scholarly journals Lymphatic endothelium

2003 ◽  
Vol 163 (2) ◽  
pp. 209-213 ◽  
Author(s):  
Michael S. Pepper ◽  
Mihaela Skobe
Keyword(s):  
Tumor Cells ◽  
Interstitial Fluid ◽  
Molecular Mechanisms ◽  
Lymphatic Vessels ◽  
Traditional View ◽  
Lymphatic Endothelium ◽  
Point Of Entry ◽  
Recent Advances ◽  
And Function

The lymphatic microvasculature is uniquely adapted for the continuous removal of interstitial fluid and proteins, and is an important point of entry for leukocytes and tumor cells. The traditional view that lymphatic capillaries are passive participants in these tasks is currently being challenged. This overview highlights recent advances in our understanding of the molecular mechanisms underlying the formation and function of lymphatic vessels.

scholarly journals Secondary lymphedema: Pathogenesis

2021 ◽  
Vol 3 ◽  
pp. 7-15
Author(s):  
Smitha Ancy Varghese
Keyword(s):  
Interstitial Fluid ◽  
Molecular Mechanisms ◽  
Subcutaneous Tissue ◽  
Lymphatic Vessels ◽  
Therapeutic Interventions ◽  
Elastic Fibers ◽  
Therapeutic Approaches ◽  
Secondary Lymphedema ◽  
Common Causes ◽  
The Common

Secondary lymphedema follows an acquired defect in the lymphatic system. The common causes leading to a defective lymphatic function include infection, inflammation, malignancy, trauma, obesity, immobility, and therapeutic interventions. Understanding the pathogenesis of lymphedema is of prime importance in offering effective treatment. The pathogenetic mechanisms such as lymphatic valvular insufficiency, obliteration/ disruption of lymphatic vessels, and decreased lymphatic contractility aggravate lymphatic hypertension and lymphstasis. Accumulation of lymph, interstitial fluid, proteins, and glycosaminoglycans within the skin and subcutaneous tissue eventually stimulates collagen production by fibroblasts, causes disruption of elastic fibers, and activates keratinocytes, fibroblasts, and adipocytes. These result in thickening of skin and cause fibrosis of subcutaneous tissue. However, the sequence of these pathomechanisms, their inter-relationship and progression vary depending on the specific etiology of the lymphedema. In this article, we discuss the possible cellular and molecular mechanisms involved in the pathogenesis. Further studies to delineate the exact sequence of pathogenic processes surrounding the primary triggering event can help to formulate tailored therapeutic approaches.

scholarly journals Targeting Raf Kinase Inhibitory Protein Regulation and Function

Cancers ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 306 ◽  
Author(s):  
Ali Yesilkanal ◽  
Marsha Rosner
Keyword(s):  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Signaling Networks ◽  
Metastasis Suppressor ◽  
Metastatic Progression ◽  
Inhibitory Protein ◽  
Raf Kinase ◽  
Raf Kinase Inhibitory Protein ◽  
And Function

Raf Kinase Inhibitory Protein (RKIP) is a highly conserved kinase inhibitor that functions as a metastasis suppressor in a variety of cancers. Since RKIP can reprogram tumor cells to a non-metastatic state by rewiring kinase networks, elucidating the mechanism by which RKIP acts not only reveals molecular mechanisms that regulate metastasis, but also represents an opportunity to target these signaling networks therapeutically. Although RKIP is often lost during metastatic progression, the mechanism by which this occurs in tumor cells is complex and not well understood. In this review, we summarize our current understanding of RKIP regulation in tumors and consider experimental and computational strategies for recovering or mimicking its function by targeting mediators of metastasis.

scholarly journals Secondary lymphedema: Pathogenesis

2021 ◽  
Vol 3 ◽  
pp. 7-15
Author(s):  
Smitha Ancy Varghese
Keyword(s):  
Interstitial Fluid ◽  
Molecular Mechanisms ◽  
Subcutaneous Tissue ◽  
Lymphatic Vessels ◽  
Therapeutic Interventions ◽  
Elastic Fibers ◽  
Therapeutic Approaches ◽  
Secondary Lymphedema ◽  
Common Causes ◽  
The Common

Secondary lymphedema follows an acquired defect in the lymphatic system. The common causes leading to a defective lymphatic function include infection, inflammation, malignancy, trauma, obesity, immobility, and therapeutic interventions. Understanding the pathogenesis of lymphedema is of prime importance in offering effective treatment. The pathogenetic mechanisms such as lymphatic valvular insufficiency, obliteration/ disruption of lymphatic vessels, and decreased lymphatic contractility aggravate lymphatic hypertension and lymphstasis. Accumulation of lymph, interstitial fluid, proteins, and glycosaminoglycans within the skin and subcutaneous tissue eventually stimulates collagen production by fibroblasts, causes disruption of elastic fibers, and activates keratinocytes, fibroblasts, and adipocytes. These result in thickening of skin and cause fibrosis of subcutaneous tissue. However, the sequence of these pathomechanisms, their inter-relationship and progression vary depending on the specific etiology of the lymphedema. In this article, we discuss the possible cellular and molecular mechanisms involved in the pathogenesis. Further studies to delineate the exact sequence of pathogenic processes surrounding the primary triggering event can help to formulate tailored therapeutic approaches.

scholarly journals Impact of TCM on Tumor-Infiltrating Myeloid Precursors in the Tumor Microenvironment

2021 ◽  
Vol 9 ◽  
Author(s):  
Jinlong Liu ◽  
Yuchen Wang ◽  
Zhidong Qiu ◽  
Guangfu Lv ◽  
Xiaowei Huang ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Lymphatic Vessels ◽  
Suppressor Cells ◽  
Tumor Immunotherapy ◽  
Tumor Stroma ◽  
Therapeutic Effects ◽  
Tumor Associated Macrophage ◽  
And Function

The tumor microenvironment (TME) is composed of tumor cells, blood/lymphatic vessels, the tumor stroma, and tumor-infiltrating myeloid precursors (TIMPs) as a sophisticated pathological system to provide the survival environment for tumor cells and facilitate tumor metastasis. In TME, TIMPs, mainly including tumor-associated macrophage (TAM), tumor-associated dendritic cells (DCs), and myeloid-derived suppressor cells (MDSCs), play important roles in repressing the antitumor activity of T cell or other immune cells. Therefore, targeting those cells would be one novel efficient method to retard cancer progression. Numerous studies have shown that traditional Chinese medicine (TCM) has made extensive research in tumor immunotherapy. In the review, we demonstrate that Chinese herbal medicine (CHM) and its components induce tumor cell apoptosis, directly inhibiting tumor growth and invasion. Further, we discuss that TCM regulates TME to promote effective antitumor immune response, downregulates the numbers and function of TAMs/MDSCs, and enhances the antigen presentation ability of mature DCs. We also review the therapeutic effects of TCM herbs and their ingredients on TIMPs in TME and systemically analyze the regulatory mechanisms of TCM on those cells to have a deeper understanding of TCM in tumor immunotherapy. Those investigations on TCM may provide novel ideas for cancer treatment.

Different role of CD73 in leukocyte trafficking via blood and lymph vessels

Blood ◽  
2011 ◽  
Vol 117 (16) ◽  
pp. 4387-4393 ◽  
Author(s):  
Annika Ålgars ◽  
Marika Karikoski ◽  
Gennady G. Yegutkin ◽  
Patrizia Stoitzner ◽  
Jussi Niemelä ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Lymphatic Vessels ◽  
Nucleotide Metabolism ◽  
Lymphatic Endothelium ◽  
Lymphocyte Migration ◽  
Lymph Vessels ◽  
Atp Metabolism ◽  
And Function ◽  
Afferent Lymph

Abstract CD73 is involved in the extracellular ATP metabolism by dephosphorylating extracellular AMP to adenosine and thus regulating permeability of the blood vessels and leukocyte traffic into the tissues. It is also present on lymphatic vessels where its distribution and function have not been characterized. We found that CD73 is expressed on a subpopulation of afferent lymph vessels but is absent on efferent lymphatics, unlike LYVE-1 and podoplanin, which are expressed on both types of lymphatics. The extracellular nucleotide metabolism on lymphatic endothelium differs from that on blood vessel endothelium as lymphatic endothelium has lower NTPDase and higher ecto-5′-nucleotidase/CD73 activity than blood vascular endothelium. In knockout mice, the lack of CD73 on lymphocytes decreases migration of lymphocytes to the draining lymph nodes more than 50% while CD73-deficient lymph vessels mediate lymphocyte trafficking as efficiently as the wild-type lymphatics. Thus, although endothelial CD73 is important for permeability and leukocyte extravasation in blood vessels, it does not have a role in these functions on lymphatics. Instead, lymphocyte CD73 is intimately involved in lymphocyte migration via afferent lymphatic vessels.

scholarly journals Recent advances in understanding the molecular mechanisms of the development and function of T h17 cells

2013 ◽  
Vol 18 (4) ◽  
pp. 247-265 ◽  
Author(s):  
Yutaka Kurebayashi ◽  
Shigenori Nagai ◽  
Ai Ikejiri ◽  
Shigeo Koyasu
Keyword(s):  
Molecular Mechanisms ◽  
Recent Advances ◽  
And Function

scholarly journals Cerebrovascular Injuries Induce Lymphatic Invasion into Brain Parenchyma to Guide Vascular Regeneration in Zebrafish

2018 ◽  
Author(s):  
Jingying Chen ◽  
Jianbo He ◽  
Qifen Yang ◽  
Yaoguang Zhang ◽  
Lingfei Luo
Keyword(s):  
Blood Vessels ◽  
Brain Edema ◽  
Interstitial Fluid ◽  
Molecular Mechanisms ◽  
Lymphatic Vessels ◽  
Lymphatic Invasion ◽  
Brain Parenchyma ◽  
Genetic Ablation ◽  
Vascular Regeneration ◽  
Promising Therapeutic Approach

SUMMARYDamage to regional cerebrovascular network and neuronal tissues occurs during acute cerebrovascular diseases, such as ischemic stroke. The promotion of vascular regeneration is the most promising therapeutic approach. To understand cellular and molecular mechanisms underlying brain vascular regeneration, we developed two zebrafish cerebrovascular injury models using genetic ablation and photochemical thrombosis. Although brain parenchyma is physiologically devoid of lymphatic vasculature, we found that cerebrovascular injuries induce rapid ingrowth of meningeal lymphatics into the injured parenchyma. The ingrown lymphatics on one hand become lumenized drain interstitial fluid to resolve brain edema, on the other hand act as “growing tracks” for nascent blood vessels. The ingrown lymphatic vessels undergo apoptosis and clearance after cerebrovascular regeneration. This study reveals a pathological function of meningeal lymphatics, through previously unexpected ingrowth into brain parenchyma and a newly identified lymphatic function as vascular “growing tracks”.HIGHLIGHTSCerebrovascular injuries induce lymphatic ingrowth into the injured brain parenchyma The ingrown lymphatics drain interstitial fluid to resolve brain edema Nascent blood vessels use the ingrown lymphatic vessels as “growing tracks” The ingrown lymphatic vessels undergo apoptosis after vascular regeneration completes

scholarly journals Mechanisms and Clinical Significance of Tumor Lymphatic Invasion

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2585
Author(s):  
Noriki Fujimoto ◽  
Lothar C. Dieterich
Keyword(s):  
Tumor Cells ◽  
Prognostic Value ◽  
Molecular Mechanisms ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Lymphatic Invasion ◽  
Malignant Cells ◽  
Single Tumor ◽  
Draining Lymph Nodes ◽  
Gain Access

Tumor-associated lymphatic vessels play an important role in tumor progression, mediating lymphatic dissemination of malignant cells to tumor-draining lymph nodes and regulating tumor immunity. An early, necessary step in the lymphatic metastasis cascade is the invasion of lymphatic vessels by tumor cell clusters or single tumor cells. In this review, we discuss our current understanding of the underlying cellular and molecular mechanisms, which include tumor-specific as well as normal, developmental and immunological processes “hijacked” by tumor cells to gain access to the lymphatic system. Furthermore, we summarize the prognostic value of lymphatic invasion, discuss its relationship with local recurrence, lymph node and distant metastasis, and highlight potential therapeutic options and challenges.

A Mucin-Specific Protease Enables Molecular and Functional Analysis of Human Cancer-Associated Mucins

2018 ◽  
Author(s):  
Stacy A. Malaker ◽  
Kayvon Pedram ◽  
Michael J. Ferracane ◽  
Elliot C. Woods ◽  
Jessica Kramer ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Molecular Mechanisms ◽  
Cultured Cells ◽  
High Resolution Mass Spectrometry ◽  
Human Cancer ◽  
Glycosylation Sites ◽  
Bacterial Protease ◽  
Specific Protease ◽  
To Come ◽  
And Function

<div> <div> <div> <p>Mucins are a class of highly O-glycosylated proteins that are ubiquitously expressed on cellular surfaces and are important for human health, especially in the context of carcinomas. However, the molecular mechanisms by which aberrant mucin structures lead to tumor progression and immune evasion have been slow to come to light, in part because methods for selective mucin degradation are lacking. Here we employ high resolution mass spectrometry, polymer synthesis, and computational peptide docking to demonstrate that a bacterial protease, called StcE, cleaves mucin domains by recognizing a discrete peptide-, glycan-, and secondary structure- based motif. We exploited StcE’s unique properties to map glycosylation sites and structures of purified and recombinant human mucins by mass spectrometry. As well, we found that StcE will digest cancer-associated mucins from cultured cells and from ovarian cancer patient-derived ascites fluid. Finally, using StcE we discovered that Siglec-7, a glyco-immune checkpoint receptor, specifically binds sialomucins as biological ligands, whereas the related Siglec-9 receptor does not. Mucin-specific proteolysis, as exemplified by StcE, is therefore a powerful tool for the study of glycoprotein structure and function and for deorphanizing mucin-binding receptors. </p> </div> </div> </div>

Sign in / Sign up

Export Citation Format

Share Document