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To observe the expression of MMP-2 and MMP-9 and of the FAK/PI3K/Akt signaling pathway in HSK. Fifty BALB/c mice were infected to establish the model and killed on days 0, 2, 7, 14, and 28. The cornea samples were prepared, respectively. Slit lamp examination, immunofluorescence staining, reverse transcription PCR, and Western blot were used to detect the index. After HSV-1 infection, different degrees of epithelial or stromal damage and corneal opacity were observed. Immunofluorescence staining showed that the expressions of MMP-2 and MMP-9 at different levels of corneal tissue were observed on the 0d, 2d, 7d, 14d, and 28d. Compared with 0d, the relative expression levels of MMP-2 and MMP-9 mRNA at 2d, 7d, 14d, and 28d were significantly increased (all P< 0.05). Compared with 14d, the relative expression of MMP-2 and MMP-9 mRNA decreased on the 2d, 7d, and 28d (all P< 0.05). Western blot showed that the protein expressions of p-FAK, p-PI3K, p-Akt, MMP-2, and MMP-9 at 2d, 14d, and 28d were all significantly higher than 0d (all P< 0.05). At 14 d, the expressions of p-FAK, p-PI3K, p-Akt, and MMP-2 were significantly higher than those at 2d, 7d, and 28d (all P< 0.05). The protein expression of FAK, PI3K, and Akt in corneal of mice in each time period had no significant (all P> 0.05). These data suggest that FAK/PI3K/Akt signaling pathway and MMP-2 and MMP-9 may be involved in the development of HSK. [ABSTRACT FROM AUTHOR]

The pathogenesis of osteoporosis is considered extremely intricate. Osteoblast differentiation and angiogenesis can greatly affect bone development and formation, given their coupling role in these processes. Exosome-mediated miRNA regulates cellular senescence, proliferation, and differentiation. However, whether senescent osteoblasts can regulate the senescence of vascular endothelial cell by miRNA through exosomal pathway remains unclear. In this study, senescent osteoblasts could regulate endothelial cell function, promote cell senescence and apoptosis, and decrease cell proliferation via exosomal pathway. miR-139-5p showed high expression in senescent osteoblasts and their exosomes. After senescent osteoblast-derived exosome treatment, miR-139-5p was also upregulated in endothelial cells. Furthermore, transfection of miR-139-5p mimic promoted the senescence and apoptosis of vascular endothelial cells and inhibited their proliferation and migration, whereas transfection of miR-139-5p inhibitor rescued the effect of D-galactose. Using double luciferase assay, TBX1 was confirmed to be a direct target gene of miR-139-5p. In conclusion, senescent osteoblast-derived exosome-mediated miR-139-5p regulated endothelial cell function via exosomal pathway. Our study revealed the role of osteoblast-derived exosomes in the bone environment during aging, providing a clue for inventing a new target therapy. [ABSTRACT FROM AUTHOR]