Lymphangiogenesis: Recapitulation of Angiogensis in Health and Disease

Shin, William S.; Rockson, Stanley G.

doi:10.1007/1-4020-4327-9_8

Cited by 4 publications

(25 citation statements)

References 248 publications

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“…In the early 20th century, Sabin suggested that initial lymph sacs emerge by budding from embryonic veins, and that these primitive lymphatics then spread out throughout the body to form lymphatic networks 44,45 . Several lymphatic‐specific markers including vascular endothelial growth factor receptor‐3 (VEGFR‐3), lymphatic vessel endothelial hyaluronan receptor (LYVE‐1), and the transcription factor prospero‐related homeobox 1 (PROX‐1) are expressed in endothelial cells that form the budding lymph sacs in mouse embryos, supporting Sabin's theory of lymphatic development 1,10,46–48 …”

Section: Embryonic Lymphatic Developmentmentioning

confidence: 92%

“…The lymphatic system is a part of both the circulatory and immune systems 1,2 . In addition to maintaining tissue fluid homeostasis through the evacuation of protein‐rich lymph from tissues, with transport to the blood vascular system for recirculation, the lymphatics serve as conduits for the transport of lymphocytes and antigen‐presenting dendritic cells to regional lymph nodes 3 .…”

Section: The Lymphatic System: Structure and Functionmentioning

confidence: 99%

“…The lymphatic system is essential for homeostasis of the circulatory and immune systems, and lymphatic dysfunction can manifest within a predictable spectrum of sequelae, 11 ranging from isolated immune impairment to a debilitating form of regional swelling termed lymphedema , in which inadequate transport of interstitial fluid, impaired immunity, and fibrosis are observed. Historically, the pathologic expression of lymphedema has been poorly understood 1 . According to the classical model, an imbalance between lymphatic load and transport capacity predicates the accumulation of protein and obligate fluid in the interstitial space, 13–15 which results in further edema formation as a consequence of increases in tissue colloid osmotic pressure.…”

Section: Disease As a Manifestation Of Lymphatic Dysfunctionmentioning

confidence: 99%

“…The VEGF family comprises seven identified growth factors, namely VEGF (VEGF‐A), VEGF‐B, VEGF‐C, VEGF‐D, orf virus VEGF (VEGF‐E), VEGF‐F, and PIGF, which bind to three receptors, VEGFR‐1, VEGFR‐2, and VEGFR‐3, with varying specificities 1,11,51 . VEGFRs are high‐affinity receptor kinases that are believed to mediate VEGF signaling by undergoing dimerization and transphosphorylation upon ligand binding 10 .…”

Section: Lymphatic Competencementioning

confidence: 99%

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Animal Models for the Molecular and Mechanistic Study of Lymphatic Biology and Disease

Shin

Rockson

2008

Annals of the New York Academy of Sciences

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The development of animal model systems for the study of the lymphatic system has resulted in an explosion of information regarding the mechanisms governing lymphatic development and the diseases associated with lymphatic dysfunction. Animal studies have led to a new molecular model of embryonic lymphatic vascular development, and have provided insight into the pathophysiology of both inherited and acquired lymphatic insufficiency. It has become apparent, however, that the importance of the lymphatic system to human disease extends, beyond its role in lymphedema, to many other diverse pathologic processes, including, very notably, inflammation and tumor lymphangiogenesis. Here, we have undertaken a systematic review of the models as they relate to molecular and functional characterization of the development, maturation, genetics, heritable and acquired diseases, and neoplastic implications of the lymphatic system. The translation of these advances into therapies for human diseases associated with lymphatic dysfunction will require the continued study of the lymphatic system through robust animal disease models that simulate their human counterparts.

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Section: Embryonic Lymphatic Developmentmentioning

confidence: 92%

Section: The Lymphatic System: Structure and Functionmentioning

confidence: 99%

Section: Disease As a Manifestation Of Lymphatic Dysfunctionmentioning

confidence: 99%

Section: Lymphatic Competencementioning

confidence: 99%

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Animal Models for the Molecular and Mechanistic Study of Lymphatic Biology and Disease

Shin

Rockson

2008

Annals of the New York Academy of Sciences

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“…6 VEGF-C knockout mice demonstrate complete abrogation of early lymphatic vessel formation, 7 thus underscoring the vital role that VEGF-C plays during embryonic lymphangiogenesis. 8 Although PROX-1 expression is not inhibited in these VEGF-C-deficient mice, PROX-1-positive, lymphatically specified endothelial cells are unable to bud from the embryonic cardinal vein to form initial lymph sacs, suggesting that LEC specification and subsequent cell migration are Stanford University School of Medicine, Stanford, California. controlled by distinct signaling pathways.…”

Section: Genetic Models Of Lymphatic Developmentmentioning

confidence: 98%

Animal Models for the Mechanistic Study of Systemic Lymphangiomatosis

Rockson

2011

Lymphatic Research and Biology

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The systematic study of focused animal models has produced an explosion of information regarding the mechanisms governing lymphatic development and the diseases associated with lymphatic dysfunction. Nevertheless, the pathogenesis of systemic lymphangiomatosis has, thus far, eluded mechanistic comprehension. In this review, recent molecular advances in lymphatic vascular development are considered within the context of the animal models that have produced evolving insights. The emerging role of the zebrafish within lymphatic investigation is discussed. Specific models of the human disease pathology are considered in detail. While much has been learned about the molecular framework that surrounds normal lymphatic vascular development, the defect responsible for systemic lymphangiomatosis remains elusive. Development of more robust, recapitulative models will also be invaluable to investigate new and emerging therapeutics for the often devastating disease of systemic lymphangiomatosis.

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