Renal PKC epsilon deficiency attenuates acute kidney injury and ischemic allograft 1 injury via TNF alpha dependent inhibition of apoptosis and inflammation

نویسندگان

  • Song Rong
  • Katja Hueper
  • Torsten Kirsch
  • Robert Greite
  • Christian Klemann
  • Matthias Meier
  • Jan Menne
  • Michael Leitges
  • Nathan Susnik
  • Martin Meier
  • Hermann Haller
  • Nelli Shushakova
  • Faikah Gueler
چکیده

1 injury via TNF alpha dependent inhibition of apoptosis and inflammation 2 3 Song Rong, Katja Hueper, Torsten Kirsch, Robert Greite, Christian Klemann, Michael 4 Mengel, Matthias Meier, Jan Menne, Michael Leitges, Nathan Susnik, Martin Meier, 5 Hermann Haller, Nelli Shushakova, Faikah Gueler 6 7 8 Correspondence to: 9 Prof. Faikah Gueler, 10 Department of Nephrology 11 Medical School Hannover, 12 Carl-Neuberg-Str.1, 30625 Hannover, 13 Tel: 0049-511-532 3722, Fax: 0049-511-552366 14 email: [email protected] 15 16 Department of Nephrology, Hannover Medical School, Hannover, Germany 17 Phenos GmbH, Hannover, Germany 18 The Transplantation Center of the affiliated hospital, Zunyi Medical College, China 19 Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, 20 Canada 21 The Biotechnology Centre of Oslo, University of Oslo 22 Institute for Diagnostic and Interventional Radiology, Medical School Hannover, Hannover, 23 Germany 24 Articles in PresS. Am J Physiol Renal Physiol (July 23, 2014). doi:10.1152/ajprenal.00372.2013

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Renal PKC-ε deficiency attenuates acute kidney injury and ischemic allograft injury via TNF-α-dependent inhibition of apoptosis and inflammation.

Acute kidney injury (AKI) increases the risk of morbidity and mortality after major surgery and transplantation. We investigated the effect of PKC-ε deficiency on AKI and ischemic allograft damage after kidney transplantation. PKC-ε-deficient and wild type (WT) control mice were subjected to 35 min of renal pedicle clamping to induce AKI. PKC-ε deficiency was associated with a marked improvemen...

متن کامل

Protective role of remote ischemic per-conditioning in acute renal injury induced by ischemia reperfusion via TLR-4 and TNF-α signaling pathway in rats

sIntroduction: Acute kidney injury (AKI) induced by ischemia-reperfusion (I / R) of the kidney as an inflammatory process in which multiple inflammatory factors are involved. Recently, one of the modalities of inflammation in AKI is Remote Ischemic Per-Conditioning (RIPerC). Materials and Methods: In this study, bilateral renal artery and vein occlusion were done for 45 minute and reperfusion a...

متن کامل

In vivo effects of allogeneic mesenchymal stem cells in a rat model of acute ischemic kidney injury

Objective(s): Renal ischemia-reperfusion injury (IRI) as a severe condition of acute kidney injury (AKI) is the most common clinical problem with high mortality rates of 35-60% deaths in hospital. Mesenchymal stem cells (MSC) due to unique regenerative characteristics are ideal candidates for the treatment of the ischemic injuries. This work is focused on the administration of MSC to IRI-induce...

متن کامل

Ischemic proximal tubular injury primes mice to endotoxin-induced TNF-alpha generation and systemic release.

Endotoxemia (LPS) can exacerbate ischemic tubular injury and acute renal failure (ARF). The present study tested the following hypothesis: that acute ischemic damage sensitizes the kidney to LPS-mediated TNF-alpha generation, a process that can worsen inflammation and cytotoxicity. CD-1 mice underwent 15 min of unilateral renal ischemia. LPS (10 mg/kg iv), or its vehicle, was injected either 45...

متن کامل

p38 MAP kinase inhibition ameliorates cisplatin nephrotoxicity in mice.

Cisplatin is an important chemotherapeutic agent but can cause acute renal injury. Part of this acute renal injury is mediated through tumor necrosis factor-alpha (TNF-alpha). The pathway through which cisplatin mediates the production of TNF-alpha and injury is not known. Cisplatin activates p38 MAPK and induces apoptosis in cancer cells. p38 MAPK activation leads to increased production of TN...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2014