Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance
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 endothelia...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Cardiology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2020/1278465 |
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| author | Juan Liu Xiangbin Xing Xinlin Wu Xiang Li Shun Yao Zi Ren Haitao Zeng Shaohong Wu |
| author_facet | Juan Liu Xiangbin Xing Xinlin Wu Xiang Li Shun Yao Zi Ren Haitao Zeng Shaohong Wu |
| author_sort | Juan Liu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-fb92070cb4b242fa894dc7e9bc71f962 |
| institution | Kabale University |
| issn | 2090-8016 2090-0597 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Cardiology Research and Practice |
| spelling | doaj-art-fb92070cb4b242fa894dc7e9bc71f9622025-08-20T03:25:34ZengWileyCardiology Research and Practice2090-80162090-05972020-01-01202010.1155/2020/12784651278465Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose ToleranceJuan Liu0Xiangbin Xing1Xinlin Wu2Xiang Li3Shun Yao4Zi Ren5Haitao Zeng6Shaohong Wu7Department of Endocrinology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Traditional Chinese Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Ultrasound, Guangzhou Development District Hospital, Guangzhou 510080, ChinaDepartment of Cardiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaCenter for Reproductive Medicine, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaCenter for Reproductive Medicine, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Ultrasound, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, ChinaBackground. 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.http://dx.doi.org/10.1155/2020/1278465 |
| spellingShingle | Juan Liu Xiangbin Xing Xinlin Wu Xiang Li Shun Yao Zi Ren Haitao Zeng Shaohong Wu 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 |
| title | Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance |
| title_full | Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance |
| title_fullStr | Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance |
| title_full_unstemmed | Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance |
| title_short | Reduced Circulating Endothelial Progenitor Cells and Downregulated GTCPH I Pathway Related to Endothelial Dysfunction in Premenopausal Women with Isolated Impaired Glucose Tolerance |
| title_sort | reduced circulating endothelial progenitor cells and downregulated gtcph i pathway related to endothelial dysfunction in premenopausal women with isolated impaired glucose tolerance |
| url | http://dx.doi.org/10.1155/2020/1278465 |
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