Inflammation-induced lymphangiogenesis and lymphatic dysfunction

Liao, Shan; Weid, Pierre‐Yves von der

doi:10.1007/s10456-014-9416-7

Cited by 74 publications

(61 citation statements)

References 104 publications

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“…Similar findings have been reported in chronic inflammation (eg, of the gastrointestinal tract, indicating that lymphatic vessel expansion may represent a compensatory mechanism to maintain interstitial fluid clearance and fluid homeostasis). 27 When imaged through the skin surface, lymphatic capillaries in the mouse tail normally have a honeycomb-like pattern. 17,28 Evaluation of the lymphatic capillaries in unoperated control mice with NIR imaging confirmed the 869 870 871 872 873 874 875 876 877 878 879 880 881 882 883 884 885 886 887 888 889 890 891 892 893 894 895 896 897 898 899 900 901 902 903 904 905 906 907 908 909 ...…”

Section: Spatiotemporal Changes In Lymphedemamentioning

confidence: 99%

Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema

Gousopoulos

Proulx

Scholl

et al. 2016

The American Journal of Pathology

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Lymphedema is a common complication that occurs after breast cancer treatment in up to 30% of the patients undergoing surgical lymph node excision. It is associated with tissue swelling, fibrosis, increased risk of infection, and impaired wound healing. Despite the pronounced clinical manifestations of the disease, little is known about the morphological and functional characteristics of the lymphatic vasculature during the course of lymphedema progression. We used an experimental murine tail lymphedema model where sustained fluid stasis was generated on disruption of lymphatic flow, resulting in chronic edema formation with fibrosis and adipose tissue deposition. Morphological analysis of the lymphatic vessels revealed a dramatic expansion during the course of the disease, with active proliferation of lymphatic endothelial cells at the early stages of lymphedema. The lymphatic capillaries exhibited progressively impaired tracer filling and retrograde flow near the surgery site, whereas the collecting lymphatic vessels showed a gradually decreasing contraction amplitude with unchanged contraction frequency, leading to lymphatic contraction arrest at the later stages of the disease. Lymphedema onset was associated with pronounced infiltration by immune cells, predominantly Ly6G(+) and CD4(+) cells, which have been linked to impaired lymphatic vessel function.

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Section: Spatiotemporal Changes In Lymphedemamentioning

confidence: 99%

Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema

Gousopoulos

Proulx

Scholl

et al. 2016

The American Journal of Pathology

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“…In addition to marking lymphatic endothelial cells, LYVE1 expression also identifies activated macrophages in adult tissues (262, 775). Macrophages have indeed recently been implicated as paracrine regulators of both angiogenesis and lymphangiogenesis (526, 537, 602, 775). Their phenotypic overlap also highlights the emerging area of research focused on lymphatic endothelial cell lineage during lymphangiogenesis in adult tissues and the and the potential for macrophages or circulating progenitor cells to differentiate into both blood and lymphatic endothelial cells (204, 303, 411, 658, 829, 844).…”

Section: Lymphangiogenesis and Relationships With Angiogenesis Duringmentioning

confidence: 99%

Lymphatic Vessel Network Structure and Physiology

Breslin

Yang

Scallan

et al. 2018

Comprehensive Physiology

277

258

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The lymphatic system is comprised of a network of vessels interrelated with lymphoid tissue, which has the holistic function to maintain the local physiologic environment for every cell in all tissues of the body. The lymphatic system maintains extracellular fluid homeostasis favorable for optimal tissue function, removing substances that arise due to metabolism or cell death, and optimizing immunity against bacteria, viruses, parasites, and other antigens. This article provides a comprehensive review of important findings over the past century along with recent advances in the understanding of the anatomy and physiology of lymphatic vessels, including tissue/organ specificity, development, mechanisms of lymph formation and transport, lymphangiogenesis, and the roles of lymphatics in disease.

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“…The interaction of VEGFC or VEGFD with VEGFR3 mediates lymphangiogenesis (Veikkola et al, 2001). The role of lymphangiogenesis in chronic inflammation is poorly understood (Liao and von der Weid, 2014). Stimulation of lymphangiogenesis via transgenic overexpression of VEGFC or VEGFD reduced the severity of inflammation in a contact hypersensitivity dermatitis model (Huggenberger et al, 2010) raising the possibility that the lack of lymphangiogenesis in cpdm mice contributes to the chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Lymphangiogenesis refers to the formation of new lymphatics resulting in remodeling of the lymphatic network in tissues. Chronic inflammation can be accompanied by dilation of lymphatics and lymphangiogenesis (Liao and von der Weid, 2014). Angiogenesis and lymphangiogenesis are potential therapeutic targets for chronic inflammatory diseases, and it is therefore important to understand the role and processes underlying these processes in chronic inflammation (Tas et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis

HogenEsch

Sola

Stearns

et al. 2016

Experimental and Molecular Pathology

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Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and antiangiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.

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Inflammation-induced lymphangiogenesis and lymphatic dysfunction

Cited by 74 publications

References 104 publications

Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema

Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema

Lymphatic Vessel Network Structure and Physiology

Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis

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