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PMID |
Sentence |
1 |
16960101
|
We found expression of S1P1, S1P2, and S1P3 receptors on NOD aortic endothelial cells.
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2 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
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3 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
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4 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
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5 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
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6 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
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7 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
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8 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
9 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
10 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
11 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
12 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
13 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
14 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
15 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
16 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
17 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
18 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
19 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
20 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
21 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
22 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
23 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
24 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
25 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
26 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
27 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
28 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
29 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
30 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
31 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
32 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
33 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
34 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
35 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
36 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
37 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
38 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
39 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
40 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
41 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
42 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
43 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
44 |
19139947
|
The S1P(2) receptor expressed in human platelets is linked to the RhoA-Rho kinase pathway and is down regulated in type 2 diabetes.
|
45 |
19139947
|
S1P(2) receptor expression (Western blotting) was detected in washed human platelets from healthy volunteers.
|
46 |
19139947
|
The S1P-induced increase in Ca(2+) was sensitive to the S1P(2) receptor antagonist JTE-013 but not the S1P(1/3) antagonist VPC23019.
|
47 |
19139947
|
Platelets from patients with type 2 diabetes demonstrated an attenuated aggregability to S1P as well as decreased levels of the full-length S1P(2) protein.
|
48 |
19139947
|
The S1P(2) antibody used identified a 45 kDa receptor cleavage product in patients with diabetes that could also be generated from healthy human platelet lysates by the addition of the Ca(2+)-activated protease, mu-calpain.
|
49 |
19139947
|
These results indicate that the S1P(2) receptor is involved in S1P-induced platelet aggregation and Rho kinase activation.
|
50 |
19139947
|
Moreover, in platelets from patients with type 2 diabetes, responses to S1P are attenuated via a phenomenon attributed to the calpain-dependent cleavage of the S1P(2) receptor.
|
51 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
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52 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
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53 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
54 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
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55 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
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56 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
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57 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
58 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
59 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
60 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
61 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
62 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
63 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
64 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
65 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
66 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
67 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
68 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
69 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
70 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
71 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
72 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
73 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
74 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
75 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
76 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
77 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
78 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
79 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
80 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
81 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
82 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
83 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
84 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
85 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
86 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
87 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
88 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
89 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
90 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
91 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
92 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
93 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
94 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
95 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
96 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
97 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
98 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
99 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
100 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
101 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
102 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
103 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
104 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
105 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
106 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
107 |
19261455
|
Sphingosine 1-phosphate (Sph-1-P) regulates vascular homeostasis through its receptors like S1P1 and S1P2.
|
108 |
19261455
|
While S1P1 works to protect vasculature, S1P2 works antagonistically against it.
|
109 |
19261455
|
Therefore, the balance of S1P1 and S1P2 determines the regulation of vascular permeability.
|
110 |
19261455
|
Therefore, we hypothesized that the balance of S1P1 and S1P2 expression becomes inappropriate in glomeruli of diabetic nephropathy.
|
111 |
19261455
|
The analysis by real-time PCR revealed that the ratio of S1P2/S1P1 mRNA in the renal cortex of the diabetic rats was significantly higher than that in the non-diabetic control group.
|
112 |
19261455
|
Immunohistochemistry revealed that S1P1 was expressed by endothelial and mesangial cells, while S1P2 was mainly expressed by mesangial cells in glomeruli.
|
113 |
19261455
|
Furthermore, the ratio of the staining intensity of S1P2 to that of S1P1 in the glomeruli was significantly higher in the diabetic rats.
|
114 |
19261455
|
In conclusion, Sph-1-P signals are preferentially transmitted through S1P2, rather than S1P1, in the glomeruli of rats with diabetic nephropathy.
|
115 |
19662499
|
In skeletal muscle cells S1P, through engagement of its S1P(2) receptor, is found to produce a transient burst of reactive oxygen species through a calcium-dependent activation of the small GTPase Rac1.
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116 |
19662499
|
S1P-induced redox-signaling is sensed by protein tyrosine phosphatase-1B, the main negative regulator of insulin receptor phosphorylation, which undergoes oxidation and enzymatic inhibition.
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117 |
20060809
|
In this study, we investigated the potential role of S1P(2) in streptozotocin (STZ)-induced apoptosis of pancreatic beta-cells and progression of diabetes.
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118 |
20060809
|
S1P(2)(-/-) mice showed higher insulin/glucose ratios (an index of relative insulin deficiency) and larger insulin-positive islet areas to administration of a low dose of STZ than WT mice.
|
119 |
20060809
|
Our findings indicate that blockade of S1P(2) signaling attenuates STZ-induced apoptosis of pancreatic beta-cells and decreases the incidence of diabetes.
|
120 |
20060809
|
In this study, we investigated the potential role of S1P(2) in streptozotocin (STZ)-induced apoptosis of pancreatic beta-cells and progression of diabetes.
|
121 |
20060809
|
S1P(2)(-/-) mice showed higher insulin/glucose ratios (an index of relative insulin deficiency) and larger insulin-positive islet areas to administration of a low dose of STZ than WT mice.
|
122 |
20060809
|
Our findings indicate that blockade of S1P(2) signaling attenuates STZ-induced apoptosis of pancreatic beta-cells and decreases the incidence of diabetes.
|
123 |
21270296
|
SOCE was observed in VSMCs lacking either S1P(2) or S1P(3) receptors, suggesting that S1P acts via multiple signaling pathways.
|
124 |
21270296
|
Finally, S1P-induced SOCE was larger in proliferative than in contractile VSMCs, correlating with increases in STIM1, Orai1, S1P(1), and S1P(3) receptor mRNA.
|
125 |
22406263
|
S1P2 receptor mediates sphingosine-1-phosphate-induced fibronectin expression via MAPK signaling pathway in mesangial cells under high glucose condition.
|
126 |
22406263
|
S1P2 receptor mediated fibronectin expression through the activation of S1P-S1P2-MAPK (ERK1/2 and p38MAPK) axis in mesangial cells under high glucose condition, suggesting that it might be a potential therapeutic target for diabetic nephropathy treatment.
|
127 |
22406263
|
S1P2 receptor mediates sphingosine-1-phosphate-induced fibronectin expression via MAPK signaling pathway in mesangial cells under high glucose condition.
|
128 |
22406263
|
S1P2 receptor mediated fibronectin expression through the activation of S1P-S1P2-MAPK (ERK1/2 and p38MAPK) axis in mesangial cells under high glucose condition, suggesting that it might be a potential therapeutic target for diabetic nephropathy treatment.
|