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Int. J. Mol. Sci. 2016, 17(7), 1051; doi:10.3390/ijms17071051

Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple Signaling Pathways

Department of Nephrology, Shengjing Affiliated Hospital of China Medical University, Shenyang 110036, China
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Author to whom correspondence should be addressed.
Academic Editor: Ritva Tikkanen
Received: 4 April 2016 / Revised: 5 June 2016 / Accepted: 27 June 2016 / Published: 12 July 2016
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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Abstract

Stanniocalcin-1 (STC-1) protects against renal ischemia-reperfusion injury (RIRI). However, the molecular mechanisms remain widely unknown. STC-1 inhibits reactive oxygen species (ROS), whereas most ROS-mediated pathways are associated with ischemic injury. Therefore, to explore the mechanism, the effects of STC-1 on ROS-medicated pathways were studied. Non-traumatic vascular clamps were used to establish RIRI mouse models. The serum levels of STC-1, interleukin-6 (IL-6), interferon (IFN) γ, P53, and capase-3 were measured by ELISA kits. Superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by fluorescence spectrofluorometer. All these molecules changed significantly in a RIRI model mouse when compared with those in a sham control. Kidney cells were isolated from sham and model mice. STC-1 was overexpressed or knockout in these kidney cells. The molecules in ROS-medicated pathways were measured by real-time quantitative PCR and Western blot. The results showed that STC-1 is an effective ROS scavenger. The serum levels of STC-1, MDA and SOD activity were increased while the serum levels of IL-6, iIFN-γ, P53, and capase-3 were decreased in a model group when compared with a sham control (p < 0.05). Furthermore, the levels of STC-1,p53, phosphorylated mitogen-activated protein kinase kinase (p-MEKK-1), c-Jun N-terminal kinase (p-JNK), extracellular signal-regulated kinase (p-ERK), IkB kinase (p-IKK), nuclear factor (NF) κB, apoptosis signal-regulating kinase 1 (ASK-1) and caspase-3 changed significantly in kidney cells isolated from a RIRI model when compared to those isolated from a sham control (p < 0.05). Meanwhile, STC-1 overexpression or silence caused significant changes of the levels of these ROS-mediated molecules. Therefore, STC-1 maybe improve anti-inflammation, anti-oxidant and anti-apoptosis activities by affecting ROS-mediated pathways, especially the phospho-modifications of the respective proteins, resulting in the increase of SOD and reduce of capase-3, p53, IL-6 and IFN-γ. View Full-Text
Keywords: stanniocalcin-1; renal ischemia-reperfusion injury; apoptosis signal-regulating kinase 1; p-IkB kinase; extracellular signal-regulated kinase; protein kinase C; p-NF-κB; caspase-3; reactive oxygen species-mediated pathways; phosphorylated mitogen-activated protein kinase kinase stanniocalcin-1; renal ischemia-reperfusion injury; apoptosis signal-regulating kinase 1; p-IkB kinase; extracellular signal-regulated kinase; protein kinase C; p-NF-κB; caspase-3; reactive oxygen species-mediated pathways; phosphorylated mitogen-activated protein kinase kinase
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MDPI and ACS Style

Liu, D.; Shang, H.; Liu, Y. Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple Signaling Pathways. Int. J. Mol. Sci. 2016, 17, 1051.

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