Tubular Chimerism Occurs Regularly in Renal Allografts and Is Not Correlated to Outcome

Mengel, Michael; Jonigk, Danny; Marwedel, Magali; Kleeberger, Wolfram; Bredt, Martin; Lehmann, Ulrich; Gwinner, Wilfried; Haller, Hermann; Kreipe, Hans

doi:10.1097/01.asn.0000120369.92378.54

Cited by 40 publications

(30 citation statements)

References 33 publications

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“…At the time of biopsy, the presence of endothelial chimerism correlates moderately with the presence of tubular atrophy, but the presence of endothelial chimerism has no relation to a vast number of clinical parameters, including graft function and outcome. This is in line with the results from a recent study in epithelial chimerism in tubular epithelial cells of renal transplants [8], because also in this study, chimerism did not correlate with allograft function [8].…”

Section: Discussionsupporting

confidence: 94%

Endothelial cell chimerism occurs more often and earlier in female than in male recipients of kidney transplants

Poelgeest

Baelde

Lagaaij

et al. 2005

Kidney International

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Section: Discussionsupporting

confidence: 94%

Endothelial cell chimerism occurs more often and earlier in female than in male recipients of kidney transplants

Poelgeest

Baelde

Lagaaij

et al. 2005

Kidney International

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“…Using this marker, our group recently reported that TGFβ, presented either in solution or on the surface of T lymphocytes, could induce EMT of cultured human RCEC, and also showed a spatial association between EMT and intratubular T cells in kidney transplant biopsy sections (4). The possibility that EMT plays a major role during the development of chronic renal allograft nephropathy is entirely consistent with studies showing that relatively few recipient‐derived cells re‐populate the parenchyma of damaged human kidneys following transplantation (30).…”

Section: Discussionsupporting

confidence: 77%

Chronic Allograft Nephropathy: Intraepithelial Signals Generated by Transforming Growth Factor-β and Bone Morphogenetic Protein-7

Tyler

Robertson

Booth

et al. 2006

American Journal of Transplantation

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It has been suggested that TGFb can cause chronic allograft nephropathy by inducing epithelial to mesenchymal transition (EMT); some studies show a reverse transition can be produced by bone morphogenetic protein-7 (BMP7). The current study assessed the relative contribution of signals generated within tubular epithelial cells by TGFb and BMP7 in normal kidney and after transplantation. Epithelial cells in normal human kidneys expressed phosphorylated forms of both Smad2/3 and Smad1/5/8 within their nuclei; cell culture experiments showed that these signaling molecules were generated in response to TGFb and BMP7, respectively. Phospho(p)-Smad2/3 was expressed at increased levels by tubular epithelial cells during acute renal allograft rejection and chronic allograft nephropathy but pSmad1/5/8 was expressed at very low levels; this staining profile was associated with induction of the EMT marker, S100A4. Further in vitro experiments demonstrated that this pattern of Smad signaling was a consequence of the stimulation of tubular epithelial cells with TGFb in the absence of BMP7. Importantly, addition of BMP7 to TGFb -stimulated cells enhanced the expression of pSmad1/5/8 and reduced expression of S100A4. These results suggest that exogenous BMP7 could restore the homeostatic balance of pSmad signaling found in normal kidneys, thereby preventing or reversing the development of chronic allograft nephropathy.

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“…This phenomenon also indicated that recipient-derived cells might actively participate in the regeneration of injured tubular epithelium after ACR. Recently, Mengel et al reported that epithelial microchimerism by re- cipient-derived cells was not correlated to morphologic or functional outcome in renal allografts (12), which seems conflicting with our present results and also with some other types of organ transplantation (13)(14).…”

Section: Discussioncontrasting

confidence: 75%

Recipient-Derived Cells in the Tissue Repair of Renal Allografts

Liu

et al. 2006

Transplantation

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To observe the roles of recipient-derived cells in renal allografts with acute cellular rejection (ACR), eight male patients who had received a female donor kidney were enrolled, with protocol renal allograft biopsies. Three of them suffered from ACR, and the other five with normal function. Biopsy sections were detected for the presence of recipient-derived cells and their phenotypes. Recipient-derived cells appeared in the tubular epithelium as early as 13 days posttransplant, with the phenotype of cytokeratin(+)/CD45(-). They also localized in the medium walls of arterioles and expressed alpha-SMA. In patients with ACR, recipient-derived tubular cells increased persistently during the first 6 months (3.8 to 6.6%). Long-term follow up showed a decline in their number when ACR ameliorated. In patients without ACR, the infiltration rate remained stable (0.6-2.3%). Recipient-derived cells participate the remodeling of renal allografts. They might have a close relationship with ACR outcome and with vascular structure remodeling.

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Tubular Chimerism Occurs Regularly in Renal Allografts and Is Not Correlated to Outcome

Cited by 40 publications

References 33 publications

Endothelial cell chimerism occurs more often and earlier in female than in male recipients of kidney transplants

Endothelial cell chimerism occurs more often and earlier in female than in male recipients of kidney transplants

Chronic Allograft Nephropathy: Intraepithelial Signals Generated by Transforming Growth Factor-β and Bone Morphogenetic Protein-7

Recipient-Derived Cells in the Tissue Repair of Renal Allografts

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