Developmental change in type VI collagen in human cerebral vessels

Kamei, Atsushi; Houdou, Sadataka; Mito, Takashi; Konomi, Hiroshi; Takashima, Sachio

doi:10.1016/0887-8994(92)90065-7

Cited by 32 publications

(12 citation statements)

References 13 publications

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“…Animal studies have found marked increases in astrocyte number, size, and their connectivity with each other and blood vessels with increased brain development (72,91). Additionally, the capacity of the local arterioles to increase local CBF through the neurovascular coupling cascade is likely to increase with age, in accordance with histological studies showing enhanced structural development of the arterioles and capillary beds, which continues until close to term age in the human fetal cortex (87,101,134). Moreover, cerebral vessel density and volume have been shown to approximately double in the cortex when newborn and adult primates are compared, with the bulk of this increase occurring at the capillary level (166).…”

Section: Cerebral Blood Flow-metabolism Coupling In the Pre-mentioning

confidence: 69%

Cerebral vascular regulation and brain injury in preterm infants

Brew

Walker

Wong

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Cerebrovascular lesions, mainly germinal matrix hemorrhage and ischemic injury to the periventricular white matter, are major causes of adverse neurodevelopmental outcome in preterm infants. Cerebrovascular lesions and neuromorbidity increase with decreasing gestational age, with the white matter predominantly affected. Developmental immaturity in the cerebral circulation, including ongoing angiogenesis and vasoregulatory immaturity, plays a major role in the severity and pattern of preterm brain injury. Prevention of this injury requires insight into pathogenesis. Cerebral blood flow (CBF) is low in the preterm white matter, which also has blunted vasoreactivity compared with other brain regions. Vasoreactivity in the preterm brain to cerebral perfusion pressure, oxygen, carbon dioxide, and neuronal metabolism is also immature. This could be related to immaturity of both the vasculature and vasoactive signaling. Other pathologies arising from preterm birth and the neonatal intensive care environment itself may contribute to impaired vasoreactivity and ineffective CBF regulation, resulting in the marked variations in cerebral hemodynamics reported both within and between infants depending on their clinical condition. Many gaps exist in our understanding of how neonatal treatment procedures and medications have an impact on cerebral hemodynamics and preterm brain injury. Future research directions for neuroprotective strategies include establishing cotside, real-time clinical reference values for cerebral hemodynamics and vasoregulatory capacity and to demonstrate that these thresholds improve long-term outcomes for the preterm infant. In addition, stimulation of vascular development and repair with growth factor and cell-based therapies also hold promise.

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Section: Cerebral Blood Flow-metabolism Coupling In the Pre-mentioning

confidence: 69%

Cerebral vascular regulation and brain injury in preterm infants

Brew

Walker

Wong

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Decorin, NG2, and type VI collagen display an overlapping pattern of expression in many developing tissues, including developing blood vessels (21,25,42,43), skin (44,45), 2 cartilage (20,21,46), and peripheral nerves (47)(48)(49). An increase in decorin synthesis may result in a decreased association of type VI collagen with NG2 and the cell surface.…”

Section: Discussionmentioning

confidence: 99%

Binding of the NG2 Proteoglycan to Type VI Collagen and Other Extracellular Matrix Molecules

Burg

Tillet

Timpl

et al. 1996

Journal of Biological Chemistry

182

143

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Previous studies have suggested that the NG2 proteoglycan interacts with type VI collagen. We have further characterized this interaction using a solid phase binding assay in which purified NG2 was shown to bind to pepsin-solubilized type VI collagen. In addition, NG2 bound a recombinant ␣2 (VI) collagen chain but did not appreciably bind to the recombinant ␣1 (VI) chain or the N-terminal domain of ␣3 (VI) (N9 -N2). Binding of NG2 to type VI collagen was shown to be concentration-dependent and saturable and to depend mainly on the NG2 core protein, since chondroitinase-treated NG2 bound the collagen as well as undigested samples. In addition, the binding studies revealed several other possible ligands for NG2, including type II collagen, type V collagen, tenascin, and laminin. Binding of the proteoglycan to these molecules was also shown to be mediated by domains contained within the NG2 core protein. The ability of NG2 to bind to these extracellular matrix molecules was compared with that of the chondroitin sulfate proteoglycan decorin, revealing an almost identical binding pattern of the two proteoglycans to the different collagen types. In addition, decorin was found to effectively inhibit the ability of NG2 to bind to collagen, thus suggesting that the two proteoglycans may bind to some of the same regions on the collagen substrates. In contrast, decorin did not bind tenascin and was ineffective in inhibiting the binding of NG2 to tenascin or laminin, indicating that NG2 may bind these two molecules using a separate domain that is distinct from its collagen binding region.Proteoglycans represent a diverse class of macromolecules the defining feature of which is the addition of one or more glycosaminoglycan sugar chains to a core glycoprotein. Characterization of this group of molecules has expanded in recent years, revealing an enormous diversity in number, structure, and function (for review, see Refs. 1-4). Although early work emphasized the importance of the glycosaminoglycan chains in mediating proteoglycan interactions with other ligands, sequence information obtained from the growing list of cloned proteoglycan core proteins has revealed the presence of binding motifs similar to those found in other proteins (3). This suggests that proteoglycan core proteins may, in fact, be responsible for many of the interactions attributed to proteoglycans. Proteoglycans contained within the extracellular matrix (ECM), 1 which include the large aggregating proteoglycans aggrecan (5) and versican (6), the smaller leucine-rich family of proteoglycans typified by decorin, and the basement membrane proteoglycan perlecan, all have been shown to interact with several other matrix components, including laminin (7), fibronectin (8, 9), tenascin (10), hyaluronic acid (5, 6, 11), and collagen (12-14). These interactions are believed to be important for the proper assembly, maintenance, and function of the ECM. In addition, cell surface proteoglycans such as syndecan and CD44 have been shown to bind matrix molecules, including...

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“…A predisposing factor in the pathogenesis of IVH in preterm infants is the microvascular architecture of the germinal matrix, which is at the end zone of thalamo-striatal arteries and in the venule structure zone of the ventricular side of terminal vein (Takashima et al, 1978). Hypotension or hypoxemia may induce focal hypoxic-ischemic changes in the arterial end zone within the germinal matrix, and with reperfusion or over-perfusion following hypoxia-ischemia, venous hemorrhage may occur due to the paucity of supportive connective tissue (Kamei et al, 1992). In addition, the microvasculature of the germinal matrix is frail because of an abundance of angiogenic blood vessels (Ballabh et al, 2007) that possess few pericytes, an incomplete and immature basal lamina, and an investment of astrocytic processes (“end-feet”) with a deficiency of glial fibrillary acidic protein (GFAP) (El-Khoury et al, 2006).…”

Section: Perinatal Hypoxiamentioning

confidence: 99%

Vulnerability of the developing brain to hypoxic-ischemic damage: contribution of the cerebral vasculature to injury and repair?

Baburamani¹,

Ek²,

Walker³

et al. 2012

Front. Physio.

119

112

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As clinicians attempt to understand the underlying reasons for the vulnerability of different regions of the developing brain to injury, it is apparent that little is known as to how hypoxia-ischemia may affect the cerebrovasculature in the developing infant. Most of the research investigating the pathogenesis of perinatal brain injury following hypoxia-ischemia has focused on excitotoxicity, oxidative stress and an inflammatory response, with the response of the developing cerebrovasculature receiving less attention. This is surprising as the presentation of devastating and permanent injury such as germinal matrix-intraventricular haemorrhage (GM-IVH) and perinatal stroke are of vascular origin, and the origin of periventricular leukomalacia (PVL) may also arise from poor perfusion of the white matter. This highlights that cerebrovasculature injury following hypoxia could primarily be responsible for the injury seen in the brain of many infants diagnosed with hypoxic-ischemic encephalopathy (HIE). Interestingly the highly dynamic nature of the cerebral blood vessels in the fetus, and the fluctuations of cerebral blood flow and metabolic demand that occur following hypoxia suggest that the response of blood vessels could explain both regional protection and vulnerability in the developing brain. However, research into how blood vessels respond following hypoxia-ischemia have mostly been conducted in adult models of ischemia or stroke, further highlighting the need to investigate how the developing cerebrovasculature responds and the possible contribution to perinatal brain injury following hypoxia. This review discusses the current concepts on the pathogenesis of perinatal brain injury, the development of the fetal cerebrovasculature and the blood brain barrier (BBB), and key mediators involved with the response of cerebral blood vessels to hypoxia.

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Developmental change in type VI collagen in human cerebral vessels

Cited by 32 publications

References 13 publications

Cerebral vascular regulation and brain injury in preterm infants

Cerebral vascular regulation and brain injury in preterm infants

Binding of the NG2 Proteoglycan to Type VI Collagen and Other Extracellular Matrix Molecules

Vulnerability of the developing brain to hypoxic-ischemic damage: contribution of the cerebral vasculature to injury and repair?

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