Poster Topical Area: Nutrient-Gene Interactions

Location: Hall D

Poster Board Number: 429

P17-006 - Altered expression levels of Tet methylcytosine dioxygenases in endothelial progenitor cells of patients of type 2 diabetes with complications

Sunday, Jun 10
8:00 AM – 6:00 PM

Objectives: Endothelial progenitor cells (EPCs) repair microvascular to prevent the complications in patients with diabetes. Epigenetic changes such as DNA methylation alter the functions of cells. Tet methylcytosine dioxygenases (TETs) are enzymes responsible for the conversion of 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine, cytosine derivatives in genomic DNA during the process of demethylation. Here, we determined the TETs expression levels in EPCs of patients with diabetic complications.


Methods: Subjects who were non-diabetic (ND), diabetic only (D) and diabetic with complications (DC) were recruited for the collection of EPCs during June 2016 to October 2016. EPCs from blood samples of 22 ND, 29 D, and 22 DC subjects with signed informed consent form were isolated and subjected to analysis. The expression levels of TET1/2/3 mRNA and proteins were determined using real-time PCR and immunoblot, respectively.


Results: The TET1 mRNA expression level in ND group is higher than that in D and DC groups. The TET3 mRNA level in ND is higher than that in D group, which is higher than that in DC group. The TET1 protein level in DC group, but not D group, is higher than that in ND group. The TET2 protein level in DC group, but not D group, is lower than that in ND group. The TET3 protein level in ND group is higher than that in D group, which is higher than that in DC group. TET3 protein level in DC group is the lowest in the three group. The results of TETs mRNA and protein levels largely matched to each other.


Conclusions: The expression levels of TET 1 and 3 proteins are lowered in EPCs of patients with diabetic complications, suggesting the changes of genomic DNA methylation and the functions of EPCs. This phenomenon may contribute to microvascular complications in diabetic patients.




Funding Source: The National Natural Science Foundation of China for financial support (No.81370942 to S. Zhao).

CoAuthors: Shi Zhao – Wuhan Central Hospital; Zihui Xu – Wuhan Central Hospital; Ting Jia – Wuhan Central Hospital; Yang Tang – Nanyang Technological University; Hong Mao – Wuhan Central Hospital; Wei Wei – Wuhan Central Hospital; Peirong Zhong – Wuhan University; Lu Ma – Wuhan University; Rui Li – Wuhan University

Guoxun Chen


The University of Tennessee, Knoxville
Knoxville, Tennessee