Circulating endothelial cells: life, death, detachment and repair of the endothelial cell layer

Woywodt, Alexander; Bahlmann, Ferdinand H.; Groot, Kirsten de; Haller, Hermann; Haubitz, Marion

doi:10.1093/ndt/17.10.1728

Cited by 136 publications

(107 citation statements)

References 18 publications

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“…In the early post-transplantation period, serum creatinine level does not reflect the degree of damage to the graft well 7 . Likewise, the increased count of CD 146+ circulating endothelial cells in peripheral blood is not specific as a marker of vascular toxic damage to the graft 58,59 . In our pilot study which prospectively monitored histological and ultrasound findings of very well functioning grafts affected by subclinical rejection 60 , no sufficiently sensitive and specific parameter for toxicity was identified (unpublished data).…”

Section: Nephrotoxicity Diagnostic Optionsmentioning

confidence: 96%

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Krejčí¹,

Tichý²,

Bachleda³

et al. 2010

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The introduction of the calcineurin inhibitors (CI) cyclosporine and tacrolimus into immunosuppressive protocols initiated a new era in organ transplantation with excellent short-term graft survival. Nevertheless, the chronic nephrotoxicity of these drugs represents a significant adverse factor limiting their long-term use. Patients treated with a CI can be at risk for developing renal failure and this problem is especially pronounced in patients after renal transplantation.Methods and Results. In a review paper we summarize the clinical aspects, histological manifestations and pitfalls of diagnostics of acute and chronic CI nephrotoxicity in patients after kidney transplantation. We look in detail at the disputed relationship between blood concentrations of cyclosporine and tacrolimus and histological manifestation of toxicity and summarize data showing that for toxic effects, local renal exposure to CI and their metabolites can play a more significant role than systemic exposure. We also include recent views on the pathophysiologic and molecular mechanisms underlying these changes; factors influencing local susceptibility to CI nephrotoxicity are discussed, including variability of expression and activity of P-glycoprotein and cytochrome P450. Last but not least we summarize our own experience with clinically manifest and subclinical forms of nephrotoxicity and their impact on the progression of chronic graft changes.Conclusions. Owing to their unique effects, CI remain the cornerstone of most immunosuppressive protocols for renal transplantation. Together with optimization of local kidney exposure to CI and their metabolites, efforts to reduce systemic levels as much as possible are the most important preventive measure for reducing toxic renal graft damage.

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Section: Nephrotoxicity Diagnostic Optionsmentioning

confidence: 96%

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Krejčí¹,

Tichý²,

Bachleda³

et al. 2010

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Loss of integrity of the endothelial layer eventually leads to cell detachment of cells 40 . Such detachment can be caused by defective adhesive properties of the endothelial cells, by action of proteases and/or cytokines or, by mechanical injury.…”

Section: Phenotype and Mechanisms Of Detachment Of Cec In Vasculitismentioning

confidence: 99%

“…Such detachment can be caused by defective adhesive properties of the endothelial cells, by action of proteases and/or cytokines or, by mechanical injury. Endothelial adhesive molecules of the integrin and cadherin family, such as vitronectin and fibronectin and VE cadherin, respectively, promote adhesion of endothelial cells to matrix [40][41] . Loss of these survival signals triggers detachment and apoptosis of endothelial cells 42 .…”

Section: Phenotype and Mechanisms Of Detachment Of Cec In Vasculitismentioning

confidence: 99%

“…It has been speculated that CEC themselves could be pro-inflammatory 40 . In general, damaged eukaryotic cells have been shown to release a variety of pro-inflammatory factors, to initiate pro-inflammatory pathways in other cell subsets, such as a Toll-like-receptor-2/NFκB-dependent reaction in monocytes 51 .…”

Section: Circulating Endothelial Cells As Potential Mediators Of Diseasementioning

confidence: 99%

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Markers of Vascular Damage and Repair

Erdbruegger¹,

Dhaygude²,

Woywodt³

2011

Advances in the Etiology, Pathogenesis and Pathology of Vasculitis

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“…It is only after the tumour cells develop, that an angiogenic phenotype is produced, and the appropriate growth factors are released, that the tumour may develop its own network of blood vessels and acquires the ability to grow further and metastasize to distant tissues [47]. Apart from neoplastic diseases, pathologic angiogenesis can be seen in conditions of hypoxia and in chronic inflammation [7,56].…”

Section: Angiogenesismentioning

confidence: 99%

The Contribution of Endothelial Marker Proteins in the Determination of Vascular Angiogenic Potential, in Normal Physiological Conditions and in Neoplasia

Konwerska

Janik

Malińska

et al. 2011

Advances in Cell Biology

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Summary: Recently, the most significant studies in the field of angiogenesis are related to trials concerning the evaluation of the prognostic significance of endothelial markers. By using an estimation of the expression of endothelial cell markers, immunohistochemical studies can assess for the continuity of the vascular intima, as well as allow for the distinction of early, late and mature forms of endothelial cells. The determination of the endothelial cell phenotype using markers such as CD34, CD31, CD133, e-NOS and von Willebrand factor may provide a valuable tool for the monitoring of both normal physiology as well as neoplastic diseases.

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Circulating endothelial cells: life, death, detachment and repair of the endothelial cell layer

Cited by 136 publications

References 18 publications

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Calcineurin Inhibitor-Induced Renal Allograft Nephrotoxicity

Markers of Vascular Damage and Repair

The Contribution of Endothelial Marker Proteins in the Determination of Vascular Angiogenic Potential, in Normal Physiological Conditions and in Neoplasia

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