| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-140 |
Sentence |
denotes |
Vitamin D suppression of endoplasmic reticulum stress promotes an antiatherogenic monocyte/macrophage phenotype in type 2 diabetic patients. |
| T2 |
141-361 |
Sentence |
denotes |
Cardiovascular disease is the leading cause of morbidity/mortality in patients with type 2 diabetes mellitus (T2DM), but there is a lack of knowledge about the mechanism(s) of increased atherosclerosis in these patients. |
| T3 |
362-602 |
Sentence |
denotes |
In patients with T2DM, the prevalence of 25-hydroxy vitamin D (25(OH)D) deficiency is almost twice that for nondiabetics and doubles the relative risk of developing cardiovascular disease compared with diabetic patients with normal 25(OH)D. |
| T4 |
603-783 |
Sentence |
denotes |
We tested the hypothesis that monocytes from vitamin D-deficient subjects will have a proatherogenic phenotype compared with vitamin D-sufficient subjects in 43 patients with T2DM. |
| T5 |
784-939 |
Sentence |
denotes |
Serum 25(OH)D level inversely correlated with monocyte adhesion to endothelial cells even after adjustment for demographic and comorbidity characteristics. |
| T6 |
940-1262 |
Sentence |
denotes |
Vitamin D-sufficient patients (≥30 ng/ml 25(OH)D) had lower monocyte endoplasmic reticulum (ER) stress, a predominance of M1 over M2 macrophage membrane receptors, and decreased mRNA expression of monocyte adhesion molecules PSGL-1, β(1)-integrin, and β(2)-integrin compared with patients with 25(OH)D levels of <30 ng/ml. |
| T7 |
1263-1415 |
Sentence |
denotes |
In vitamin D-deficient macrophages, activation of ER stress increased adhesion and adhesion molecule expression and induced an M2-predominant phenotype. |
| T8 |
1416-1568 |
Sentence |
denotes |
Moreover, adding 1,25(OH)(2)D(3) to vitamin D-deficient macrophages shifted their phenotype toward an M1-predominant phenotype with suppressed adhesion. |
| T9 |
1569-1740 |
Sentence |
denotes |
Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients activated ER stress, accelerated adhesion, and increased adhesion molecule expression. |
| T10 |
1741-1949 |
Sentence |
denotes |
The absence of ER stress protein CCAAT enhancer-binding protein homologous protein suppressed monocyte adhesion, adhesion molecule expression, and the M2-predominant phenotype induced by vitamin D deficiency. |
| T11 |
1950-2060 |
Sentence |
denotes |
Thus, vitamin D is a natural ER stress reliever that induced an antiatherogenic monocyte/macrophage phenotype. |
