Akt1-dependent expression of angiopoietin 1 and 2 in vascular smooth muscle cells leads to vascular stabilization

Ha Jung Min; Jin Seo Yeon; Lee Hye Sun; Kum Hye Jin; Vafaeinik Farzaneh; Ha Hong Koo; Song Sang Heon; Kim Chi Dae; Bae Sun Sik

doi:10.1038/s12276-022-00819-8

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저자정보: Ha Jung Min (Pusan National University School of Medicine) Jin Seo Yeon (Pusan National University School of Medicine) Lee Hye Sun (Pusan National University School of Medicine) Kum Hye Jin (Pusan National University School of Medicine) Vafaeinik Farzaneh (Pusan National University School of Medicine) Ha Hong Koo (Pusan National University School of Medicine) Song Sang Heon (Pusan National University School of Medicine) Kim Chi Dae (Pusan National University School of Medicine) Bae Sun Sik (Pusan National University School of Medicine)

저널정보: 대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제54권

발행연도: 2022.8

수록면: 1 - 13 (13page)

DOI: 10.1038/s12276-022-00819-8

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Retinal angiogenesis was delayed in VSMC-specific Akt1-deficient mice (Akt1?SMC) but not in Akt2?SMC mice. The proliferation of ECs, recruitment of pericytes, and coverage of VSMCs to the endothelium were defective in Akt1?SMC. The silencing of Akt1 in VSMCs led to the downregulation of angiopoietin 1 (Ang1) and the upregulation of Ang2. The activation of Notch3 in VSMCs was significantly reduced in the retinas of Akt1?SMC mice. Silencing Akt1 suppressed the activation of Notch3. Moreover, the silencing of Notch3 downregulated Ang1, whereas the overexpression of Notch3 intracellular domain (NICD3) enhanced Ang1 expression. The nuclear localization and transcriptional activity of yes-associated protein (YAP) were affected by the expression level of Akt1. Silencing YAP downregulated Ang2 expression, whereas overexpression of YAP showed the opposite results. Ang1 antibody and Ang2 suppressed endothelial sprouting of wild-type aortic tissues, whereas the Ang2 antibody and Ang1 facilitated the endothelial sprouting of aortic tissues from Akt1?SMC mice. Finally, severe hemorrhage was observed in Akt1?SMC mice, which was further facilitated under streptozotocin (STZ)-induced diabetic conditions. Therefore, the Akt1-Notch3/YAP-Ang1/2 signaling cascade in VSMCs might play an essential role in the paracrine regulation of endothelial function.

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