Inhibition of Prolyl-4-Hydroxylase Ameliorates Chronic Rejection of Mouse Kidney Allografts

Franceschini, Nora; Cheng, Orlena; Zhang, Xiaojie; Ruiz, Phillip; Mannon, Roslyn B.

doi:10.1034/j.1600-6143.2003.00081.x

Cited by 14 publications

(9 citation statements)

References 45 publications

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“…Therefore, novel therapies for CAN are needed to promote long-term graft survival. In the renal transplantation model of B6 donor mice to BALB/c recipient mice, the grafts develop pathological abnormalities after 6 wk that resemble chronic rejection in humans (30,31), and this model has been used in preclinical study of therapy for CAN (12). Our previous study demonstrated that pharmacological intervention of ERK1/2 signaling prolongs cardiac allograft survival (56).…”

Section: Discussionmentioning

confidence: 99%

Reduction of chronic allograft nephropathy by inhibition of extracellular signal-regulated kinase 1 and 2 signaling

Wang¹,

Jiang²,

Guan³

et al. 2008

American Journal of Physiology-Renal Physiology

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Section: Discussionmentioning

confidence: 99%

Reduction of chronic allograft nephropathy by inhibition of extracellular signal-regulated kinase 1 and 2 signaling

Wang¹,

Jiang²,

Guan³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…Mouse models are essential in the study of mechanisms of acute [1–3] and chronic kidney transplant rejection [4–6]. They are especially important for the investigation of the role of certain genes in transplant rejection by studying knockout, transgenic, congenic, and inbred mouse strains [7].…”

Section: Introductionmentioning

confidence: 99%

A Knotless Technique for Kidney Transplantation in the Mouse

Rong

Lewis

Kunter

et al. 2012

Journal of Transplantation

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Mouse models of kidney transplantation are important to study molecular mechanisms of organ transplant rejection as well as to develop new therapeutic strategies aimed at improving allograft survival. However, the surgical technique necessary to result in a viable allograft has traditionally proven to be complex and very demanding. Here, we introduce a new, simple, and rapid knotless technique for vessel anastomosis wherein the last stitch of the anastomosis is not tied to the short end of the upper tie as in the classical approach but is left free. This is a critical difference in that it allows the size of the anastomosis to be increased or decreased after graft reperfusion in order to avoid stenosis or bleeding, respectively. We compared the outcome of this new knotless technique (n = 175) with the classical approach (n = 122) in terms of local thrombosis or bleeding, time for anastomosis, and survival rates. By this modification of the suture technique, local thrombosis was significantly reduced (1.1% versus 6.6%), anastomosis time was less, and highly reproducible kidney graft survival was achieved (95% versus 84% with the classical approach). We believe that this knotless technique is easy to learn and will improve the success rates in the technically demanding model of mouse kidney transplantation.

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“…For example, blockade of prolyl-4-hydroxylase, a rate-limiting step in collagen biosynthesis (126,127), resulted not only in a reduction of fibrosis and graft inflammation but also in improved graft function compared with vehicle-treated controls, with no evidence of gross toxicity in the mouse (128). Inhibition of matrix metalloproteinase enzymes, regulatory enzymes in matrix degradation, ameliorate proteinuria and histology in rat kidney allografts, depending on the time course of dosing (129).…”

Section: Abrogating Matrix Deposition: Novel Approachesmentioning

confidence: 99%

Late Kidney Allograft Loss

Jevnikar

Mannon

2008

Clinical Journal of the American Society of Nephrology

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103

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Despite dramatic improvements in immunosuppression, late graft loss after kidney transplantation remains a common and difficult problem. Histologic evaluation may reveal changes related to BK polyomavirus infection, hypertension, or calcineurin inhibitor toxicity, which can help to guide therapy. The designation chronic allograft nephropathy should thus be reserved for biopsies with tubular atrophy and interstitial fibrosis without an apparent cause. Although the cause clearly includes both antigen-dependent and antigen-independent events, the approach remains largely to exclude immune mechanisms. Although this review discusses the potential contribution of antibody to chronic injury, it focuses on the basic elements of kidney injury, the role of parenchymal cells in promoting injury, and the proliferative and inflammatory responses that accompanying injury. Strategies to manage these recipients include close attention to accompanying hypertension, diabetes, and hyperlipidemia, as well as consideration for altering immunosuppression; however, therapies that limit epithelial-to-mesenchymal transition or directly block fibrosis pathways may reduce chronic allograft fibrosis and may prove to be useful. Understanding the basic pathogenesis sufficiently to allow early intervention may finally benefit patients who are at high risk for tubular atrophy and interstitial fibrosis and promote their long-term graft function.

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Inhibition of Prolyl-4-Hydroxylase Ameliorates Chronic Rejection of Mouse Kidney Allografts

Cited by 14 publications

References 45 publications

Reduction of chronic allograft nephropathy by inhibition of extracellular signal-regulated kinase 1 and 2 signaling

Reduction of chronic allograft nephropathy by inhibition of extracellular signal-regulated kinase 1 and 2 signaling

A Knotless Technique for Kidney Transplantation in the Mouse

Late Kidney Allograft Loss

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