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Gemigliptin Inhibits Interleukin-1β–Induced Endothelial-Mesenchymal Transition via Canonical-Bone Morphogenetic Protein Pathway by Oak-Kee Hong; Seong-Su Lee; Soon Jib Yoo; Min-Kyung Lee; Mee-Kyoung Kim; Ki-Hyun Baek; Ki-Ho Song; Hyuk-Sang Kwon is a Medicine article available to read on EtoBox.
What is Gemigliptin Inhibits Interleukin-1β–Induced Endothelial-Mesenchymal Transition via Canonical-Bone Morphogenetic Protein Pathway about?
## Background Endothelial-to-mesenchymal transition (EndMT) contributes to inflammatory conditions inducing conversion of endothelial cells (ECs) into activated fibroblasts, promoting fibrotic diseases. Pro-inflammatory cytokine is the most potent inducer of EndMT. We investigated inhibition of interleukin-1β (IL-1β)-induced EndMT by gemigliptin, a dipeptidyl peptidase-IV inhibitor. ## Methods We exposed human umbilical vein endothelial cells (HUVECs) to 10 ng/mL IL-1β/20 μM gemigliptin and analyzed the expression of endothelial, smooth muscle, mesenchymal, and osteoblastic markers, bone morphogenetic protein (BMP), Smad, and non-Smad signaling pathway proteins. ## Results Morphological changes showed gemigliptin blocked IL-1β-induced EndMT, upregulated EC markers, and downregulated smooth muscle and mesenchymal markers. IL-1β activation of HUVECs is initiated by the BMP/Smad and non-smad BMP signaling pathways. Gemigliptin inhibited IL-1β induction of BMP2 and 7, activin receptor type IA, BMP receptor type IA, and BMP receptor type II. Reversal of IL-1β-mediated inhibition of BMP-induced Smad1/5/8, Smad2, and Smad3 phosphorylation by gemigliptin suggests involvement of the Smad pa
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- Author
- Oak-Kee Hong; Seong-Su Lee; Soon Jib Yoo; Min-Kyung Lee; Mee-Kyoung Kim; Ki-Hyun Baek; Ki-Ho Song; Hyuk-Sang Kwon
- Publisher
- Korean Endocrine Society
- Published
- 2020
- Language
- EN
- Field
- Medicine (Health Sciences)