Reduction of DNA hydroxymethylation in the mouse kidney insulted by ischemia reperfusion.

Abstract

Ischemia reperfusion (IR) is a frequent pathological injury to the perioperative patients. The molecular mechanism underlying IR injury is still not well characterized. In this study, we investigated the effect of IR injury on DNA hydroxymethylation in mouse kidney. Dot blot and immunochemistry analysis showed that the global level of 5-hydroxymethylcytosine (5hmC) was reduced in mouse kidney insulted by IR; however, the 5-methylcytosine (5mC) level had no significant change. hMeDIP-qPCR validated that IR injury also decreased the 5hmC enrichment at promoter regions of Cxcl10 and Ifngr2 genes. RT-qPCR analysis revealed that the mRNA levels of Cxcl10 and Ifngr2 increased in IR-injured kidney. In addition, mRNA expression of both Tet1 and Tet2 but not Tet3 was dramatically downregulated in IR-injured kidney. Taken together, our data provided the first evidence that IR injury influences DNA hydroxymethylation and Tet gene expression in mouse kidney, which may contribute to the regulation of gene transcription during renal IR injury.

• Authors: Ning Huang, Li Tan, Zhanggang Xue, Jing Cang, Hao Wang
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 422 Issue 4 Pg. 697-702 (Jun 15 2012) ISSN: 1090-2104 [Electronic] United States
• PMID: 22627137 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2012 Elsevier Inc. All rights reserved.

Chemical References

• Chemokine CXCL10
• Cxcl10 protein, mouse
• DNA-Binding Proteins
• Ifngr2 protein, mouse
• Proto-Oncogene Proteins
• Receptors, Interferon
• TET1 protein, mouse
• 5-hydroxymethylcytosine
• 5-Methylcytosine
• Cytosine
• Dioxygenases
• TET2 protein, human
• Tet3 protein, mouse

Topics

• 5-Methylcytosine (analogs & derivatives)
• Animals
• Chemokine CXCL10 (genetics)
• Cytosine (analogs & derivatives, metabolism)
• DNA Methylation
• DNA-Binding Proteins (genetics)
• Dioxygenases
• Disease Models, Animal
• Gene Expression Regulation
• Kidney (blood supply)
• Male
• Mice
• Mice, Inbred C57BL
• Proto-Oncogene Proteins (genetics)
• Receptors, Interferon (genetics)
• Reperfusion Injury (genetics)