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Receptor‐Mediated Endocytosis of Polypeptide Hormones by Vascular Endothelium

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Abstract

The sections in this article are:

1 Insulin
2 Insulin‐Like Growth Factors
3 Human Chorionic Gonadotropin (hCG)
4 Glucagon
Figure 1. Figure 1.

Schematic representation of the three basic types of blood capillaries. Organelles and routes involved in the non‐specific (bulk‐phase) transport of plasma proteins (A), continuous capillary; (B), fenestrated capillary; (C), discontinuous capillary (sinusoid). (1) transport via endothelial junctions (j) effective in inflammatory conditions); (2) vesicular transport (the main transport mechanism in continuous and fenestrated capillary endothelia); (3) transport via transendothelial channels (c) (minor contribution to the transport due to their scarcity); (4) transport through the diaphragmed fenestrae (f) (minor contribution to plasma protein transport due to their negative charge); (5) diffusion through the endothelial gaps (g) (effective and efficient transport but only in sinusoids), bl, basal lamina; va, abluminal plasmalemmal vesicle; v1, luminal plasmalemmal vesicle.

[Reproduced with permission from 27.]
Figure 2. Figure 2.

Time course of dissociation of receptor‐bound insulin and IGFs from cultured endothelial cells.

[Reproduced with permission from 7.]
Figure 3. Figure 3.

Displacement of [125I]insulin, pro‐insulin, and glucagon in the perfused heart.

[Reproduced with permission from 9.]
Figure 4. Figure 4.

125I grains over capillary endothelium (left) and cardiac muscle (right) in intact hearts perfused with [125I]insulin alone or [125I]insulin and varying concentrations of unlabeled insulin.

[Reproduced with permission from 6.]
Figure 5. Figure 5.

Localization of 125I grains in intact hearts perfused with either [125I]insulin or [125I]desoctapeptide (DOP) insulin alone or coperfused with varying concentrations of unlabeled insulin.

[Reproduced with permission from 6.]
Figure 6. Figure 6.

Effect of trypsin treatment on subsequent appearance of [125I]insulin in capillary endothelium and cardiac muscle.

[Reproduced with permission from 6.]
Figure 7. Figure 7.

Effect of anti‐insulin receptor antibody, perfused at two dilutions (1:50 and 1:250) on the subsequent appearance of [125I]insulin in capillary endothelium and cardiac muscle.

[Reproduced with permission from 6.]
Figure 8. Figure 8.

IGF‐I binding to capillary endothelium of the perfused heart (left). For comparison, IGF‐I binding to cultured microvessel endothelial cells is shown (right).

[Reproduced with permission from 4.]
Figure 9. Figure 9.

IGF‐II binding to capillary endothelium of the perfused heart (left) and to cultured microvessel endothelial cells (right).

[Reproduced with permission from 5.]
Figure 10. Figure 10.

Transcytosis of hCG‐AU5 nm through the endothelial cells of rat testicular capillaries, (a) After 5 min of perfusion with hCG‐AU5nm the tracer marks the luminal plasma membrane (pm), the coated pits (cp), and the coated vesicles (cv), but fails to label the plasmalemmal vesicles (v1) open to the capillary lumen and the endothelial junctions (j), (b‐d) After 15 min of perfusion the gold‐labeled hormone is detected in the tubular (te) and vesicular (ve) endosomes (b) and in large smooth vesicles (SV) located near the abluminal side of the endothelium (c). Some hormone is present in the multivesicular bodies (mvb) (d). (e, f) After 20 min of perfusion hCG‐Au5 nm is delivered into the interstitial space (is) via smooth vesicles (SV) (e). Some of the tracer is associated with the plasma membrane (pm) and the coated pits (cp) of the abluminal cell surface of the endothelium (f). (Inset) Control perfusion with BSA‐AU5 nm. The gold‐labeled albumin was perfused for 5 min at a concentration 20‐fold higher than the concentration of hCG‐AU5 nm ( = 2 and = 0.1 respectively). Some gold particles are present in the plasmalemmal vesicles (v1) open to the capillary lumen (L). End, endothelial cell. Bar, 0.1 μm.

[Reproduced with permission from 26.]


Figure 1.

Schematic representation of the three basic types of blood capillaries. Organelles and routes involved in the non‐specific (bulk‐phase) transport of plasma proteins (A), continuous capillary; (B), fenestrated capillary; (C), discontinuous capillary (sinusoid). (1) transport via endothelial junctions (j) effective in inflammatory conditions); (2) vesicular transport (the main transport mechanism in continuous and fenestrated capillary endothelia); (3) transport via transendothelial channels (c) (minor contribution to the transport due to their scarcity); (4) transport through the diaphragmed fenestrae (f) (minor contribution to plasma protein transport due to their negative charge); (5) diffusion through the endothelial gaps (g) (effective and efficient transport but only in sinusoids), bl, basal lamina; va, abluminal plasmalemmal vesicle; v1, luminal plasmalemmal vesicle.

[Reproduced with permission from 27.]


Figure 2.

Time course of dissociation of receptor‐bound insulin and IGFs from cultured endothelial cells.

[Reproduced with permission from 7.]


Figure 3.

Displacement of [125I]insulin, pro‐insulin, and glucagon in the perfused heart.

[Reproduced with permission from 9.]


Figure 4.

125I grains over capillary endothelium (left) and cardiac muscle (right) in intact hearts perfused with [125I]insulin alone or [125I]insulin and varying concentrations of unlabeled insulin.

[Reproduced with permission from 6.]


Figure 5.

Localization of 125I grains in intact hearts perfused with either [125I]insulin or [125I]desoctapeptide (DOP) insulin alone or coperfused with varying concentrations of unlabeled insulin.

[Reproduced with permission from 6.]


Figure 6.

Effect of trypsin treatment on subsequent appearance of [125I]insulin in capillary endothelium and cardiac muscle.

[Reproduced with permission from 6.]


Figure 7.

Effect of anti‐insulin receptor antibody, perfused at two dilutions (1:50 and 1:250) on the subsequent appearance of [125I]insulin in capillary endothelium and cardiac muscle.

[Reproduced with permission from 6.]


Figure 8.

IGF‐I binding to capillary endothelium of the perfused heart (left). For comparison, IGF‐I binding to cultured microvessel endothelial cells is shown (right).

[Reproduced with permission from 4.]


Figure 9.

IGF‐II binding to capillary endothelium of the perfused heart (left) and to cultured microvessel endothelial cells (right).

[Reproduced with permission from 5.]


Figure 10.

Transcytosis of hCG‐AU5 nm through the endothelial cells of rat testicular capillaries, (a) After 5 min of perfusion with hCG‐AU5nm the tracer marks the luminal plasma membrane (pm), the coated pits (cp), and the coated vesicles (cv), but fails to label the plasmalemmal vesicles (v1) open to the capillary lumen and the endothelial junctions (j), (b‐d) After 15 min of perfusion the gold‐labeled hormone is detected in the tubular (te) and vesicular (ve) endosomes (b) and in large smooth vesicles (SV) located near the abluminal side of the endothelium (c). Some hormone is present in the multivesicular bodies (mvb) (d). (e, f) After 20 min of perfusion hCG‐Au5 nm is delivered into the interstitial space (is) via smooth vesicles (SV) (e). Some of the tracer is associated with the plasma membrane (pm) and the coated pits (cp) of the abluminal cell surface of the endothelium (f). (Inset) Control perfusion with BSA‐AU5 nm. The gold‐labeled albumin was perfused for 5 min at a concentration 20‐fold higher than the concentration of hCG‐AU5 nm ( = 2 and = 0.1 respectively). Some gold particles are present in the plasmalemmal vesicles (v1) open to the capillary lumen (L). End, endothelial cell. Bar, 0.1 μm.

[Reproduced with permission from 26.]
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How to Cite

Robert S. Bar, Ngozi E. Erondu. Receptor‐Mediated Endocytosis of Polypeptide Hormones by Vascular Endothelium. Compr Physiol 2011, Supplement 20: Handbook of Physiology, The Endocrine System, Cellular Endocrinology: 39-47. First published in print 1998. doi: 10.1002/cphy.cp070103