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While adiponectin (APN) was known to significantly abolish the diabetic endothelial inflammatory response, the specific mechanisms have yet to be elucidated. Aortic vascular tissues from mice fed normal and high-fat diets (HFD) were analyzed by transcriptome analysis. GO functional annotation showed that APN inhibited vascular endothelial inflammation in an APPL1-dependent manner. We confirmed that activation of the Wnt/β-catenin signaling plays a key role in APN-mediated anti-inflammation. Mechanistically, APN promoted APPL1/reptin complex formation and β-catenin nuclear translocation. Simultaneously, we identified APN promoted the expression of CD44 by activating TCF/LEF in an APPL1-mediated manner. Clinically, the serum levels of APN and CD44 were decreased in diabetes; the levels of these two proteins were positively correlated. Functionally, treatment with CD44 C-terminal polypeptides protected diabetes-induced vascular endothelial inflammation in vivo. Collectively, we provided a roadmap for APN-inhibited vascular inflammatory effects and CD44 might represent potential targets against the diabetic endothelial inflammatory effect.

The changes of biomechanical properties, especially the elasticity of the ocular tissues, are closely related to some ophthalmic diseases. Currently, the ophthalmic optical coherence elastography (OCE) systems are dedicated either to the anterior segment or to the retina. The elasticity measurements of the whole eye remain challenging. Here we demonstrated an acoustic radiation force optical coherence elastography (ARF-OCE) method to quantify the elasticity of the cornea and the retina. The experiment results show that the Young’s moduli of the cornea and the retina were 16.66 ± 6.51 kPa and 207.96 ± 4.75 kPa, respectively. Our method can measure the elasticity of the anterior segment and the posterior segment, and provides a powerful tool to enhance ophthalmology research.