Fig 1: PFN2 involved molecular signaling pathway. (A) PFN2 expression level in HUVECs treated with PI3K inhibitor and PI3K expression level in OE and KD, n = 3, normalized to control. (B) PFN2 expression level in HUVECs treated with ERK inhibitor and ERK expression level in OE and KD, n = 3, normalized to control. (C) ERK and PFN2 expression levels in the heart tissue of MI mice treated with different exosomes, n = 3, normalized to control. (D) Statistical result of (C). *p < 0.05, Student's t-test and one-way ANOVA (Tukey).
Fig 2: PFN2 protects ECs after LPS treatment. (A) PFN2 and Alix expression levels in LPS-treated EC exosomes, n = 3, normalized to control. (B) PCNA expression levels of ECs under LPS stimulus after treatment with various exosomes, n = 3, normalized to control. (C) Viability of ECs under LPS stimulation after treatment with various exosomes. n = 8. *p < 0.05, one-way ANOVA (Tukey).
Fig 3: Exosomal PFN2 enhances the proliferation ability of ECs and OE-exo treated zebrafish showed significantly increased vessel number than exo and control. (A) The exosomes secreted from ECs were identified by electron microscopy. (B) PFN2 expression in exosomes (n = 3, the expression levels were normalized to control). (C) Exosomes could be internalized by ECs. (D) PFN2 and PCNA expression levels in CTL, exosomes from normal ECs (exo), PFN2-overexpressing ECs (OE-exo), and PFN2 knockdown ECs (KD-exo), n = 3, and the expression levels were normalized to control. (E) OE-exo-treated zebrafish showed significantly increased vessel number than exo and control. Exo, exosomes from normal ECs; OE-exo, exosomes from PFN2-overexpressing ECs; CTL, PBS as control. *p < 0.05, one-way ANOVA (Tukey).
Fig 4: PFN2-overexpressing ECs (OE-exo) treated MI mice showed improvement in infarction volume, cardiac function and motor ability, and PFN2/ OE-exo significantly enhanced EC proliferation, migration, tube formation ability and angiogenesis.
Fig 5: PFN2 promotes proliferation and migration of ECs, as well as tube formation and reaches the maximum level in 10-day embryo. (A) The mRNA levels of PFN2 and VEGFA at different developmental stages of gerbils (n = 15) embryo (prenatal), brain and heart (postnatal). (B) PFN2 significantly promoted proliferation of HUVECs (n = 3) and RBMECs (n = 3), as well as showed a positive effect on migration of HUVECs (n = 3) and RBMECs (n = 3). (C) The tube length in PFN2-overexpressing ECs (OE) was significantly increased than that in blank CTL and PFN2 knockdown ECs (KD), n = 3. *p < 0.05, one-way ANOVA and repeated-measures ANOVA (Tukey).
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