Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance

Joint Authors

Liu, Juan
Xing, Xiangbin
Wu, Xinlin
Li, Xiang
Yao, Shun
Ren, Zi
Zeng, Haitao
Wu, Shaohong

Source

Cardiology Research and Practice

Issue

Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.

Publisher

Hindawi Publishing Corporation

Publication Date

2020-01-25

Country of Publication

Egypt

No. of Pages

12

Main Subjects

Diseases

Abstract EN

Background.

Individuals at a prediabetic stage have had an augmented cardiovascular disease (CVD) risk and CVD-related mortality compared to normal glucose tolerance (NGT) individuals, which may be attributed to the impaired vascular endothelial repair capacity.

In this study, circulating endothelial progenitor cells’ (EPCs) number and activity were evaluated, and the underlying mechanisms in premenopausal women with impaired glucose regulation were explored.

Methods.

Circulating EPCs’ number and activity and flow-mediated dilation (FMD) were compared in premenopausal women with NGT, isolated impaired fasting glucose (i-IFG), or isolated impaired glucose tolerance (i-IGT).

Plasma nitric oxide (NO), EPCs-secreted NO, and intracellular BH4 levels were also measured.

The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.

Results.

It was observed that the i-IGT premenopausal women not i-IFG premenopausal women had a significant reduction in circulating EPCs’ number and activity as well as reduced FMD when compared to NGT subjects.

Plasma NO levels or EPCs-secreted NO also decreased only in i-IGT women.

The expression of GTCPH I as well as intracellular BH4 levels declined in i-IGT women; however, the alternations of key proteins’ expression in the Tie2/Akt/eNOS signaling pathway were not observed in either i-IGT or i-IFG women.

Conclusions.

The endothelial repair capacity was impaired in i-IGT premenopausal women but was preserved in i-IFG counterparts.

The underlying mechanism may be associated with the downregulated GTCPH I pathway and reduced NO productions.

American Psychological Association (APA)

Liu, Juan& Xing, Xiangbin& Wu, Xinlin& Li, Xiang& Yao, Shun& Ren, Zi…[et al.]. 2020. Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance. Cardiology Research and Practice،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1152313

Modern Language Association (MLA)

Liu, Juan…[et al.]. Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance. Cardiology Research and Practice No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1152313

American Medical Association (AMA)

Liu, Juan& Xing, Xiangbin& Wu, Xinlin& Li, Xiang& Yao, Shun& Ren, Zi…[et al.]. Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance. Cardiology Research and Practice. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1152313

Data Type

Journal Articles

Language

English

Notes

Includes bibliographical references

Record ID

BIM-1152313