Growth Hormone Promotes Lymphangiogenesis

Bänziger-Tobler, Nadja E.; Halin, Cornelia; Kajiya, Kentaro; Detmar, Michael

doi:10.2353/ajpath.2008.080060

Cited by 39 publications

(30 citation statements)

References 71 publications

(99 reference statements)

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“…Finally, the arterial marker ephrinB2 was up-regulated only by NICD, but not by Hey1, Hey2, or Hes1. We also found that activated NICD strongly down-regulated a number of other previously reported lymphatic markers, including coxsackie virus and adenovirus receptor, 42,43 c-Maf, 14,44 plakoglobin, 13 transforming growth factor-␣, 14 aldehyde dehydrogenase 1 A1, 14 and growth hormone receptor 14,45 (Table 2). Taken together, these data indicate that Notch signal suppresses the lymphatic phenotypes and possibly augments the arterial phenotype in postdevelopmental LECs.…”

Section: Notch Signal Regulates Other Lymphatic Markerssupporting

confidence: 64%

An exquisite cross-control mechanism among endothelial cell fate regulators directs the plasticity and heterogeneity of lymphatic endothelial cells

Kang

Yoo

Lee

et al. 2010

Blood

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111

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Arteriovenous-lymphatic endothelial cell fates are specified by the master regulators, namely, Notch, COUP-TFII, and Prox1. Whereas Notch is expressed in the arteries and COUP-TFII in the veins, the lymphatics express all 3 cell fate regulators. Previous studies show that lymphatic endothelial cell (LEC) fate is highly plastic and reversible, raising a new concept that all 3 endothelial cell fates may coreside in LECs and a subtle alteration can result in a reprogramming of LEC fate. We provide a molecular basis verifying this concept by identifying a crosscontrol mechanism among these cell fate regulators. We found that Notch signal down-regulates Prox1 and COUP-TFII through Hey1 and Hey2 and that activated Notch receptor suppresses the lymphatic phenotypes and induces the arterial cell fate. On the contrary, Prox1 and COUP-TFII attenuate vascular endothelial growth factor signaling, known to induce Notch, by repressing vascular endothelial growth factor receptor-2 and neuropilin-1. We show that previously reported podoplanin-based LEC heterogeneity is associated with differential expression of Notch1 in human cutaneous lymphatics. We propose that the expression of the 3 cell fate regulators is controlled by an exquisite feedback mechanism working in LECs and that LEC fate is a consequence of the Prox1-directed lymphatic equilibrium among the cell fate regulators. (Blood. 2010;116(1):140-150)

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Section: Notch Signal Regulates Other Lymphatic Markerssupporting

confidence: 64%

An exquisite cross-control mechanism among endothelial cell fate regulators directs the plasticity and heterogeneity of lymphatic endothelial cells

Kang

Yoo

Lee

et al. 2010

Blood

Self Cite

111

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“…Newly identified lymphangiogenic factors include the growth hormone (GH), 88 and the multifunctional peptide adrenomedullin (AM), which signals via the calcitonin receptor-like receptor (calcrl) associated with the receptor activity modifying protein (RAMP) 2. In addition to AM signaling having a role in lymphatic development as revealed by knockout mice for either AM itself or calcrl or RAMP2 (Table 1), adrenomedullin treatment promotes the proliferation of cultured human LECs.…”

Section: Lymphangiogenesis In the Adultmentioning

confidence: 99%

The Lymphatic System in Health and Disease

Cueni

Detmar

2008

Lymphatic Research and Biology

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252

216

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The lymphatic vascular system has an important role in the regulation of tissue pressure, immune surveillance and the absorption of dietary fat in the intestine. There is growing evidence that the lymphatic system also contributes to a number of diseases, such as lymphedema, cancer metastasis and different inflammatory disorders. The discovery of various molecular markers allowing the distinction of blood and lymphatic vessels, together with the availability of a increasing number of in vitro and in vivo models to study various aspects of lymphatic biology, has enabled tremendous progress in research into the development and function of the lymphatic system. This review discusses recent advances in our understanding of the embryonic development of the lymphatic vasculature, the molecular mechanisms mediating lymphangiogenesis in the adult, the role of lymphangiogenesis in chronic inflammation and lymphatic cancer metastasis, and the emerging importance of the lymphatic vasculature as a therapeutic target.

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“…Growth hormone is produced steadily during childhood, doubles in production during puberty [13], and is known to promote lymphangiogenesis [14]. Recently, a study of LM tissue found an overexpression of GH receptors (65%) compared to the control tissue (25.8%), which suggests that GH may play a role in LM pathophysiology and influencing disease progression [15].…”

Section: Discussionmentioning

confidence: 99%

Natural History of Lymphatic Malformation Progression in Children: A Retrospective Study

Patel¹,

Tu²,

Teng³

2017

J Clin Exp Dermatol Res

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Background/Objectives: Lymphatic malformation (LM) is a challenging lifetime disorder that can significantly impact children's lives, and a key challenge in management is knowing when interventions might be appropriate. The purpose of this study was to determine (i) natural progression of complications associated with lymphatic malformations during childhood and adolescence, (ii) risk factors associated with complications, and (iii) whether early intervention decreases LM complication rates in adolescents or young adults.

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Growth Hormone Promotes Lymphangiogenesis

Cited by 39 publications

References 71 publications

An exquisite cross-control mechanism among endothelial cell fate regulators directs the plasticity and heterogeneity of lymphatic endothelial cells

An exquisite cross-control mechanism among endothelial cell fate regulators directs the plasticity and heterogeneity of lymphatic endothelial cells

The Lymphatic System in Health and Disease

Natural History of Lymphatic Malformation Progression in Children: A Retrospective Study

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