Circulating Endothelial Cells in Renal Transplant Recipients

Mohamed, Amier; Thomson, Jackie; McDonald, Kenneth J; Hillyard, DZ; Mark, Patrick B.; Elliott, Henry L.; Jardine, Alan G.

doi:10.1016/j.transproceed.2005.03.126

Cited by 11 publications

(6 citation statements)

References 10 publications

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“…Consistent with this, data from FISH analysis 38 in humans suggest that in patients that underwent prior BM or kidney transplantation, ECs can be replaced by the recipient's cells. 39,40 This special allogenic situation is also associated with increased numbers of circulating mature ECs, [41][42][43] which might become integrated into the renal microvasculature.…”

Section: Discussionmentioning

confidence: 99%

Extrarenal Progenitor Cells Do Not Contribute to Renal Endothelial Repair

Sradnick

Rong

Luedemann

et al. 2015

JASN

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Endothelial progenitor cells (EPCs) may be relevant contributors to endothelial cell (EC) repair in various organ systems. In this study, we investigated the potential role of EPCs in renal EC repair. We analyzed the major EPC subtypes in murine kidneys, blood, and spleens after induction of selective EC injury using the concanavalin A/anti-concanavalin A model and after ischemia/reperfusion (I/R) injury as well as the potential of extrarenal cells to substitute for injured local EC. Bone marrow transplantation (BMTx), kidney transplantation, or a combination of both were performed before EC injury to allow distinction of extrarenal or BM-derived cells from intrinsic renal cells. During endothelial regeneration, cells expressing markers of endothelial colony-forming cells (ECFCs) were the most abundant EPC subtype in kidneys, but were not detected in blood or spleen. Few cells expressing markers of EC colony-forming units (EC-CFUs) were detected. In BM chimeric mice (C57BL/6 with tandem dimer Tomato-positive [tdT+] BM cells), circulating and splenic EC-CFUs were BM-derived (tdT+), whereas cells positive for ECFC markers in kidneys were not. Indeed, most BM-derived tdT+ cells in injured kidneys were inflammatory cells. Kidneys from C57BL/6 donors transplanted into tdT+ recipients with or without prior BMTx from C57BL/6 mice were negative for BM-derived or extrarenal ECFCs. Overall, extrarenal cells did not substitute for any intrinsic ECs. These results demonstrate that endothelial repair in mouse kidneys with acute endothelial lesions depends exclusively on local mechanisms.

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Section: Discussionmentioning

confidence: 99%

Extrarenal Progenitor Cells Do Not Contribute to Renal Endothelial Repair

Sradnick

Rong

Luedemann

et al. 2015

JASN

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“…In recent years, several methods and markers for endothelial dysfunction have been studied in kidney allograft recipients due to higher cardiovascular mortality in these patients in comparison with healthy subjects [1][2][3][4][5][6][7][8][9][10]. While uremic status and related factors such as calcium-phosphorus balance, hypervolemia, anemia, oxidative stress, hyperparathyroidism, inflammation and hyperhomocysteinemia resolve after transplantation, we do not know clearly whether kidney transplantation improves long-term changes of uremia in the cardiovascular system (left ventricular structural abnormality, coronary calcification, arterial changes induced by arteriosclerosis).…”

Section: Discussionmentioning

confidence: 99%

“…In recent studies, there has been an increased interest in the evaluation of endothelial dysfunction as an early abnormality in atherosclerosis not only in patients with end stage renal disease but also in RTx recipients [2][3][4][5][6][7]. Various endothelial dysfunction markers and methods including flowmediated dilatation (FMD), high-sensitive C-reactive protein (CRP), fetuin-A, visfatin, homocysteine, several cytokines, circulating endothelial cells and progenitor cells, plasma soluble von Willebrand factor antigen and adhesion molecules have been defined [2][3][4][5][6][7][8][9]. In recent years, thrombomodulin (TM), which is a transmembrane cofactor of the endothelial cells, and endothelial protein C receptor (EPCR), which plays an important role in activation of protein C in the coagulation cascade, have been described as new markers of endothelial dysfunction, and the soluble forms of both markers increase in situations of endothelial damage such as vasculitis, systemic lupus erythematosus (SLE) and sepsis [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Soluble endothelial cell protein C receptor and thrombomodulin levels after renal transplantation

et al. 2009

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“…Woywodt et al demonstrated that patients with acute vascular rejection had the highest cell numbers compared with other patients [61]. Mohamed et al found that the cells seemed to be derived from the graft itself [81]. Therefore, kidney transplantation may have a remarkable effect on endothelial damage.…”

Section: Clinical Value Of Circulating Endothelial Cells In Transpmentioning

confidence: 99%

Circulating Endothelial Cells and Chronic Kidney Disease

Zhang

Yin

Lin

2014

BioMed Research International

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Endothelial dysfunction may play a crucial role in initiation of the pathogenesis of vascular disease and atherosclerosis. The identification and quantification of circulating endothelial cells (CEC) have been developed as a novel marker of endothelial function. We describe, in great detail, mechanisms of endothelial dysfunction and CEC detachment. We also review the relationship between numbers of CEC and disease severity and response to treatment. In addition, we describe the possible clinical use of CEC in chronic kidney disease (CKD) and kidney transplantation. In summary, CEC have been developed as a novel approach to assess the endothelial damage. Measurement of the CEC level would provide an important diagnostic and prognostic value on the endothelium status and the long-term outcome of vascular dysfunction.

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Circulating Endothelial Cells in Renal Transplant Recipients

Cited by 11 publications

References 10 publications

Extrarenal Progenitor Cells Do Not Contribute to Renal Endothelial Repair

Extrarenal Progenitor Cells Do Not Contribute to Renal Endothelial Repair

Soluble endothelial cell protein C receptor and thrombomodulin levels after renal transplantation

Circulating Endothelial Cells and Chronic Kidney Disease

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