scholarly journals The role of tissue inhibitors of metalloproteinases in microvascular endothelial cell barrier dysfunction during sepsis

2019 ◽  
Vol Volume 6 ◽  
pp. 1-12
Author(s):  
Devika P. Jayawardena ◽  
Nidhi P. Kulkarni ◽  
Sean E. Gill
Keyword(s):  
Endothelial Cell ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Microvascular Endothelial Cell ◽  
Barrier Dysfunction ◽  
Tissue Inhibitors ◽  
Microvascular Endothelial

scholarly journals mCRP triggers angiogenesis by inducing F3 transcription and TF signalling in microvascular endothelial cells

2017 ◽  
Vol 117 (02) ◽  
pp. 357-370 ◽  
Author(s):  
Esther Peña ◽  
Raquel de la Torre ◽  
Gemma Arderiu ◽  
Mark Slevin ◽  
Lina Badimon
Keyword(s):  
Endothelial Cell ◽  
Wound Repair ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial Cell ◽  
Angiogenic Effect ◽  
Supplementary Material ◽  
Microvascular Endothelial ◽  
Inflammatory Molecules ◽  
Slow Onset

SummaryInflammation contributes to vascular disease progression. However, the role of circulating inflammatory molecules on microvascular endothelial cell (mECs) is not fully elucidated. The aim of this study was to investigate the effects of the short pentraxin CRP on microvascular endothelial cell angiogenic function. Subcutaneously implanted collagen plugs seeded with human mECs exposed to monomeric CRP (mCRP) in mice showed formation of an extended network of microvessels both in the plug and the overlying skin tissue, while mECs exposure to pentameric native CRP (nCRP) induced a much milder effect. To understand the mechanisms behind this angiogenic effects, mECs were exposed to both CRP forms and cell migration, wound repair and tube-like formation were investigated. nCRP effects were moderate and of slow-onset whereas mCRP induced rapid, and highly significant effects. We investigated how circulating nCRP is transformed into mCRP by confocal microscopy and western blot. nCRP is transformed into mCRP on the mECs membranes in a time dependent fashion. This transformation is specific and in part receptor dependent, and the formed mCRP triggers F3 gene transcription and TF-protein expression in mECs to induce angiogenesis. F3-silenced mECs are unable to form angiotubes. In agreement, mCRP induced upregulation of the TF signalling pathway in mECs with downstream phosphorylation of AKT and activation of the transcription factor ETS1 leading to increased CCL2 release. The circulating pentraxin nCRP with little pro-angiogenic effect when dissociated into mCRP on the surface of mECs is able to trigger potent proangiogenic effects by inducing F3-gene upregulation and TF signalling.Supplementary Material to this article is available online at www.thrombosis-online.com.

scholarly journals The Role of Brain Microvascular Endothelial Cell and Blood-Brain Barrier Dysfunction in Schizophrenia

2020 ◽  
Vol 6 (1-2) ◽  
pp. 30-46
Author(s):  
Sovannarath Pong ◽  
Rakesh Karmacharya ◽  
Marianna Sofman ◽  
Jeffrey R. Bishop ◽  
Paulo Lizano
Keyword(s):  
Blood Brain Barrier ◽  
Association Studies ◽  
Central Element ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Genome Wide Association Studies ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
Microvascular Endothelial

Background: Despite decades of research, little clarity exists regarding pathogenic mechanisms related to schizophrenia. Investigations on the disease biology of schizophrenia have primarily focused on neuronal alterations. However, there is substantial evidence pointing to a significant role for the brain’s microvasculature in mediating neuroinflammation in schizophrenia. Summary: Brain microvascular endothelial cells (BMEC) are a central element of the microvasculature that forms the blood-brain barrier (BBB) and shields the brain against toxins and immune cells via paracellular, transcellular, transporter, and extracellular matrix proteins. While evidence for BBB dysfunction exists in brain disorders, including schizophrenia, it is not known if BMEC themselves are functionally compromised and lead to BBB dysfunction. Key Messages: Genome-wide association studies, postmortem investigations, and gene expression analyses have provided some insights into the role of the BBB in schizophrenia pathophysiology. However, there is a significant gap in our understanding of the role that BMEC play in BBB dysfunction. Recent advances differentiating human BMEC from induced pluripotent stem cells (iPSC) provide new avenues to examine the role of BMEC in BBB dysfunction in schizophrenia.

Role of nitric oxide in human pulmonary microvascular endothelial cell adhesion

Life Sciences ◽  
2000 ◽  
Vol 67 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Hirokazu Tsukahara ◽  
Eisei Noiri ◽  
Mi Zu Jiang ◽  
Masahiro Hiraoka ◽  
Mitsufumi Mayumi
Keyword(s):  
Nitric Oxide ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Microvascular Endothelial Cell ◽  
Pulmonary Microvascular Endothelial Cell ◽  
Microvascular Endothelial ◽  
Endothelial Cell Adhesion
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