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Inhibition of the Semaphorin 4D-Plexin-B1 axis prevents calcification in vascular smooth muscle cells
Hyun-Joo Park1 (Post Doc.), Yeon Kim1 (Research worker), Mi-Kyoung Kim1 (Research worker), Hyung Joon Kim1 (Professor), Soo-Kyung Bae1 (Professor), Moon-Kyoung Bae1,* (Professor)
1School of Dentistry, Pusan National University
Vascular calcification is common in cardiovascular diseases including atherosclerosis, and is associated with an increased risk of pathological events and mortality. Some semaphorin family members play an important role in atherosclerosis. In the present study, we show that Semaphoring 4D/Sema4D and its Plexin-B1 receptor were significantly upregulated in calcified aorta of a rat chronic kidney disease model. Significantly higher Sema4D and Plexin-B1 expression was also observed during inorganic phosphate-induced calcification of vascular smooth muscle cells. Knockdown of Sema4D or Plexin-B1 genes attenuated both the phosphate-induced osteogenic phenotype of vascular smooth muscle cells, through regulation of SMAD1/5 signaling, as well as apoptosis of vascular smooth muscle cells, through modulation of the Gas6/Axl/Akt survival pathway. Taken together, our results offer new insights on the role of Sema4D and Plexin-B1 as potential therapeutic targets against vascular calcification.
Abstract, Accepted Manuscript(in press) [Submitted on October 20, 2022, Accepted on November 26, 2022]
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