STAT5 activation induced by diabetic LDL depends on LDL glycation and occurs via src kinase activity
Diabetes, ISSN: 0012-1797, Vol: 51, Issue: 11, Page: 3311-3317
2002
- 23Citations
- 15Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations23
- Citation Indexes22
- CrossRef22
- 22
- Patent Family Citations1
- 1
- Captures15
- Readers15
- 15
Article Description
Advanced glycation end products (AGEs) have been implicated in the accelerated vascular injury occurring in diabetes. We recently reported that LDL prepared from type 2 diabetic patients (dm-LDL), but not normal LDL (n-LDL) triggered signal transducers and activators of transcription STAT5 activation and p21 expression in endothelial cells (ECs). The aims of the present study were to investigate the role of LDL glycation in dm-LDL-mediated signals and to analyze the molecular mechanisms leading to STAT5 activation. We found that glycated LDL (gly-LDL) triggered STAT5 activation, the formation of a prolactin inducible element (PIE)-binding complex containing STAT5, and increased p21 expression through the activation of the receptor for AGE (RAGE). We also demonstrated that dm-LDL and gly-LDL, but not n-LDL treatment induced the formation of a stable complex containing the activated STAT5 and RAGE. Moreover, gly-LDL triggered src but not JAK2 kinase activity. Pretreatment with the src kinase inhibitor PP1 abrogated both STAT5 activation and the expression of p21 induced by gly-LDL. Consistently, gly-LDL failed to activate STAT5 in src fibroblasts. Collectively, our results provide evidence for the role of glycation in dm-ldl-mediated effects and for a specific role of src kinase in STAT5-dependent p21 expression.
Bibliographic Details
American Diabetes Association
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