“…Similar sleeves of basement membrane have been described in the tunica vasculosa lentis (22) and in tumors treated with AG-013736 or VEGF Trap (42).…”
Section: Discussionsupporting
confidence: 72%
“…Pericytes can persist at least temporarily in empty basement membrane sleeves (6). However, pericytes on some regressing blood vessels undergo apoptosis (22,67).…”
Section: Discussionmentioning
confidence: 99%
“…These sleeves have been described in regressing vessels of the tunica vasculosa lentis during postnatal eye development (22,51), as part of the pathology of diabetes (70), and after inhibition of VEGF signaling in tumor models and in the trachea (5,42).…”
The vasculature of the embryo requires vascular endothelial growth factor (VEGF) during development, but most adult blood vessels lose VEGF dependence. However, some capillaries in the respiratory tract and selected other organs of adult mice regress after VEGF inhibition. The present study sought to identify the sequence of events and the fate of endothelial cells, pericytes, and vascular basement membrane during capillary regression in mouse tracheas after VEGF signaling was blocked with a VEGF-receptor tyrosine kinase inhibitor AG-013736 or soluble receptor construct (VEGF Trap or soluble adenoviral VEGFR-1). Within 1 day, patency was lost and fibrin accumulated in some tracheal capillaries. Apoptotic endothelial cells marked by activated caspase-3 were present in capillaries without blood flow. VEGF inhibition was accompanied by a 19% decrease in tracheal capillaries over 7 days and 30% over 21 days. During this period, desmin/NG2-immunoreactive pericytes moved away from regressing capillaries onto surviving vessels. Empty sleeves of basement membrane, left behind by regressing endothelial cells, persisted for about 2 wk and served as a scaffold for vascular regrowth after treatment ended. The amount of regrowth was limited by the number of surviving basement membrane sleeves. These findings demonstrate that, after inhibition of VEGF signaling, some normal capillaries regress in a systematic sequence of events initiated by a cessation of blood flow and followed by apoptosis of endothelial cells, migration of pericytes away from regressing vessels, and formation of empty basement membrane sleeves that can facilitate capillary regrowth.
“…Similar sleeves of basement membrane have been described in the tunica vasculosa lentis (22) and in tumors treated with AG-013736 or VEGF Trap (42).…”
Section: Discussionsupporting
confidence: 72%
“…Pericytes can persist at least temporarily in empty basement membrane sleeves (6). However, pericytes on some regressing blood vessels undergo apoptosis (22,67).…”
Section: Discussionmentioning
confidence: 99%
“…These sleeves have been described in regressing vessels of the tunica vasculosa lentis during postnatal eye development (22,51), as part of the pathology of diabetes (70), and after inhibition of VEGF signaling in tumor models and in the trachea (5,42).…”
The vasculature of the embryo requires vascular endothelial growth factor (VEGF) during development, but most adult blood vessels lose VEGF dependence. However, some capillaries in the respiratory tract and selected other organs of adult mice regress after VEGF inhibition. The present study sought to identify the sequence of events and the fate of endothelial cells, pericytes, and vascular basement membrane during capillary regression in mouse tracheas after VEGF signaling was blocked with a VEGF-receptor tyrosine kinase inhibitor AG-013736 or soluble receptor construct (VEGF Trap or soluble adenoviral VEGFR-1). Within 1 day, patency was lost and fibrin accumulated in some tracheal capillaries. Apoptotic endothelial cells marked by activated caspase-3 were present in capillaries without blood flow. VEGF inhibition was accompanied by a 19% decrease in tracheal capillaries over 7 days and 30% over 21 days. During this period, desmin/NG2-immunoreactive pericytes moved away from regressing capillaries onto surviving vessels. Empty sleeves of basement membrane, left behind by regressing endothelial cells, persisted for about 2 wk and served as a scaffold for vascular regrowth after treatment ended. The amount of regrowth was limited by the number of surviving basement membrane sleeves. These findings demonstrate that, after inhibition of VEGF signaling, some normal capillaries regress in a systematic sequence of events initiated by a cessation of blood flow and followed by apoptosis of endothelial cells, migration of pericytes away from regressing vessels, and formation of empty basement membrane sleeves that can facilitate capillary regrowth.
“…The general structure of the hyaloid vasculature has been described previously in a number of species (Jack, 1972a, b ;Hamming et al, 1977 ;Balas et al, 1980 ;Bloom, Balazs and Ozanics, 1980 ;Sellheyer and Spitznas, 1987 ;Boeve, van der Linde-Sipman and Stades, 1989 ;De Schaepdrijver et al, 1989 ;Strek et al, 1993 ;El-Hifnawi et al, 1994). The present study provides new information concerning the types and distribution of cells associated with the hyaloid system and vitreous.…”
Section: Cellular Constituents and Their Relationshipssupporting
“…Regression of the hyaloid artery through the vitreous body to the lens during the development of the rat accompanied the regression of the dense meshwork of tunica vasculosa lentis covering the lens surface (Cairns, 1959), in which meshwork was lost 21 days after birth (Hollenberg & Dickson, 1971; Latker & Kuwabara, 1981; El‐Hifnawi et al ., 1994). In the gerbil, under the microscope it was examined that CBs of its eye became thinner and rudimental but remained almost without function from 21 days after birth.…”
The blood supply to the retina and the lens in 32 gerbils (Meriones unguiculatus) of both sexes from infancy to maturity was studied under light and stereoscopic microscopes, and a scanning electron microscope. Mercox (CL-2R; Dai Nippon Ink, Tokyo, Japan) was injected into the left ventricle of 30 animals in order to visualize the blood supply to the retina and the lens from the ophthalmic artery. The central retinal artery arises from the ophthalmic artery, passes through the papilla of the optic nerve together with the central retinal vein and penetrates the vitreous space (cavity of the eye) between the lens and the internal limiting membrane of the retina, where it divides into the central branches covering the lens and the parietal branches to supply the retina. The former passes through the hyaloid space after branching several arterioles and then covers the lens like a network from its medial and marginal sides. Different from small experimental animals, the parietal branches, just after separating from the central one, divides into the nasal, dorsal and temporal branches in the vitreous space, each of which then subdivides to distribute across the retina on the inner limiting membrane, then delineates the membrana vasculosa retinae. This basal pattern of vasculization 1 day after birth continues to death. Both the central and parietal branches of the central retinal artery correspond to the branches of the hyaloid artery in embryo and the latter is preserved in adult gerbils.
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