Angiogenesis within the wound site is a necessary prerequisite for skin tissue regeneration during the process of wound healing. Skin vessels provide adequate nutrients and soluble bioactive factors to the wounded area and remove metabolites. In this study, we prepared a double-cross-linked hydrogel based on GelMA and PVAMA to load Myeloid-derived growth factor (MYDGF). Additionally, we evaluated the healing-promoting effect of the hydrogel using a full-thickness skin injury mouse model. Compared with the control and MYDGF-free hydrogels, the MYDGF-loaded hydrogels significantly increased the percentage of wound healing and promoted granulation tissue proliferation and epidermization. In vitro experiments have shown that MYDGF may augment the migration and angiogenesis of human umbilical vein endothelial cells (HUVECs) by upregulating the expression of phosphorylated ERK and phosphorylated P38. These findings indicate that MYDGF-loaded hydrogels promote wound healing by accelerating angiogenesis.
Retinal neovascularization (RNV) is a potential vision-threatening process characterized by the abnormal growth of retinal vessels. Despite its clinical prevalence, the precise mechanisms governing RNV initiation and progression remain incompletely defined. Here we identify myeloid-derived growth factor (MYDGF) as a critical regulator of retinal vascular dynamics. Using single-cell RNA sequencing and human patient validation, we show that MYDGF is upregulated in retinal endothelial cells during proliferative diabetic retinopathy and mouse models of pathological neovascularization. In vitro, MYDGF promotes retinal endothelial cell proliferation, migration, and sprouting. In vivo, endothelial-specific MYDGF depletion inhibits both normal vascular development and pathological neovascularization in neonatal mice, and disrupting adult vascular homeostasis in male mice. MYDGF drives angiogenesis by activating the Akt-mTOR cascade through the Gαi1/3-Gab1 signaling complex; genetic depleting or mutation these components suppress MYDGF-induced Akt-mTOR activation and angiogenic responses. Together, MYDGF promotes retinal angiogenesis and maintains vascular homeostasis via the Gαi1/3-Gab1-Akt-mTOR signaling axis.
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