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PMID |
Sentence |
1 |
32739209
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The effect of TGF-β, mediated by the type I TGF-β receptor, ALK5, and subsequent Smad2/3 activation results in podocyte apoptosis and loss.
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2 |
32739209
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This was associated with heightened ALK1-mediated activation of Smad1/5 in the glomerular endothelial cells (ECs).
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3 |
32739209
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Therefore, to evaluate the glomerular cell-specific effects of TGF-β in diabetic nephropathy we examined the effects of the podocyte- or EC-specific loss of Bambi (Pod-Bambi-/- or EC-Bambi-/-) in streptozotocin-induced diabetic mice with endothelial nitric oxide synthase deficiency.
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4 |
32739209
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While the podocyte or EC-specific loss of BAMBI both accelerated the progression of diabetic nephropathy, the worsened podocyte injury and loss observed in the diabetic Pod-Bambi-/- mice were associated with enhanced Smad3 activation.
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5 |
32739209
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The enhanced Smad1/5 activation in diabetic EC-Bambi-/- mice was associated with increased glomerular expression of plasmalemma vesicle-associated protein, pointing to the involvement of immature or dedifferentiated glomerular ECs in diabetic nephropathy.
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6 |
32739209
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The effect of TGF-β, mediated by the type I TGF-β receptor, ALK5, and subsequent Smad2/3 activation results in podocyte apoptosis and loss.
|
7 |
32739209
|
This was associated with heightened ALK1-mediated activation of Smad1/5 in the glomerular endothelial cells (ECs).
|
8 |
32739209
|
Therefore, to evaluate the glomerular cell-specific effects of TGF-β in diabetic nephropathy we examined the effects of the podocyte- or EC-specific loss of Bambi (Pod-Bambi-/- or EC-Bambi-/-) in streptozotocin-induced diabetic mice with endothelial nitric oxide synthase deficiency.
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9 |
32739209
|
While the podocyte or EC-specific loss of BAMBI both accelerated the progression of diabetic nephropathy, the worsened podocyte injury and loss observed in the diabetic Pod-Bambi-/- mice were associated with enhanced Smad3 activation.
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10 |
32739209
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The enhanced Smad1/5 activation in diabetic EC-Bambi-/- mice was associated with increased glomerular expression of plasmalemma vesicle-associated protein, pointing to the involvement of immature or dedifferentiated glomerular ECs in diabetic nephropathy.
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11 |
32828232
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Furthermore, they showed that bone morphogenetic protein (BMP) and activin membrane-bound inhibitor, an endogenous modulator of transforming growth factor-β signaling, plays a cell type-specific role and may be a good target for intervention against diabetic kidney disease.
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