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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: closed (26 July 2024) | Viewed by 3996

Special Issue Editor

Prof. Dr. Alexandre Mironov

E-Mail Website
Guest Editor
Istituto FIRC di Oncologia Molecolare (IFOM-IEO Campus), Via Adamello 16, 20139 Milan, Italy
Interests: intracellular transport Golgi complex; endothelium, atherosclerosis; electron microscopy
Special Issues, Collections and Topics in MDPI journals

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

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Published Papers (4 papers)

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Research

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16 pages, 3087 KiB  
Article
During Postnatal Ontogenesis, the Development of a Microvascular Bed in an Intestinal Villus Depends on Intussusceptive Angiogenesis
by Anna V. Zaytseva, Natalia R. Karelina, Eugeny V. Bedyaev, Pavel S. Vavilov, Irina S. Sesorova and Alexander A. Mironov
Int. J. Mol. Sci. 2024, 25(19), 10322; https://doi.org/10.3390/ijms251910322 - 25 Sep 2024
Viewed by 483
Abstract
The mechanisms responsible for the growth and development of vascular beds in intestinal villi during postnatal ontogenesis remain enigmatic. For instance, according to the current consensus, in the sprouting type of angiogenesis, there is no blood flow in the rising capillary sprout. However, [...] Read more.
The mechanisms responsible for the growth and development of vascular beds in intestinal villi during postnatal ontogenesis remain enigmatic. For instance, according to the current consensus, in the sprouting type of angiogenesis, there is no blood flow in the rising capillary sprout. However, it is known that biomechanical forces resulting from blood flow play a key role in these processes. Here, we present evidence for the existence of the intussusception type of angiogenesis during the postnatal development of micro-vessel patterns in the intestinal villi of rats. This process is based on the high-level flattening of blood capillaries on the flat surfaces of intestinal villi, contacts among the opposite apical plasma membrane of endothelial cells in the area of inter-endothelial contacts, or the formation of bridges composed of blood leucocytes or local microthrombi. We identified factors that, in our opinion, ensure the splitting of the capillary lumen and the formation of two parallel vessels. These phenomena are in agreement with previously described features of intussusception angiogenesis. Full article
(This article belongs to the Special Issue Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions)
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17 pages, 4948 KiB  
Article
Equine Endothelial Cells Show Pro-Angiogenic Behaviours in Response to Fibroblast Growth Factor 2 but Not Vascular Endothelial Growth Factor A
by Elizabeth J. T. Finding, Ashton Faulkner, Lilly Nash and Caroline P. D. Wheeler-Jones
Int. J. Mol. Sci. 2024, 25(11), 6017; https://doi.org/10.3390/ijms25116017 - 30 May 2024
Cited by 2 | Viewed by 1046
Abstract
Understanding the factors which control endothelial cell (EC) function and angiogenesis is crucial for developing the horse as a disease model, but equine ECs remain poorly studied. In this study, we have optimised methods for the isolation and culture of equine aortic endothelial [...] Read more.
Understanding the factors which control endothelial cell (EC) function and angiogenesis is crucial for developing the horse as a disease model, but equine ECs remain poorly studied. In this study, we have optimised methods for the isolation and culture of equine aortic endothelial cells (EAoECs) and characterised their angiogenic functions in vitro. Mechanical dissociation, followed by magnetic purification using an anti-VE-cadherin antibody, resulted in EC-enriched cultures suitable for further study. Fibroblast growth factor 2 (FGF2) increased the EAoEC proliferation rate and stimulated scratch wound closure and tube formation by EAoECs on the extracellular matrix. Pharmacological inhibitors of FGF receptor 1 (FGFR1) (SU5402) or mitogen-activated protein kinase (MEK) (PD184352) blocked FGF2-induced extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and functional responses, suggesting that these are dependent on FGFR1/MEK-ERK signalling. In marked contrast, vascular endothelial growth factor-A (VEGF-A) had no effect on EAoEC proliferation, migration, or tubulogenesis and did not promote ERK1/2 phosphorylation, indicating a lack of sensitivity to this classical pro-angiogenic growth factor. Gene expression analysis showed that unlike human ECs, FGFR1 is expressed by EAoECs at a much higher level than both VEGF receptor (VEGFR)1 and VEGFR2. These results suggest a predominant role for FGF2 versus VEGF-A in controlling the angiogenic functions of equine ECs. Collectively, our novel data provide a sound basis for studying angiogenic processes in horses and lay the foundations for comparative studies of EC biology in horses versus humans. Full article
(This article belongs to the Special Issue Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions)
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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
Cited by 2 | Viewed by 1323
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
(This article belongs to the Special Issue Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions)
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Review

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18 pages, 1253 KiB  
Review
Responses of Endothelial Progenitor Cells to Chronic and Acute Physical Activity in Healthy Individuals
by Marta Tkacz, Katarzyna Zgutka, Patrycja Tomasiak and Maciej Tarnowski
Int. J. Mol. Sci. 2024, 25(11), 6085; https://doi.org/10.3390/ijms25116085 - 31 May 2024
Viewed by 638
Abstract
Endothelial progenitor cells (EPCs) are circulating cells of various origins that possess the capacity for renewing and regenerating the endothelial lining of blood vessels. During physical activity, in response to factors such as hypoxia, changes in osmotic pressure, and mechanical forces, endothelial cells [...] Read more.
Endothelial progenitor cells (EPCs) are circulating cells of various origins that possess the capacity for renewing and regenerating the endothelial lining of blood vessels. During physical activity, in response to factors such as hypoxia, changes in osmotic pressure, and mechanical forces, endothelial cells undergo intense physiological stress that results in endothelial damage. Circulating EPCs participate in blood vessel repair and vascular healing mainly through paracrine signalling. Furthermore, physical activity may play an important role in mobilising this important cell population. In this narrative review, we summarise the current knowledge on the biology of EPCs, including their characteristics, assessment, and mobilisation in response to both chronic and acute physical activity in healthy individuals. Full article
(This article belongs to the Special Issue Activation, Proliferation and Migration of Endothelial Cells under Normal and Pathological Conditions)
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