed the activity of β-glucan in angiogenesis through in vitro and ex vivo assays including cell migration, tube formation, and aortic ring analyses. Specifically, application of an HDAC5 inhibitor repressed MEF2 transcriptional activation in both in vitro and ex vivo angiogenesis. HDAC5 inhibitor LMK235 inhibited the proangiogenic activity of beta-glucan, suggesting that β-glucan induces angiogenesis through HDAC5.

These findings suggest that HDAC5 is essential for angiogenesis, and that β-glucan induces angiogenesis. In conclusion, this study demonstrates that β-glucan induces angiogenesis through HDAC5. It also suggests that β-glucan has potential value as a novel therapeutic agent for modulating angiogenesis.The major hurdles for cancer therapy include controlling tumor growth and metastasis. Herein, we developed a novel platelet-derived growth factor receptor-β (PDGFR-β)-recognizing cyclic peptide (PDGFB)-conjugated copper-gadolinium oxide (CGO) nanocluster (PDGFB-CGO) to suppress tumor growth and metastasis via copper overload-mediated apoptosis and anti-angiogenesis. The developed PDGFB-CGO showed not only ultra-strong Fenton-catalytic activity and PT performance but also excellent T1 contrast ability. It effectively recognized the tumor tissue, thereby significantly improving its tumor-specific delivery and upon laser irradiation, quickly ablated tumor cells contributing to PTT. In addition, PDGFB-CGO quickly produced abundance of highly active Cu(I) which catalyzed endogenous hydrogen peroxide (H2O2) into hydroxyl radical (·OH), achieving ultra-high cancer CDT efficiency. In addition, the influx of Cu(I) broke copper homeostasis, thereby suppressing epithelial-mesenchymal transition (EMT) and tumor angiogenesis. This process restricted cell migration and invasion, which dramatically blocked cancer metastasis. In addition, the systemic delivery of PDGFB-CGO significantly enhanced the MRI signal in the tumor, which would be beneficial for the accurate diagnosis of cancer. Thus, this work provides a promising strategy to develop advanced biomaterials for efficient theranostic applications in cancer.

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Mishita
Jornal co-ordinator
Journal of Heart and Cardiovascular Research