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Article ; Online: Transplantation-Induced Ischemia-Reperfusion Injury Modulates Antigen Presentation by Donor Renal CD11c

Aiello, Sistiana / Podestà, Manuel Alfredo / Rodriguez-Ordonez, Pamela Y / Pezzuto, Francesca / Azzollini, Nadia / Solini, Samantha / Carrara, Camillo / Todeschini, Marta / Casiraghi, Federica / Noris, Marina / Remuzzi, Giuseppe / Benigni, Ariela

Journal of the American Society of Nephrology : JASN

2020 Volume 31, Issue 3, Page(s) 517–531

Abstract: Background: In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen ... ...

Abstract	Background: In donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen presentation. After injury, however, resident renal macrophages coexpressing these surface markers acquire a proreparative phenotype, which is pivotal in controlling inflammation and fibrosis. No data are currently available regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resident renal macrophages to act as professional antigen-presenting cells. Methods: We evaluated the phenotype and function of intragraft CD11c Results: Cold ischemia and reversible ischemia-reperfusion injury dampened antigen presentation by renal macrophages, skewed their polarization toward the M Conclusions: IL-1R8 is a key regulator of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and antigen-presenting role of these cells. It may therefore represent an intriguing pathway to explore with respect to modulating responses against autoantigens and alloantigens after kidney transplant.
MeSH term(s)	Adaptive Immunity/genetics ; Animals ; Antigen Presentation ; CD11c Antigen/immunology ; CD11c Antigen/metabolism ; Cells, Cultured ; Cold Ischemia/methods ; Disease Models, Animal ; Gene Expression Regulation/genetics ; Kidney Transplantation/adverse effects ; Kidney Transplantation/methods ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Receptors, Interleukin-1/genetics ; Receptors, Interleukin-1/immunology ; Reperfusion Injury/genetics ; Reperfusion Injury/prevention & control ; Sensitivity and Specificity ; Signal Transduction/genetics
Chemical Substances	CD11c Antigen ; Receptors, Interleukin-1 ; SIGIRR protein, human
Language	English
Publishing date	2020-01-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2019080778
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Article ; Online: Effect of Timing and Complement Receptor Antagonism on Intragraft Recruitment and Protolerogenic Effects of Mesenchymal Stromal Cells in Murine Kidney Transplantation.

Casiraghi, Federica / Todeschini, Marta / Azzollini, Nadia / Cravedi, Paolo / Cassis, Paola / Solini, Samantha / Fiori, Sonia / Rota, Cinzia / Karachi, Aida / Carrara, Camillo / Noris, Marina / Perico, Norberto / Remuzzi, Giuseppe

Transplantation

2019 Volume 103, Issue 6, Page(s) 1121–1130

Abstract: Background: Mesenchymal stromal cells (MSCs) have protolerogenic effects in renal transplantation, but they induce long-term regulatory T cells (Treg)-dependent graft acceptance only when infused before transplantation. When given posttransplant, MSCs ... ...

Abstract	Background: Mesenchymal stromal cells (MSCs) have protolerogenic effects in renal transplantation, but they induce long-term regulatory T cells (Treg)-dependent graft acceptance only when infused before transplantation. When given posttransplant, MSCs home to the graft where they promote engraftment syndrome and do not induce Treg. Unfortunately, pretransplant MSC administration is unfeasible in deceased-donor kidney transplantation. Methods: To make MSCs a therapeutic option also for deceased organ recipients, we tested whether MSC infusion at the time of transplant (day 0) or posttransplant (day 2) together with inhibition of complement receptors prevents engraftment syndrome and allows their homing to secondary lymphoid organs for promoting tolerance. We analyzed intragraft and splenic MSC localization, graft survival, and alloimmune response in mice recipients of kidney allografts and syngeneic MSCs given on day 0 or on posttransplant day 2. C3a receptor (C3aR) or C5a receptor (C5aR) antagonists were administered to mice in combination with the cells or were used together to treat MSCs before infusion. Results: Syngeneic MSCs given at day 0 homed to the spleen increased Treg numbers and induced long-term graft acceptance. Posttransplant MSC infusion, combined with a short course of C3aR or C5aR antagonist or administration of MSCs pretreated with C3aR and C5aR antagonists, prevented intragraft recruitment of MSCs and graft inflammation, inhibited antidonor T-cell reactivity, but failed to induce Treg, resulting in mild prolongation of graft survival. Conclusions: These data support testing the safety/efficacy profile of administering MSCs on the day of transplant in deceased-donor transplant recipients and indicate that complement is crucial for MSC recruitment into the kidney allograft.
MeSH term(s)	Animals ; Complement Inactivating Agents/administration & dosage ; Drug Administration Schedule ; Female ; Graft Rejection/immunology ; Graft Rejection/prevention & control ; Graft Survival/drug effects ; Kidney Transplantation ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/drug effects ; Mesenchymal Stem Cells/immunology ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Complement/antagonists & inhibitors ; Receptors, Complement/immunology ; Receptors, G-Protein-Coupled/antagonists & inhibitors ; Receptors, G-Protein-Coupled/immunology ; Spleen/drug effects ; Spleen/immunology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Time Factors ; Transplantation Tolerance/drug effects ; Transplantation, Homologous ; Transplantation, Isogeneic
Chemical Substances	C3a-derived anaphylatoxin receptor, mouse ; Complement Inactivating Agents ; Receptors, Complement ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2019-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0000000000002611
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Autotaxin Inhibitor Protects from Chronic Allograft Injury in Rat Kidney Allotransplantation.

Cortinovis, Monica / Aiello, Sistiana / Mister, Marilena / Conde-Knape, Karin / Noris, Marina / Novelli, Rubina / Solini, Samantha / Rodriguez Ordonez, Pamela Y / Benigni, Ariela / Remuzzi, Giuseppe

Nephron

2019 Volume 144, Issue 1, Page(s) 38–48

Abstract: Background: Tissue fibrosis is the final common phase of chronic allograft injury, the leading cause of late graft loss in kidney transplantation. Preclinical evidence points to the involvement of lysophosphatidic acid (LPA), a bioactive phospholipid, ... ...

Abstract	Background: Tissue fibrosis is the final common phase of chronic allograft injury, the leading cause of late graft loss in kidney transplantation. Preclinical evidence points to the involvement of lysophosphatidic acid (LPA), a bioactive phospholipid, in the development of renal fibrosis. Objectives: We assessed whether treatment with an orally available inhibitor of autotaxin (ATXi), the main LPA-producing enzyme, could slow the progression of chronic allograft injury in a fully major histocompatibility complex-mismatched rat kidney transplant model and compared its effects with those of the angiotensin-converting enzyme inhibitor lisinopril. Methods: Kidney allograft recipients were given ciclosporin for the first 15 postoperative days to prevent early acute rejection. Thereafter, they received either no treatment or ATXi or lisinopril and were followed for 180 days after transplantation. Results: Renal LPA levels were increased in allograft rats, providing the rationale for using ATXi in this model. Chronic treatment with ATXi or lisinopril limited progressive proteinuria and ameliorated tubulointerstitial fibrosis compared with allograft rats, although the effects were more robust under ATX inhibition. The administration of ATXi, but not lisinopril, attenuated systemic hypertension, reduced intragraft T cell infiltration, and eventually improved renal graft survival. Conclusions: In summary, ATXi had protective effects on indices of chronic allograft injury and could be of therapeutic add-on value in the kidney transplant setting. Notably, an ATX inhibitor is currently being investigated in 2 large phase 3 studies in idiopathic pulmonary fibrosis, underscoring the clinical relevance of our findings.
MeSH term(s)	Animals ; Chronic Disease ; Graft Rejection ; Kidney/metabolism ; Kidney Transplantation/adverse effects ; Lysophospholipids/metabolism ; Male ; Phosphoric Diester Hydrolases/drug effects ; Rats ; Rats, Inbred Strains ; Transplantation, Homologous/adverse effects
Chemical Substances	Lysophospholipids ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; alkylglycerophosphoethanolamine phosphodiesterase (EC 3.1.4.39) ; lysophosphatidic acid (PG6M3969SG)
Language	English
Publishing date	2019-09-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000502908
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Zs.A 169: Show issues

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Article: Autotaxin Inhibitor Protects from Chronic Allograft Injury in Rat Kidney Allotransplantation

Cortinovis, Monica / Aiello, Sistiana / Mister, Marilena / Conde-Knape, Karin / Noris, Marina / Novelli, Rubina / Solini, Samantha / Rodriguez Ordonez, Pamela Y. / Benigni, Ariela / Remuzzi, Giuseppe

Nephron

2019 Volume 144, Issue 1, Page(s) 38–48

Institution	Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy Global Research at Novo Nordisk, Målov, Denmark L. Sacco Department of Biomedical and Clinical Sciences, University of Milan, Milan, Italy
Abstract	Background: Tissue fibrosis is the final common phase of chronic allograft injury, the leading cause of late graft loss in kidney transplantation. Preclinical evidence points to the involvement of lysophosphatidic acid (LPA), a bioactive phospholipid, in the development of renal fibrosis. Objectives: We assessed whether treatment with an orally available inhibitor of autotaxin (ATXi), the main LPA-producing enzyme, could slow the progression of chronic allograft injury in a fully major histocompatibility complex-mismatched rat kidney transplant model and compared its effects with those of the angiotensin-converting enzyme inhibitor lisinopril. Methods: Kidney allograft recipients were given ciclosporin for the first 15 postoperative days to prevent early acute rejection. Thereafter, they received either no treatment or ATXi or lisinopril and were followed for 180 days after transplantation. Results: Renal LPA levels were increased in allograft rats, providing the rationale for using ATXi in this model. Chronic treatment with ATXi or lisinopril limited progressive proteinuria and ameliorated tubulointerstitial fibrosis compared with allograft rats, although the effects were more robust under ATX inhibition. The administration of ATXi, but not lisinopril, attenuated systemic hypertension, reduced intragraft T cell infiltration, and eventually improved renal graft survival. Conclusions: In summary, ATXi had protective effects on indices of chronic allograft injury and could be of therapeutic add-on value in the kidney transplant setting. Notably, an ATX inhibitor is currently being investigated in 2 large phase 3 studies in idiopathic pulmonary fibrosis, underscoring the clinical relevance of our findings.
Keywords	Kidney transplantation ; Chronic allograft injury ; Fibrosis ; Lysophosphatidic acid ; Autotaxin
Language	English
Publishing date	2019-09-24
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Experimental Nephrology and Genetics: Research Article
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000502908
Database	Karger publisher's database

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Zs.A 169: Show issues

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Article ; Online: Rabbit anti-rat thymocyte immunoglobulin preserves renal function during ischemia/reperfusion injury in rat kidney transplantation.

Aiello, Sistiana / Cassis, Paola / Mister, Marilena / Solini, Samantha / Rocchetta, Federica / Abbate, Mauro / Gagliardini, Elena / Benigni, Ariela / Remuzzi, Giuseppe / Noris, Marina

Transplant international : official journal of the European Society for Organ Transplantation

2011 Volume 24, Issue 8, Page(s) 829–838

Abstract: Ischemia/reperfusion (I/R) injury is an important cause of renal graft dysfunction in humans. Increases in cold and warm ischemia times lead to a higher risk of early post-transplant complications including delayed graft function and acute rejection. ... ...

Abstract	Ischemia/reperfusion (I/R) injury is an important cause of renal graft dysfunction in humans. Increases in cold and warm ischemia times lead to a higher risk of early post-transplant complications including delayed graft function and acute rejection. Moreover, prolonged cold ischemia is a predictor of long-term kidney graft loss. The protective effect of rabbit anti-rat thymocyte immunoglobulin (rATG) was evaluated in a rat model of I/R injury following syngeneic kidney transplantation. Serum creatinine concentration was evaluated at 16 h and 24 h post-transplant. Animals were sacrificed 24 h post-transplant for evaluation of histology, infiltrating leukocytes, nitrotyrosine staining, and apoptosis. rATG was effective in preventing renal function impairment, tissue damage and tubular apoptosis associated with I/R only when was given 2 h before transplantation but not at the time of reperfusion. Pretransplant rATG treatment of recipient animals effectively reduced the amount of macrophages, CD4(+), CD8(+) T cells and LFA-1(+) cells infiltrating renal graft subjected to cold ischemia as well as granzyme-B expression within ischemic kidney. On the other hand, granulocyte infiltration and oxidative stress were not modified by rATG. If these results will be translated into the clinical setting, pretransplant administration of Thymoglobuline(®) could offer the additional advantage over peri-transplant administration of limiting I/R-mediated kidney graft damage.
MeSH term(s)	Animals ; Apoptosis ; CD4-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/cytology ; Granzymes/pharmacology ; Immunoglobulins/metabolism ; Ischemia/pathology ; Kidney/metabolism ; Kidney Transplantation/methods ; Male ; Microscopy, Fluorescence/methods ; Rabbits ; Rats ; Rats, Inbred Lew ; Reperfusion Injury/metabolism ; Thymocytes/cytology
Chemical Substances	Immunoglobulins ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2011-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639435-8
ISSN	1432-2277 ; 0934-0874
ISSN (online)	1432-2277
ISSN	0934-0874
DOI	10.1111/j.1432-2277.2011.01263.x
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Article ; Online: Erythropoietin, but not the correction of anemia alone, protects from chronic kidney allograft injury.

Cassis, Paola / Gallon, Lorenzo / Benigni, Ariela / Mister, Marilena / Pezzotta, Anna / Solini, Samantha / Gagliardini, Elena / Cugini, Daniela / Abbate, Mauro / Aiello, Sistiana / Rocchetta, Federica / Scudeletti, Pierangela / Perico, Norberto / Noris, Marina / Remuzzi, Giuseppe

Kidney international

2012 Volume 81, Issue 9, Page(s) 903–918

Abstract: Anemia can contribute to chronic allograft injury by limiting oxygen delivery to tissues, particularly in the tubulointerstitium. To determine mechanisms by which erythropoietin (EPO) prevents chronic allograft injury we utilized a rat model of full MHC- ... ...

Abstract	Anemia can contribute to chronic allograft injury by limiting oxygen delivery to tissues, particularly in the tubulointerstitium. To determine mechanisms by which erythropoietin (EPO) prevents chronic allograft injury we utilized a rat model of full MHC-mismatched kidney transplantation (Wistar Furth donor and Lewis recipients) with removal of the native kidneys. EPO treatment entirely corrected post-transplant anemia. Control rats developed progressive proteinuria and graft dysfunction, tubulointerstitial damage, inflammatory cell infiltration, and glomerulosclerosis, all prevented by EPO. Normalization of post-transplant hemoglobin levels by blood transfusions, however, had no impact on chronic allograft injury, indicating that EPO-mediated graft protection went beyond the correction of anemia. Compared to syngeneic grafts, control allografts had loss of peritubular capillaries, higher tubular apoptosis, tubular and glomerular oxidative injury, and reduced expression of podocyte nephrin; all prevented by EPO treatment. The effects of EPO were associated with preservation of intragraft expression of angiogenic factors, upregulation of the anti-apoptotic factor p-Akt in tubuli, and increased expression of Bcl-2. Inhibition of p-Akt by Wortmannin partially antagonized the effect of EPO on allograft injury and tubular apoptosis, and prevented EPO-induced Bcl-2 upregulation. Thus non-erythropoietic derivatives of EPO may be useful to prevent chronic renal allograft injury.
MeSH term(s)	Anemia/blood ; Anemia/drug therapy ; Anemia/etiology ; Animals ; Apoptosis/drug effects ; Biomarkers/blood ; Blood Transfusion ; Chronic Disease ; Erythropoietin/pharmacology ; Glomerulonephritis/immunology ; Glomerulonephritis/prevention & control ; Hematinics/pharmacology ; Hemoglobins/metabolism ; Histocompatibility ; Kidney/drug effects ; Kidney/immunology ; Kidney/metabolism ; Kidney/pathology ; Kidney Diseases/immunology ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Kidney Diseases/prevention & control ; Kidney Transplantation/adverse effects ; Kidney Transplantation/immunology ; Mice ; Primary Graft Dysfunction/immunology ; Primary Graft Dysfunction/prevention & control ; Proteinuria/immunology ; Proteinuria/prevention & control ; Rats ; Rats, Inbred Lew ; Rats, Inbred WF ; Time Factors
Chemical Substances	Biomarkers ; Hematinics ; Hemoglobins ; Erythropoietin (11096-26-7)
Language	English
Publishing date	2012-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2011.473
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Zs.A 797: Show issues

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Article ; Online: Prolonged cold ischemia accelerates cellular and humoral chronic rejection in a rat model of kidney allotransplantation.

Solini, Samantha / Aiello, Sistiana / Cassis, Paola / Scudeletti, Pierangela / Azzollini, Nadia / Mister, Marilena / Rocchetta, Federica / Abbate, Mauro / Pereira, Rafael Luiz / Noris, Marina

Transplant international : official journal of the European Society for Organ Transplantation

2012 Volume 25, Issue 3, Page(s) 347–356

Abstract: One of the leading causes of long-term kidney graft loss is chronic allograft injury (CAI), a pathological process triggered by alloantigen-dependent and alloantigen-independent factors. Alloantigen-independent factors, such as cold ischemia (CI) may ... ...

Abstract	One of the leading causes of long-term kidney graft loss is chronic allograft injury (CAI), a pathological process triggered by alloantigen-dependent and alloantigen-independent factors. Alloantigen-independent factors, such as cold ischemia (CI) may amplify the recipient immune response against the graft. We investigated the impact of prolonged cold ischemia and the subsequent delayed graft function on CAI in a fully MHC-mismatched rat model of kidney allotransplantation. Prolonged CI was associated with anticipation of proteinuria onset and graft function deterioration (ischemia: 90d; no ischemia: 150d), more severe tubular atrophy, interstitial fibrosis, and glomerulosclerosis, and increased mortality rate (180d survival, ischemia: 0%; no ischemia: 67%). In ischemic allografts, T and B cells were detected very early and were organized in inflammatory clusters. Higher expression of BAFF-R and TACI within the ischemic allografts indicates that B cells are mature and activated. As a consequence of B cell activity, anti-donor antibodies, glomerular C4d and IgG deposition, important features of chronic humoral rejection, appeared earlier in ischemic than in non-ischemic allograft recipients. Thus, prolonged CI time plays a main role in CAI development by triggering acceleration of cellular and humoral reactions of chronic rejection. Limiting CI time should be considered as a main target in kidney transplantation.
MeSH term(s)	Animals ; Apoptosis ; Cold Ischemia/adverse effects ; Delayed Graft Function/etiology ; Delayed Graft Function/immunology ; Delayed Graft Function/pathology ; Flow Cytometry ; Graft Rejection/etiology ; Graft Rejection/immunology ; Graft Rejection/pathology ; In Situ Nick-End Labeling ; Kidney/immunology ; Kidney/pathology ; Kidney Transplantation/immunology ; Kidney Transplantation/methods ; Kidney Transplantation/mortality ; Male ; Rats ; Rats, Inbred WF ; Real-Time Polymerase Chain Reaction ; Time Factors ; Transplantation, Homologous/immunology ; Transplantation, Homologous/methods ; Transplantation, Homologous/mortality
Language	English
Publishing date	2012-03
Publishing country	England
Document type	Evaluation Studies ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639435-8
ISSN	1432-2277 ; 0934-0874
ISSN (online)	1432-2277
ISSN	0934-0874
DOI	10.1111/j.1432-2277.2011.01425.x
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Article ; Online: Both darbepoetin alfa and carbamylated erythropoietin prevent kidney graft dysfunction due to ischemia/reperfusion in rats.

Cassis, Paola / Azzollini, Nadia / Solini, Samantha / Mister, Marilena / Aiello, Sistiana / Cugini, Daniela / Scudeletti, Pierangela / Gagliardini, Elena / Abbate, Mauro / Gallon, Lorenzo / Remuzzi, Giuseppe / Noris, Marina

Transplantation

2011 Volume 92, Issue 3, Page(s) 271–279

Abstract: Background: Ischemia/reperfusion (I/R) injury is an important cause of renal graft dysfunction. Increases in cold and warm ischemia times lead to a higher risk of early posttransplant complications including delayed graft function and acute rejection. ... ...

Abstract	Background: Ischemia/reperfusion (I/R) injury is an important cause of renal graft dysfunction. Increases in cold and warm ischemia times lead to a higher risk of early posttransplant complications including delayed graft function and acute rejection. Moreover, prolonged cold ischemia is a predictor of long-term graft loss in kidney transplant patients. Methods: Darbepoetin alfa (DA) and carbamylated nonerythropoietic derivative of erythropoietin (CEPO) protective effects were evaluated in a model of I/R injury after kidney transplantation in both syngeneic and allogeneic combinations. The effects of wortmannin (phosphorylated Akt [p-Akt] inhibitor) administration were also investigated. Serum creatinine was evaluated at 16, 24, 48 hr and at 4 and 7 days posttransplant. Animals were killed 24 hr or 7 days after transplant and kidneys were processed for histological analysis, immunohistochemistry assessment of erythropoietin receptor (EPOR) and β-common chain receptor expression, granulocyte infiltration, nitrotyrosine staining, p-Akt expression, peritubular capillary (PTC) density, apoptosis, antioxidant, and antiapoptotic gene expression. Results: DA and CEPO significantly reduced serum creatinine, tubular injury, tubular nitrotyrosine staining, and prevented I/R-induced tubular apoptosis, but only when given both to the donor and to the recipient. DA and CEPO cytoprotection was associated with prevention of I/R-induced drop of p-Akt expression in tubuli, and almost complete preservation of capillary density in the tubulointerstitium of the graft. CEPO was more effective than DA in reducing tubular oxidative stress and preserving PTCs. Conclusion: DA and CEPO when given both to the donor and to the recipient, prevented renal graft dysfunction, tubular oxidative stress, and apoptosis after I/R injury in kidney transplantation. Their cytoprotection was mediated by tubular p-Akt activation and PTC density preservation.
MeSH term(s)	Androstadienes/pharmacology ; Animals ; Antioxidants/metabolism ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/metabolism ; Cold Temperature ; Darbepoetin alfa ; Erythropoietin/analogs & derivatives ; Erythropoietin/pharmacology ; Graft Survival/drug effects ; Hematinics/pharmacology ; Immunosuppressive Agents/pharmacology ; Kidney Transplantation ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Oxidative Stress/drug effects ; Primary Graft Dysfunction/metabolism ; Primary Graft Dysfunction/pathology ; Primary Graft Dysfunction/prevention & control ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Inbred Lew ; Reperfusion Injury/drug therapy ; Tissue Donors ; Transplantation, Homologous
Chemical Substances	Androstadienes ; Antioxidants ; Apoptosis Regulatory Proteins ; Hematinics ; Immunosuppressive Agents ; carbamylated erythropoietin ; Erythropoietin (11096-26-7) ; Darbepoetin alfa (15UQ94PT4P) ; Akt1 protein, rat (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; wortmannin (XVA4O219QW)
Language	English
Publishing date	2011-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0b013e3182241106
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Embryonic stem cells, derived either after in vitro fertilization or nuclear transfer, prolong survival of semiallogeneic heart transplants.

Imberti, Barbara / Casiraghi, Federica / Cugini, Daniela / Azzollini, Nadia / Cassis, Paola / Todeschini, Marta / Solini, Samantha / Sebastiano, Vittorio / Zuccotti, Maurizio / Garagna, Silvia / Redi, Carlo Alberto / Noris, Marina / Morigi, Marina / Remuzzi, Giuseppe

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 7, Page(s) 4164–4174

Abstract: Tolerance induction toward allogeneic organ grafts represents one of the major aims of transplantation medicine. Stem cells are promising candidates for promoting donor-specific tolerance. In this study, we investigated the immunomodulatory properties of ...

Abstract	Tolerance induction toward allogeneic organ grafts represents one of the major aims of transplantation medicine. Stem cells are promising candidates for promoting donor-specific tolerance. In this study, we investigated the immunomodulatory properties of murine embryonic stem cells (ESCs), obtained either by in vitro fertilization (IVF-ESCs) or by nuclear transfer (NT-ESCs), in heart transplant mouse models. IVF-ESCs did not prolong the survival of fully allogeneic cardiac transplants but significantly prolonged the survival of semiallogeneic hearts from the same ESC donor strain for >100 d in 44% of the animals. However, 28% of transplanted animals infused with IVF-ESCs experienced development of a teratoma. NT-ESCs similarly prolonged semiallogeneic heart graft survival (>100 d in 40% of the animals) but were less teratogenic. By in vitro studies, IVF-ESC and NT-ESC immunoregulation was mediated both by cell contact-dependent mechanisms and by the release of soluble factors. By adding specific inhibitors, we identified PGE(2) as a soluble mediator of ESC immunoregulation. Expansion of regulatory T cells was found in lymphoid organs and in the grafts of IVF-ESC- and NT-ESC-tolerized mice. Our study demonstrates that both IVF-ESCs and NT-ESCs modulate recipient immune response toward tolerance to solid organ transplantation, and that NT-ESCs exhibit a lower tendency for teratoma formation. Because NT-ESCs are obtained by NT of a somatic cell from living individuals into an enucleated oocyte, they could represent a source of donor-derived stem cells to induce tolerance to solid organ allograft.
MeSH term(s)	Adoptive Transfer ; Animals ; Cell Line ; Embryonic Stem Cells/immunology ; Embryonic Stem Cells/transplantation ; Female ; Fertilization in Vitro ; Graft Rejection/prevention & control ; Graft Survival/immunology ; Heart Transplantation/immunology ; Heart Transplantation/methods ; Heart Transplantation/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Nuclear Proteins/administration & dosage ; Random Allocation ; Transplantation, Homologous/immunology ; Transplantation, Homologous/pathology
Chemical Substances	Nuclear Proteins
Language	English
Publishing date	2011-04-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1000654
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Pretransplant infusion of mesenchymal stem cells prolongs the survival of a semiallogeneic heart transplant through the generation of regulatory T cells.

Casiraghi, Federica / Azzollini, Nadia / Cassis, Paola / Imberti, Barbara / Morigi, Marina / Cugini, Daniela / Cavinato, Regiane Aparecida / Todeschini, Marta / Solini, Samantha / Sonzogni, Aurelio / Perico, Norberto / Remuzzi, Giuseppe / Noris, Marina

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 181, Issue 6, Page(s) 3933–3946

Abstract: In this study, we investigated whether mesenchymal stem cells (MSC) had immunomodulatory properties in solid organ allotransplantation, using a semiallogeneic heart transplant mouse model, and studied the mechanism(s) underlying MSC tolerogenic effects. ... ...

Abstract	In this study, we investigated whether mesenchymal stem cells (MSC) had immunomodulatory properties in solid organ allotransplantation, using a semiallogeneic heart transplant mouse model, and studied the mechanism(s) underlying MSC tolerogenic effects. Either single (portal vein, day -7) or double (portal vein, day -7 and tail vein, day -1) pretransplant infusions of donor-derived B6C3 MSC in B6 recipients induced a profound T cell hyporesponsiveness and prolonged B6C3 cardiac allograft survival. The protolerogenic effect was abrogated when donor-derived MSC were injected together with B6C3 hematopoietic stem cells (HSC), suggesting that HSC negatively impact MSC immunomodulatory properties. Both the induction (pretransplant) and the maintenance phase (>100 days posttransplant) of donor-derived MSC-induced tolerance were associated with CD4(+)CD25(+)Foxp3(+) Treg expansion and impaired anti-donor Th1 activity. MSC-induced regulatory T cells (Treg) were donor-specific since adoptive transfer of splenocytes from tolerant mice prevented the rejection of fully MHC-mismatched donor-specific secondary allografts but not of third-party grafts. In addition, infusion of recipient-derived B6 MSC tolerized a semiallogeneic B6C3 cardiac allograft, but not a fully MHC-mismatched BALB/c graft, and expanded Treg. A double i.v. pretransplant infusion of recipient-derived MSC had the same tolerogenic effect as the combined intraportal/i.v. MSC infusions, which makes the tolerogenic protocol applicable in a clinical setting. In contrast, single MSC infusions given either peritransplant or 1 day after transplant were less effective. Altogether these findings indicate that MSC immunomodulatory properties require HSC removal, partial sharing of MHC Ags between the donor and the recipient and pretransplant infusion, and are associated with expansion of donor-specific Treg.
MeSH term(s)	Animals ; Bone Marrow Cells/immunology ; Cell Differentiation/immunology ; Female ; Graft Survival/immunology ; Heart Transplantation/immunology ; Heart Transplantation/methods ; Male ; Mesenchymal Stem Cell Transplantation/methods ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; Transplantation Conditioning/methods ; Transplantation Tolerance/immunology ; Transplantation, Heterotopic ; Transplantation, Homologous ; Transplantation, Isogeneic
Language	English
Publishing date	2008-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.181.6.3933
Database	MEDical Literature Analysis and Retrieval System OnLINE

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