Vascular Endothelial Growth Factor-B Promotes In Vivo Angiogenesis

Silvestre, Jean‐Sébastien; Tamarat, Radia; Ebrahimian, Teni; Leroux, Anne; Clergue, Michel; Emmanuel, Florence; Duriez, Micheline; Schwartz, Bertrand; Branellec, Didier; Lévy, Bernard

doi:10.1161/01.res.0000081594.21764.44

Cited by 160 publications

(103 citation statements)

References 38 publications

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“…In the linkage regions of this study, there are several genes of angiogenesis factors physiologically involved in endothelial NO synthase-related pathways. [25][26][27][28][29][30][31] There is also the possibility that the vessel diameters are genetically determined by vasculogenesis factors during vascular development, and many candidate genes, for example, fibroblast growth factor 12 at 3q28, involved in this process are present in the linkage regions. Linkage regions for hypertension-adjusted retinal vessel diameters in this study overlapped with the regions of essential hypertension, 32-37 which suggested generalized retinal arteriolar narrowing preceding hypertension and contributing to the pathogenesis of hypertension.…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Linkage Study of Retinal Vessel Diameters in the Beaver Dam Eye Study

Xing

Klein

et al. 2006

Hypertension

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Abstract-Retinal vessels can be observed noninvasively and provide a window to microvascular systems elsewhere in the body. Generalized retinal arteriolar narrowing can represent structural changes resulting from persistent high blood pressure. However, data from recent studies also suggest that generalized retinal arteriolar narrowing might precede hypertension and contribute to its pathogenesis. To determine whether vessel diameters in the eye are genetically determined, we conducted a genome-wide linkage scan on retinal vessel diameters (central retinal artery equivalent and central retinal vein equivalent) using data from the Beaver Dam Eye Study. There were 7 regions on 5 chromosomes (3q28, 5q35, 7q21, 7q32, 11q14, 11q24, and 17q11) Key Words: genetics Ⅲ arterioles Ⅲ veins Ⅲ microcirculation Ⅲ retinal vessels T he retinal vessels can be observed noninvasively and are thought to characterize microvascular systems elsewhere in the body. It is believed that the retinal vessels, as an end point of the arteriolar system, are particularly susceptible to changes in blood pressure. 1 There have been several studies showing an association between past and present hypertension and narrowing of retinal arterioles. [2][3][4][5] Data from general population-based cohort studies have shown that generalized retinal arteriolar narrowing precedes hypertension and may contribute to its pathogenesis. 6,7 Moreover, independent of blood pressure, generalized retinal arteriolar narrowing was shown to be a predictor of stroke, 8 cardiovascular disease mortality, 9 and coronary heart disease. 10 Recently, Lee et al 11 investigated the familial aggregation of retinal vessel diameters and showed that it was more highly correlated between relatives than between unrelated individuals, suggesting the involvement of genetic components. To our knowledge, however, there have been no genetic linkage or association studies investigating the genetic influence on retinal vessel diameters.In the present study, we performed a genome-wide linkage scan on retinal vessel diameters using data from the Beaver Dam Eye Study. Our specific aims were: (1) to study the underlying genetic factors influencing retinal vessel diameters, and (2) to study the differences between retinal vessel diameters (venules and arterioles) in terms of the genetic background. Given the association between retinal arteriolar narrowing and hypertension, stroke, and cardiovascular disease, understanding the genetic determinants of retinal vessel diameters may provide additional insights into the pathogenesis of these complex diseases. Methods Family AscertainmentThe Beaver Dam Eye Study, as described in detail in previous reports, 12,13 is a population-based cohort study of age-related eye diseases. At the time of census 4926 subjects between 43 and 86 years of age, living in the city or township of Beaver Dam, Wis, participated in the baseline examination from 1988 to 1990. Informed consent was obtained from the participants following a protocol approved by the Institution...

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Section: Discussionmentioning

confidence: 99%

Genome-Wide Linkage Study of Retinal Vessel Diameters in the Beaver Dam Eye Study

Xing

Klein

et al. 2006

Hypertension

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“…5,7,9,33,34 On the other hand, under other conditions where blood vessels are challenged and need to struggle to survive, VEGF-B is then critically required and VEGF-B treatment can indeed lead to more (survived) blood vessels. 9,29,30,32 Under such conditions, VEGF-B can appear to be "angiogenic." 10,29,30,32 However, this "angiogenic" effect of VEGF-B is most likely only due to its survival effect on both vascular and non-vascular cells (Figs.…”

Section: Vegf-b Is a Survival Rather Than An Angiogenic Factormentioning

confidence: 99%

“…However, studies along this line have only led to inconsistent results. VEGF-B was reported to be angiogenic in some studies, [29][30][31][32] but lack of an angiogenic activity in others. 5,7,33,34 Below is an overview of the reports with regard to the angiogenic activity of VEGF-B.…”

Section: Introductionmentioning

confidence: 99%

Vegf-B

Lee

Tang

et al. 2009

Cell Adhesion & Migration

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Despite its early discovery and high sequence homology to the other VEGF family members, the biological function of VEGF-B remained debatable for a long time, and VEGF-B has received little attention from the field thus far. Recently, we and others have found that (1) VEGF-B is a potent survival factor for different types of cells by inhibiting apoptosis via suppressing the expression of BH3-only protein and other apoptotic/cell deathrelated genes. (2) VEGF-B has a negligible role in inducing blood vessel growth in most organs. Instead, it is critically required for blood vessel survival. VEGF-B targeting inhibited pathological angiogenesis by abolishing blood vessel survival in different animal models. (3) Using different types of neuro-injury and neurodegenerative disease models, VEGF-B treatment protected endangered neurons from apoptosis without inducing undesired blood vessel growth or permeability. Thus, VEGF-B is the first member of the VEGF family that has a potent survival/antiapoptotic effect, while lacking a general angiogenic activity. Our work thus advocates that the major function of VEGF-B is to act as a "survival," rather than an "angiogenic" factor and implicates a therapeutic potential of VEGF-B in treating different types of vascular and neurodegenerative diseases.

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“…14 Additional EC mitogens inducing EC proliferation include acidic fibroblast growth factor(aFGF), basic FGF(bFGF), hepatocyte growth factor (HGF), and transforming growth factor ␣, ␤(TGF-␣, -␤), while angiostatin and endostatin inhibit proliferation. 2,[15][16][17][18][19] Activated hepatic stellate cells also proliferate in response to hypoxia-induced VEGF, thereby participating in nonpathological hepatic angiogenesis. [43][44][45] (Center right) Signaling pathways that determine branching, formation of adequate basement membrane and ECM, and cell migration and differentiation are then activated.…”

Section: Molecular Insights Into the Angiogenic Processmentioning

confidence: 99%

“…EC proliferation may also be stimulated by additional members of the VEGF family: placental growth factor, which potentiates the effects of VEGF and plays a relevant role during angiogenesis; VEGF-C and VEGF-D, which regulate lymphatic angiogenesis; and VEGF-B, recently described to promote in vivo angiogenesis, particularly in the setting of inflammatory arthritis. 15,16 In addition, EC proliferation may be stimulated by other growth factors, such as acidic and basic fibroblast growth factors (aFGF and bFGF); hepatocyte growth factor (HGF); and transforming growth factor (TGF) ␣ and ␤, whose pathophysiological relevance is less well characterized. 2,17 Cytokines, lipid medi- Makes vessels too tight and inhibits sprouting Ang-2…”

Section: Molecular Insights Into the Angiogenic Processmentioning

confidence: 99%

Angiogenesis in chronic inflammatory liver disease

et al. 2004

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Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels. Of particular importance are growth factors, molecules involved in matrix remodeling and cell migration, and vessel maturation-related factors. In recent years, a number of studies have examined the expression and function of many pro-and antiangiogenic molecules in the setting of nontumoral chronic liver diseases and liver regeneration. This review examines the potential pathogenetic role of angiogenesis in the context of viral hepatitis, cirrhosis, autoimmune hepatitis, primary biliary cirrhosis, and alcoholic liver disease. The future perspectives for research in this field are outlined.

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Vascular Endothelial Growth Factor-B Promotes In Vivo Angiogenesis

Cited by 160 publications

References 38 publications

Genome-Wide Linkage Study of Retinal Vessel Diameters in the Beaver Dam Eye Study

Genome-Wide Linkage Study of Retinal Vessel Diameters in the Beaver Dam Eye Study

Vegf-B

Angiogenesis in chronic inflammatory liver disease

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