Expression and function of toll-like receptors in human circulating endothelial colony forming cells

Mazzucchelli, Iolanda; Lisini, Daniela; Garofoli, Francesca; Dragoni, Silvia; Angelini, Micol; Pozzi, Margherita; Bonetti, Elisa; Tzialla, Chryssoula; Kramer, Boris W.; Spinillo, Arsenio; Maccario, Rita; Rosti, Vittorio; Moccia, Francesco; Borghesi, A.; Stronati, Mauro

doi:10.1016/j.imlet.2015.09.014

Cited by 6 publications

(3 citation statements)

References 30 publications

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“…Finally, this was a preliminary hypothesis-generating study; we plan to confirm the results in an independent sample of patients in the near future. Further more, given that the majority of endothelium function-related markers influence the process of endothelial colony-forming cells (ECFC) 52,53 transforming into mature EC, we consider that further research about isolated ECFC from circulation is essential to explore the potential pathological procedure of endothelial injury induced by unbalanced EC markers. We suspect that intermittent hypoxia and sleep fragmentation is likely the key factors.…”

Section: Discussionmentioning

confidence: 99%

Association between Upper-airway Surgery and Ameliorative Risk Markers of Endothelial Function in Obstructive Sleep Apnea

Wang

Liu

et al. 2019

Sci Rep

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The objective of our study was to evaluate the effects of upper-airway surgery on improvement of endothelial function-related markers in patients with obstructive sleep apnea (OSA). Subjects with moderate to severe OSA who underwent upper-airway surgery, with a follow-up duration of at least 6 months, were included. Pre- and postoperative polysomnographic variables and endothelial function-related markers were compared. Subgroup and correlation analyses were conducted to find possible indicators for better endothelial function-related markers after upper-airway surgery. In total, 44 patients with OSA were included. The mean follow-up duration was 1.72 ± 0.92 years. Serum VEGFA [−20.29 (CI: −35.27, −5.31), p < 0.05], Ang2 [−0.06 (CI: −0.16, 0.03), p < 0.05], E-selectin [−7.21 (CI: −11.01, −3.41), p < 0.001], VWF [−58.83 (CI: −103.93, −13.73), p < 0.05], VWFCP [−33.52 (CI: −66.34, −0.70), p < 0.05], and TM [−0.06 (CI: −0.09, −0.03), p < 0.05] were significantly lower after upper-airway surgery. However, other risk markers of endothelial function, such as Ang1, ICAM1, VEGFR1, and VCAM, did not change significantly. Correlations between improved endothelial function-related markers and ameliorated oxyhemoglobin saturation and glucolipid metabolism were established. Upper-airway surgery might be associated with an improvement in endothelial function in patients with OSA. These changes may be associated with improved oxygen saturation after upper-airway surgery.

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Section: Discussionmentioning

confidence: 99%

Association between Upper-airway Surgery and Ameliorative Risk Markers of Endothelial Function in Obstructive Sleep Apnea

Wang

Liu

et al. 2019

Sci Rep

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“…Systemic accumulation of bacterial endotoxins such as lipopolysaccharide (LPS) signals the disruption of the endothelial barrier through an increase in [Ca 2+ ] i that causes endothelial cell contraction [ 37 , 68 ]. A number of studies demonstrated that LPS elicits intracellular Ca 2+ signals in vascular endothelial cells [ 22 , 37 ], although not in circulating ECFCs [ 275 ]. Gandhirajan et al revealed that Toll-like receptor 4 (TLR4) activation by LPS results in repetitive Ca 2+ transients in mouse pulmonary artery endothelial cells [ 22 ].…”

Section: Therapeutic Applications and Pathological Implications Of Ros-induced Endothelial Ca 2+ Signalsmentioning

confidence: 99%

Reactive Oxygen Species and Endothelial Ca2+ Signaling: Brothers in Arms or Partners in Crime?

Negri¹,

Faris²,

Moccia³

2021

IJMS

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An increase in intracellular Ca2+ concentration ([Ca2+]i) controls virtually all endothelial cell functions and is, therefore, crucial to maintain cardiovascular homeostasis. An aberrant elevation in endothelial can indeed lead to severe cardiovascular disorders. Likewise, moderate amounts of reactive oxygen species (ROS) induce intracellular Ca2+ signals to regulate vascular functions, while excessive ROS production may exploit dysregulated Ca2+ dynamics to induce endothelial injury. Herein, we survey how ROS induce endothelial Ca2+ signals to regulate vascular functions and, vice versa, how aberrant ROS generation may exploit the Ca2+ handling machinery to promote endothelial dysfunction. ROS elicit endothelial Ca2+ signals by regulating inositol-1,4,5-trisphosphate receptors, sarco-endoplasmic reticulum Ca2+-ATPase 2B, two-pore channels, store-operated Ca2+ entry (SOCE), and multiple isoforms of transient receptor potential (TRP) channels. ROS-induced endothelial Ca2+ signals regulate endothelial permeability, angiogenesis, and generation of vasorelaxing mediators and can be exploited to induce therapeutic angiogenesis, rescue neurovascular coupling, and induce cancer regression. However, an increase in endothelial [Ca2+]i induced by aberrant ROS formation may result in endothelial dysfunction, inflammatory diseases, metabolic disorders, and pulmonary artery hypertension. This information could pave the way to design alternative treatments to interfere with the life-threatening interconnection between endothelial ROS and Ca2+ signaling under multiple pathological conditions.

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“…ECFCs are a promising source for postnatal vascularization strategies and tissue repair ( 75 ) and are isolated from different sources (cord blood, peripheral blood, and lung) by outgrowth of EC colonies via limiting dilution from blood or tissues ( 76 – 79 ). ECFCs from cord blood and peripheral blood expressed mRNA for all TLRs, and umbilical cord ECFCs showed higher TLR4 expression than peripheral blood ECFCs, HUVECs, and PBMCs ( 80 ).…”

Section: Expression and Role Of Tlrs In Endothelial Cellsmentioning

confidence: 99%

When Innate Immunity Meets Angiogenesis—The Role of Toll-Like Receptors in Endothelial Cells and Pulmonary Hypertension

2020

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Toll-like receptors serve a central role in innate immunity, but they can also modulate cell function in various non-immune cell types including endothelial cells. Endothelial cells are necessary for the organized function of the vascular system, and part of their fundamental role is also the regulation of immune function and inflammation. In this review, we summarize the current knowledge of how Toll-like receptors contribute to the immune and non-immune functions of the endothelial cells.

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Expression and function of toll-like receptors in human circulating endothelial colony forming cells

Cited by 6 publications

References 30 publications

Association between Upper-airway Surgery and Ameliorative Risk Markers of Endothelial Function in Obstructive Sleep Apnea

Association between Upper-airway Surgery and Ameliorative Risk Markers of Endothelial Function in Obstructive Sleep Apnea

Reactive Oxygen Species and Endothelial Ca2+ Signaling: Brothers in Arms or Partners in Crime?

When Innate Immunity Meets Angiogenesis—The Role of Toll-Like Receptors in Endothelial Cells and Pulmonary Hypertension

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