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Differential gene expression in Lin-/VEGF-R2+ bone marrow-derived endothelial progenitor cells isolated from diabetic mice


Barthelmes, D; Zhu, L; Shen, W; Gillies, M C; Irhimeh, M R (2014). Differential gene expression in Lin-/VEGF-R2+ bone marrow-derived endothelial progenitor cells isolated from diabetic mice. Cardiovascular Diabetology, 13:42.

Abstract

Background: Diabetes is known to impair the number and function of endothelial progenitor cells in the circulation, causing structural and functional alterations in the micro- and macro-vasculature. The aim of this study was to identify early diabetes-related changes in the expression of genes that have been reported to be closely involved in endothelial progenitor cell migration and function. Methods: Based on review of current literature, this study examined the expression level of 35 genes that are known to be involved in endothelial progenitor cell migration and function in magnetically sorted Lin−/VEGF-R2+ endothelial progenitor cells obtained from the bone marrow of Akita mice in the early stages of diabetes (18 weeks) using RT-PCR and Western blotting. We used the Shapiro-Wilk and D’Agostino & Pearson Omnibus tests to assess normality. Differences between groups were evaluated by Student’s t-test for normally distributed data (including Welch correction in cases of unequal variances) or Mann–Whitney test for not normally distributed data. Results: We observed a significant increase in the number of Lin−/VEGF-R2+ endothelial progenitor cells within the bone marrow in diabetic mice compared with non-diabetic mice. Two genes, SDF-1 and SELE, were significantly differentially expressed in diabetic Lin−/VEGF-R2+ endothelial progenitor cells and six other genes, CAV1, eNOS, CLDN5, NANOG, OCLN and BDNF, showed very low levels of expression in diabetic Lin−/VEGF-R2+ progenitor cells. Conclusion: Low SDF-1 expression may contribute to the dysfunctional mobilization of bone marrow Lin−/VEGF-R2+ endothelial progenitor cells, which may contribute to microvascular injury in early diabetes.

Abstract

Background: Diabetes is known to impair the number and function of endothelial progenitor cells in the circulation, causing structural and functional alterations in the micro- and macro-vasculature. The aim of this study was to identify early diabetes-related changes in the expression of genes that have been reported to be closely involved in endothelial progenitor cell migration and function. Methods: Based on review of current literature, this study examined the expression level of 35 genes that are known to be involved in endothelial progenitor cell migration and function in magnetically sorted Lin−/VEGF-R2+ endothelial progenitor cells obtained from the bone marrow of Akita mice in the early stages of diabetes (18 weeks) using RT-PCR and Western blotting. We used the Shapiro-Wilk and D’Agostino & Pearson Omnibus tests to assess normality. Differences between groups were evaluated by Student’s t-test for normally distributed data (including Welch correction in cases of unequal variances) or Mann–Whitney test for not normally distributed data. Results: We observed a significant increase in the number of Lin−/VEGF-R2+ endothelial progenitor cells within the bone marrow in diabetic mice compared with non-diabetic mice. Two genes, SDF-1 and SELE, were significantly differentially expressed in diabetic Lin−/VEGF-R2+ endothelial progenitor cells and six other genes, CAV1, eNOS, CLDN5, NANOG, OCLN and BDNF, showed very low levels of expression in diabetic Lin−/VEGF-R2+ progenitor cells. Conclusion: Low SDF-1 expression may contribute to the dysfunctional mobilization of bone marrow Lin−/VEGF-R2+ endothelial progenitor cells, which may contribute to microvascular injury in early diabetes.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Ophthalmology Clinic
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2014
Deposited On:20 Nov 2014 07:43
Last Modified:08 Dec 2017 08:13
Publisher:BioMed Central
ISSN:1475-2840
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1186/1475-2840-13-42
PubMed ID:24521356

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