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  1. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3344: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 169: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. 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

    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 ...

    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

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 169: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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