B Moulin

University of Strasbourg, Strasburg, Alsace, France

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Publications (186)539.27 Total impact

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    ABSTRACT: Introduction Les leucémies lymphoïdes chroniques et lymphomes lymphocytaires B à petites cellules sont 2 variantes d’une même pathologie (CLL/SLL). Le spectre des atteintes rénales associées à la CLL/SLL est mal décrit dans la littérature, principalement sous forme de cas isolés de glomérulopathies à médiation immunologique ou d’infiltration interstitielle. Patients et méthodes Ce travail propose une description systématique des atteintes rénales associées aux CLL/SLL. La population est constituée des 15 patients CLL/SLL ayant bénéficié d’une biopsie rénale au CHU de Rouen entre 1989 et 2013. Les données clinico-biologiques ansi qu’une réanalyse histologique et immunohistologique des biopsies ont été colligées. Résultats L’âge moyen était de 65,2 ans. L’hémopathie précédait le diagnostic rénal dans 47 % des cas, le diagnostic était simultané dans 40 % des cas. À la date de la PBR, 11 patients présentaient une insuffisance rénale, 7 un syndrome néphrotique, 6 une dysprotéinémie (dont 3 cryoglobulinémies). Dix biopsies ont montré un infiltrat interstitiel spécifique, 9 une glomérulopathie (5 GMNP, 2 LGM, 1 GOMMID, 1 amylose AHL). Cinq patients présentaient des granulomes interstitiels. La durée moyenne de suivi était de 7,2 années. Après traitement de l’hémopathie, l’évolution a été marquée par une rémission complète du syndrome néphrotique dans 5/7 cas, une amélioration de la créatininémie chez 7/11 patients. 6/15 patients ont nécessité une prise en charge en dialyse. Discussion et conclusion Cette étude correspond, à ce jour, à la description de la plus large série de patients CLL/SLL présentant une atteinte rénale. Elle montre la diversité des lésions rénales associées à cette pathologie, infiltratives ou immunologiques, et identifie notamment une prévalence importante d’atteintes granulomateuses, rarement rapportées dans la littérature.
    Néphrologie & Thérapeutique. 09/2014; 10(5):276.
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    ABSTRACT: Introduction Les glomérulonéphrites membrano-prolifératives (GNMP) forment un groupe de maladies hétérogènes dont la classification histopathologique a été récemment modifiée en se basant sur des critères physiopathologiques. On distingue désormais deux classes de GNMP, l’une avec dépôts de C3 prédominants (GNMP C3) associée à des anomalies de la voie alterne du complément (AVAC) et l’autre avec dépôts de complexes immuns [1]. L’objectif de cette étude a été de reclasser une cohorte rétrospective de GNMP et de glomérulonéphrites à dépôts isolés de C3 (GNC3) selon la nouvelle classification, et d’évaluer l’implication de cette démarche notamment en ce qui concerne la mise en évidence d’une AVAC. Patients et méthodes Nous avons relu les comptes rendus de 2100 biopsies effectuées dans notre région sur 10 ans et retenus 128 biopsies avec un diagnostic de GNMP ou GNC3. Les biopsies ont été relues par le même néphropathologiste. Les patients greffés ont été analysés à part pour les cas récidives. Résultats Après relecture, les 128 cas étaient répartis selon l’ancienne classification en : 86 GNMP de type 1, 2 GN à dépôts denses, 10 GNMP de type 3 et 30 GNC3. Après application de la nouvelle classification on retrouvait 85 cas de GNMP à dépôts de complexes immuns (14 monotypiques et 71 polytypiques), 12 GNMP C3 et 31 cas de GNC3. La réanalyse des biopsies a abouti à un changement de classement histologique principalement pour 8 cas de GNMP type 1 reclassés en GNMP C3. Parmi les 43 cas de GNC3 + GNMP C3, seulement 17 patients avaient bénéficié d’une recherche d’AVAC qui était positive dans 8 cas, la recherche d’AVAC est en cours pour les 26 autres cas. Discussion et conclusion Notre étude régionale indique l’intérêt de reprendre les anciens diagnostics de GNMP, de les reclasser à l’aide de la nouvelle classification physiopathologique conduisant à la recherche d’ AVAC jusqu’alors non identifiées. Cette stratégie est notamment importante dans le contexte de recherche de mutation familiale ou de projet de greffe de rein.
    Néphrologie & Thérapeutique. 09/2014; 10(5):271.
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    Annales de biologie clinique 08/2014; 72(4):385-389. · 0.30 Impact Factor
  • Nephrologie & therapeutique. 06/2014;
  • Bruno Moulin, Luc Frimat
    Néphrologie & Thérapeutique 04/2014; 10(2):71-3. · 0.50 Impact Factor
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    ABSTRACT: Introduction Several studies have indicated that impaired GFR is an important predictor factor associated with impaired platelet inhibition by clopidogrel. In chronic kidney disease, the presence of low platelet inhibition by clopidogrel is associated with adverse outcome following PCI and stenting. In the present study, we sought to determine if renal transplantation per se alters clopidogrel pharmacodynamics. Patients and methods 36 patients with kidney transplantation were enrolled in one single center (Nephrology Department, Hôpitaux Universitaires de Strasbourg). Control patients were 126 patients with different degrees of chronic renal failure, tested in the same conditions. Inclusion criteria were patients under clopidogrel treatment of 75mg per day for at least 8 days. Unstable patients or those presenting with any conditions that could account for reduced platelet inhibition by clopidogrel (heart failure, shock) were excluded. Treatment and medical history were collected at inclusion. Clopidogrel pharmacodynamics was studied using the VASP assay. Results Patients with kidney transplantation were younger (58.3 vs 72.6 years, p<0.001), less likely diabetics (39% vs 57%, p=0.12), presented a lower BMI (25.2 sv 27.2 p=0,05), the estimated glomerular filtration rate with the MDRD formula is better (47.9 vs 39.5ml/mn/1.73m2, p=0.15), and there is less inflammation. 89% patients in the transplantation group were under anti-calcineurin and 50% under steroids at low dose. Platelet reactivity Index a marker of the extent of P2Y12 inhibition was significantly higher in the transplantation group vs controls (60.1% vs 51.2% p=0.014). By multivariate analysis, high BMI and kidney transplantation were important predictors of residual platelet reactivity under clopidogrel treatment. After adjustment on eGFR with the MDRD formula, kidney transplantation remains an important predictor of alter P2Y12 inhibition. Conclusion In kidney transplantation patients treated by clopidogrel, impaired platelet inhibition exist, even after adjustment on estimated glomerular filtration rate. The mechanisms by which immunosuppressive treatments may alter clopidogrel pharmacodynamics requires further investigation
    Archives of Cardiovascular Diseases Supplements 04/2014; 6:4.
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    ABSTRACT: EBV contributes the pathogenesis of PTLD in more than 70% of the cases. EBV DNAemia surveillance has been reported to assist in prevention and treatment of PTLD in hematopoietic stem-cell transplantation recipients (HSCT). Derived from experience in HSCT and taking into account that PCR-based EBV monitoring techniques are currently available in most solid organ transplant (SOT) centres there is a great interest in EBV surveillance and prevention of PTLD in SOT recipients. In the present document we have tried to address from a practical perspective different important topics regarding the prevention and management of EBV-related in SOT. To this end, available information in SOT was analysed and combined with potentially useful data from HSCT and expert observations. The document is therefore structured according to different specific questions each of them culminated by a consensus opinion of the panel of European experts, grading the answers according to internationally recognized levels of evidence. The addressed issues were grouped in the following topics:1) Timing and epidemiological data of PTLD. Prophylaxis guided by clinical risk factors of early and late PTLD in SOT.2) Relationship of EBV DNAemia load monitoring and the development of PTLD in solid organ transplant recipients. 3) Monitoring of EBV DNAemia after SOT. Which population should be monitored?. What is the optimal timing of the monitoring?.4)Management of SOT recipients with persistent and/or increasing EBV DNAemia. This article is protected by copyright. All rights reserved.
    Clinical Microbiology and Infection 01/2014; · 4.58 Impact Factor
  • Néphrologie & Thérapeutique. 01/2014;
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    ABSTRACT: In a six-month, multicenter, open-label trial, de novo kidney transplant recipients at low immunological risk were randomized to steroid avoidance or steroid withdrawal with IL-2 receptor antibody (IL-2RA) induction, enteric-coated mycophenolate sodium (EC-MPS: 2160 mg/day to week 6, 1440 mg/day thereafter), and cyclosporine. Results from a 30-month observational follow-up study are presented. Of 166 patients who completed the core study on treatment, 131 entered the follow-up study (70 steroid avoidance, 61 steroid withdrawal). The primary efficacy endpoint of treatment failure (clinical biopsy-proven acute rejection (BPAR) graft loss, death, or loss to follow-up) occurred in 21.4% (95% CI 11.8-31.0%) of steroid avoidance patients and 16.4% (95% CI 7.1-25.7%) of steroid withdrawal patients by month 36 (P = 0.46). BPAR had occurred in 20.0% and 11.5%, respectively (P = 0.19). The incidence of adverse events with a suspected relation to steroids during months 6-36 was 22.9% versus 37.1% (P = 0.062). By month 36, 32.4% and 51.7% of patients in the steroid avoidance and steroid withdrawal groups, respectively, were receiving oral steroids. In conclusion, IL-2RA induction with early intensified EC-MPS dosing and CNI therapy in de novo kidney transplant patients at low immunological risk may achieve similar three-year efficacy regardless of whether oral steroids are withheld for at least three months.
    Journal of Transplantation 01/2014; 2014:171898.
  • Néphrologie & Thérapeutique. 01/2014;
  • Néphrologie & Thérapeutique 10/2013; · 0.50 Impact Factor
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    ABSTRACT: The risk of fractures after kidney transplantation is high. Hyperparathyroidism frequently persists after successful kidney transplantation and contributes to bone loss, but its impact on fracture has not been demonstrated. This longitudinal study was designed to evaluate hyperparathyroidism and its associations with mineral disorders and fractures in the 5 posttransplant years. We retrospectively analyzed 143 consecutive patients who underwent kidney transplantation between August 2004 and April 2006. The biochemical parameters were determined at transplantation and at 3, 12 and 60 months posttransplantation, and fractures were recorded. The median intact parathyroid hormone (PTH) level was 334 ng/L (interquartile 151-642) at the time of transplantation and 123 ng/L (interquartile 75-224) at 3 months. Thirty fractures occurred in 22 patients. The receiver operating characteristic (ROC) curve analysis for PTH at 3 months (area under the ROC curve = 0.711, p = 0.002) showed that a good threshold for predicting fractures was 130 ng/L (sensitivity = 81%, specificity = 57%). In a multivariable analysis, independent risk factors for fracture were PTH >130 ng/L at 3 months (adjusted hazard ratio [AHR] = 7.5, 95% CI 2.18-25.50), and pretransplant osteopenia (AHR = 2.7, 95% CI 1.07-7.26). In summary, this study demonstrates for the first time that persistent hyperparathyroidism is an independent risk factor for fractures after kidney transplantation.
    American Journal of Transplantation 08/2013; · 6.19 Impact Factor
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    ABSTRACT: Overimmunosuppression is a widely recognized risk factor for BK virus (BKV) infection, particularly with the combination of tacrolimus, mycophenolate mofetil (MMF), and steroids. Nevertheless, the exact impact of exposure to tacrolimus and MMF is not well understood. We examined 240 kidney recipients between 2006 and 2008. BKV was monitored every 2 months in the urine or blood. A kidney biopsy was performed when viremia exceeded 10 copies/mL. Ninety-five (40%) patients had sustained viruria, 48 (20%) sustained viremia, and 17 (7%) biopsy-proven polyomavirus-associated nephropathy. The mean time-to-occurrence was 7.6, 7.9, and 9.7 months for viruria, viremia, and polyomavirus-associated nephropathy. Risk factors associated with BKV infection in univariate analyses were retransplantation, panel-reactive antibody more than 0%, cytomegalovirus D+/R-, cold ischemia time, delayed graft function, induction with antithymocyte globulins, acute rejection before month 3 (M3), tacrolimus trough levels more than 10 ng/mL, and M3 AUC0-12 hr more than 50 hr mg/L. Multivariate analyses showed that cytomegalovirus D+/R- (adjusted hazard ratio [AHR], 2.03; P=0.05), acute rejection (AHR, 5.4; P<0.001), and mycophenolic acid AUC0-12 hr more than 50 hr mg/L (AHR, 3.6; P=0.001) were risk factors for BKV. This study identified a link between a state of increased immunosuppression and BKV infection, especially in patients with higher MMF exposure and elevated tacrolimus trough levels at M3.
    Transplantation 06/2013; 95(12):1498-505. · 3.78 Impact Factor
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    ABSTRACT: Atypical hemolytic-uremic syndrome is a genetic, life-threatening, chronic disease of complement-mediated thrombotic microangiopathy. Plasma exchange or infusion may transiently maintain normal levels of hematologic measures but does not treat the underlying systemic disease. We conducted two prospective phase 2 trials in which patients with atypical hemolytic-uremic syndrome who were 12 years of age or older received eculizumab for 26 weeks and during long-term extension phases. Patients with low platelet counts and renal damage (in trial 1) and those with renal damage but no decrease in the platelet count of more than 25% for at least 8 weeks during plasma exchange or infusion (in trial 2) were recruited. The primary end points included a change in the platelet count (in trial 1) and thrombotic microangiopathy event-free status (no decrease in the platelet count of >25%, no plasma exchange or infusion, and no initiation of dialysis) (in trial 2). A total of 37 patients (17 in trial 1 and 20 in trial 2) received eculizumab for a median of 64 and 62 weeks, respectively. Eculizumab resulted in increases in the platelet count; in trial 1, the mean increase in the count from baseline to week 26 was 73×10(9) per liter (P<0.001). In trial 2, 80% of the patients had thrombotic microangiopathy event-free status. Eculizumab was associated with significant improvement in all secondary end points, with continuous, time-dependent increases in the estimated glomerular filtration rate (GFR). In trial 1, dialysis was discontinued in 4 of 5 patients. Earlier intervention with eculizumab was associated with significantly greater improvement in the estimated GFR. Eculizumab was also associated with improvement in health-related quality of life. No cumulative toxicity of therapy or serious infection-related adverse events, including meningococcal infections, were observed through the extension period. Eculizumab inhibited complement-mediated thrombotic microangiopathy and was associated with significant time-dependent improvement in renal function in patients with atypical hemolytic-uremic syndrome. (Funded by Alexion Pharmaceuticals; C08-002 ClinicalTrials.gov numbers, NCT00844545 [adults] and NCT00844844 [adolescents]; C08-003 ClinicalTrials.gov numbers, NCT00838513 [adults] and NCT00844428 [adolescents]).
    New England Journal of Medicine 06/2013; 368(23):2169-81. · 54.42 Impact Factor
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    ABSTRACT: Parathyroid hormone related protein (PTHrP) belongs to vasoactive factors that regulate blood pressure and renal hemodynamics both by reducing vascular tone and raising renin release. PTHrP is expressed in systemic and renal vasculature. Here we wanted to assess the contribution of vascular smooth muscle cell endogenous PTHrP to the regulation of cardiovascular and renal functions. We generated a mouse strain (SMA-CreER(T2)/PTHrP(L2/L2) or premutant PTHrP(SM-/-)) which allows temporally-controlled, smooth muscle targeted PTHrP knockdown in adult mice. Tamoxifen treatment induced efficient recombination of PTHrP floxed alleles, and decreased PTHrP expression in vascular and visceral smooth muscle cells of PTHrP(SM-/-) mice. Blood pressure remained unchanged in PTHrP(SM-/-) mice, but plasma renin concentration and creatinine clearance were reduced. Renal hemodynamics were further analyzed during clearance measurements in anaesthetized mice. Conditional knockdown of PTHrP decreased renal plasma flow and glomerular filtration rate with concomitant reduction in filtration fraction. Similar measurements were repeated during acute saline volume expansion. Saline volume expansion induced a rise in renal plasma flow and reduced filtration fraction; both were blunted in PTHrP(SM-/-) mice leading to impaired diuresis. These findings show that endogenous vascular smooth muscle PTHrP controls renal hemodynamics under basal conditions, and is an essential factor in renal vasodilation elicited by saline volume expansion.
    AJP Renal Physiology 05/2013; · 4.42 Impact Factor
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    ABSTRACT: Patients with chronic kidney disease (CKD) represent an increasing proportion of the population undergoing percutaneous coronary intervention (PCI) and up to 40% of the patients treated for acute coronary syndrome (ACS). Several studies and registries in the setting of ACS and elective PCI have reported a negative association between CKD and mortality, stent thrombosis, post-procedural ischaemic events and bleeding events. Pharmacological inhibition of the adenosine diphosphate receptor by thienopyridines or ticagrelor and disruption of the cyclooxygenase pathway by aspirin constitute the current standards of care to prevent thrombotic complications following stent-based PCI. In CKD patients, the avoidance of anti-platelet therapy may be driven by the lack of clinical trial data to support its efficacy, by errors or omissions, or by a reluctance to use this therapy in a population characterized by its enhanced bleeding risk. However, there is growing evidence to suggest that a severely decreased glomerular filtration rate per se, independent of the presence of diabetes mellitus, is an important determinant of high residual platelet reactivity under a clopidogrel maintenance dose. Recent reports have emphasized that the impact of impaired platelet inhibition by thienopyridines is of paramount importance in CKD patients, with an enhanced mortality rate in low-responder patients. Pharmacodynamic studies indicate the phosphodiesterase 3 inhibitor, cilostazol, the third generation thienopyridine prasugrel and the reversible P2Y12 antagonist ticagrelor to be potent strategies to overcome this biological resistance. In clinical practice, platelet function testing should be considered in CKD patients undergoing PCI, especially in those who experience thrombotic events despite dual therapy. Newer agents should be contemplated in patients who display higher residual platelet aggregability after standard treatment. Among these, the non-thienopyridine P2Y12 receptor antagonist ticagrelor, which does not require biotransformation, could be the drug of choice in CKD patients with ACS. In this population, ticagrelor has been found to reduce mortality and ischaemic events with an acceptable bleeding risk.
    Nephrology Dialysis Transplantation 03/2013; · 3.37 Impact Factor
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    ABSTRACT: PURPOSEPost-transplantation lymphoproliferative disorder (PTLD) is associated with significant mortality in kidney transplant recipients. We conducted a prospective survey of the occurrence of PTLD in a French nationwide population of adult kidney recipients over 10 years. PATIENTS AND METHODSA French registry was established to cover a nationwide population of transplant recipients and prospectively enroll all adult kidney recipients who developed PTLD between January 1, 1998, and December 31, 2007. Five hundred patient cases of PTLD were referred to the French registry. The prognostic factors for PTLD were investigated using Kaplan-Meier and Cox analyses.ResultsPatients with PTLD had a 5-year survival rate of 53% and 10-year survival rate of 45%. Multivariable analyses revealed that age > 55 years, serum creatinine level > 133 μmol/L, elevated lactate dehydrogenase levels, disseminated lymphoma, brain localization, invasion of serous membranes, monomorphic PTLD, and T-cell PTLD were independent prognostic indicators of poor survival. Considering five variables at diagnosis (age, serum creatinine, lactate dehydrogenase, PTLD localization, and histology), we constructed a prognostic score that classified patients with PTLD as being at low, moderate, high, or very high risk for death. The 10-year survival rate was 85% for low-, 80% for moderate-, 56% for high-, and 0% for very high-risk recipients. CONCLUSION This nationwide study highlights the prognostic factors for PTLD and enables the development of a new prognostic score. After validation in an independent cohort, the use of this score should allow treatment strategies to be better tailored to individual patients in the future.
    Journal of Clinical Oncology 02/2013; · 18.04 Impact Factor
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    ABSTRACT: Atypical hemolytic and uremic syndrome (aHUS) is a severe disease strongly associated with genetic abnormalities in the complement alternative pathway. In renal posttransplantation, few data are available on recurrence risk and graft outcome according to genetic background in aHUS patients. The aim of this study was to identify risk factors for recurrence and transplant outcome and, in particular, the role of complement gene abnormalities. We retrospectively studied 57 aHUS patients who had received 71 renal transplants. A mutation in complement gene was identified in 39 (68%), in factor H (CFH), factor I (CFI), membrane cofactor-protein (MCP), C3 and factor B (CFB). At 5 years, death-censored graft survival was 51%. Disease recurrence was associated with graft loss (p = 0.001). Mutations in complement genes were associated with higher risk of recurrence (p = 0.009). Patients with CFH or gain of function (C3, CFB) mutations had a highest risk of recurrence. M-TOR inhibitor was associated with significant risk of recurrence (p = 0.043) but not calcineurin inhibitor immunosuppressive treatment (p = 0.29). Preemptive plasmatherapy was associated with a trend to decrease recurrence (p = 0.07). Our study highlights that characterization of complement genetic abnormalities predicts the risk of recurrence-related graft loss and paves the way for future genetically based individualized prophylactic therapeutic strategies.
    American Journal of Transplantation 01/2013; · 6.19 Impact Factor
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    ABSTRACT: BACKGROUND AND OBJECTIVES: Atypical hemolytic uremic syndrome (aHUS) is a rare complement-mediated kidney disease that was first recognized in children but also affects adults. This study assessed the disease presentation and outcome in a nationwide cohort of patients with aHUS according to the age at onset and the underlying complement abnormalities. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: A total of 214 patients with aHUS were enrolled between 2000 and 2008 and screened for mutations in the six susceptibility factors for aHUS and for anti-factor H antibodies. RESULTS: Onset of aHUS occurred as frequently during adulthood (58.4%) as during childhood (41.6%). The percentages of patients who developed the disease were 23%, 40%, 70%, and 98% by age 2, 18, 40, and 60 years, respectively. Mortality was higher in children than in adults (6.7% versus 0.8% at 1 year) (P=0.02), but progression to ESRD after the first aHUS episode was more frequent in adults (46% versus 16%; P<0.001). Sixty-one percent of patients had mutations in their complement genes. The renal outcome was not significantly different in adults regardless of genetic background. Only membrane cofactor protein (MCP) and undetermined aHUS were less severe in children than adults. The frequency of relapse after 1 year was 92% in children with MCP-associated HUS and approximately 30% in all other subgroups. CONCLUSION: Mortality rate was higher in children than adults with aHUS, but renal prognosis was worse in adults than children. In children, the prognosis strongly depends on the genetic background.
    Clinical Journal of the American Society of Nephrology 01/2013; · 5.07 Impact Factor
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    ABSTRACT: Glomerulonephritis is characterized by the proliferation and apoptosis of mesangial cells (MC). The parathyroid-hormone related protein (PTHrP) is a locally active cytokine that affects these phenomena in many cell types, through either paracrine or intracrine pathways. The aim of this study was to evaluate the effect of both PTHrP pathways on MC proliferation and apoptosis. In vitro studies were based on MC from male transgenic mice allowing PTHrP-gene excision by a CreLoxP system. MC were also transfected with different PTHrP constructs: wild type PTHrP, PTHrP devoid of its signal peptide, or of its nuclear localization sequence. The results showed that PTHrP deletion in MC reduced their proliferation even in the presence of serum and increased their apoptosis when serum-deprived. PTH1R activation by PTHrP(1-36) or PTH(1-34) had no effect on proliferation but improved MC survival. Transfection of MC with PTHrP devoid of its signal peptide significantly increased their proliferation and minimally reduced their apoptosis. Overexpression of PTHrP devoid of its nuclear localization sequence protected cells from apoptosis without changing their proliferation. Wild type PTHrP transfection conferred both mitogenic and survival effects, which seem independent of midregion and C-terminal PTHrP fragments. PTHrP-induced MC proliferation was associated with p27(Kip1) down-regulation and c-Myc/E2F1 up-regulation. PTHrP increased MC survival through the activation of cAMP/protein kinase A and PI3-K/Akt pathways. These results reveal that PTHrP is a cytokine of multiple roles in MC, acting as a mitogenic factor only through an intracrine pathway, and reducing apoptosis mainly through the paracrine pathway. Thus, PTHrP appears as a probable actor in MC injuries.
    Endocrinology 01/2013; · 4.72 Impact Factor

Publication Stats

2k Citations
539.27 Total Impact Points

Institutions

  • 1999–2013
    • University of Strasbourg
      Strasburg, Alsace, France
  • 2010–2012
    • Université René Descartes - Paris 5
      Lutetia Parisorum, Île-de-France, France
    • Hospices Civils de Lyon
      Lyons, Rhône-Alpes, France
  • 1992–2010
    • CHRU de Strasbourg
      Strasburg, Alsace, France
  • 2006–2009
    • IHU de Strasbourg
      Strasburg, Alsace, France
  • 2007
    • Civil Hospital, Raikot
      Rāikot, Punjab, India
  • 2003
    • Centre Hospitalier Universitaire de Reims
      • Service de Neurologie
      Reims, Champagne-Ardenne, France
  • 1990–1995
    • Centre Hospitalier Universitaire Rouen
      Rouen, Upper Normandy, France
  • 1988–1995
    • Université de Rouen
      Mont-Saint-Aignan, Upper Normandy, France
  • 1989–1990
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France