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Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 26 July 2024 | Viewed by 668

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Istituto FIRC di Oncologia Molecolare (IFOM-IEO Campus), Via Adamello 16, 20139 Milan, Italy
Interests: intracellular transport Golgi complex; endothelium, atherosclerosis; electron microscopy
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Special Issue Information

Dear Colleagues,

Vascular endothelium is found in almost all organs and tissues. Its role in understanding the mechanisms of various diseases is difficult to overestimate. This became especially clear after the COVID-19 epidemic, when, due to the similarity of the protein composition of the receptors of the ciliated cells of the airways and vascular endothelium, various, and often very severe, complications developed following the disease. It has long been known that the endothelium of elastic-type arteries is involved in the pathogenesis of atherosclerosis, and the endothelium of this and other parts of the vascular bed is involved in the pathogenesis of many other diseases. Knowledge of the mechanisms associated with damage to this endothelium and its subsequent repair is very important now. Although tremendous progress has been made recently in deciphering the molecular mechanisms of vascular endothelium functioning. Most of these discoveries were made in vitro. It is necessary to bring this knowledge to the tissue level. Additionally, rather little information is available on the role of itracell, ulat transport and endocytosis within endothelial cells. We would greatly appreciate all researchers who take the time to contribute to this Special Issue.

Prof. Dr. Alexandre Mironov
Guest Editor

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Keywords

  • endothelial cell
  • regeneration
  • angiogenesis
  • migration
  • molecular mechanism
  • intracellular transport
  • Golgi
  • signaling
  • transcription
  • miRNA
  • tumorigenesis
  • COVID

Published Papers (1 paper)

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Research

20 pages, 7084 KiB  
Article
BMPR2 Loss Activates AKT by Disrupting DLL4/NOTCH1 and PPARγ Signaling in Pulmonary Arterial Hypertension
by Keytam S. Awad, Shuibang Wang, Edward J. Dougherty, Ali Keshavarz, Cumhur Y. Demirkale, Zu Xi Yu, Latonia Miller, Jason M. Elinoff and Robert L. Danner
Int. J. Mol. Sci. 2024, 25(10), 5403; https://doi.org/10.3390/ijms25105403 - 15 May 2024
Viewed by 376
Abstract
Pulmonary arterial hypertension (PAH) is a progressive cardiopulmonary disease characterized by pathologic vascular remodeling of small pulmonary arteries. Endothelial dysfunction in advanced PAH is associated with proliferation, apoptosis resistance, and endothelial to mesenchymal transition (EndoMT) due to aberrant signaling. DLL4, a cell membrane [...] Read more.
Pulmonary arterial hypertension (PAH) is a progressive cardiopulmonary disease characterized by pathologic vascular remodeling of small pulmonary arteries. Endothelial dysfunction in advanced PAH is associated with proliferation, apoptosis resistance, and endothelial to mesenchymal transition (EndoMT) due to aberrant signaling. DLL4, a cell membrane associated NOTCH ligand, plays a pivotal role maintaining vascular integrity. Inhibition of DLL4 has been associated with the development of pulmonary hypertension, but the mechanism is incompletely understood. Here we report that BMPR2 silencing in pulmonary artery endothelial cells (PAECs) activated AKT and suppressed the expression of DLL4. Consistent with these in vitro findings, increased AKT activation and reduced DLL4 expression was found in the small pulmonary arteries of patients with PAH. Increased NOTCH1 activation through exogenous DLL4 blocked AKT activation, decreased proliferation and reversed EndoMT. Exogenous and overexpression of DLL4 induced BMPR2 and PPRE promoter activity, and BMPR2 and PPARG mRNA in idiopathic PAH (IPAH) ECs. PPARγ, a nuclear receptor associated with EC homeostasis, suppressed by BMPR2 loss was induced and activated by DLL4/NOTCH1 signaling in both BMPR2-silenced and IPAH ECs, reversing aberrant phenotypic changes, in part through AKT inhibition. Directly blocking AKT or restoring DLL4/NOTCH1/PPARγ signaling may be beneficial in preventing or reversing the pathologic vascular remodeling of PAH. Full article
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