The optimum marker for the detection of lymphatic vessels

Kong, Lingling; Yang, Nianzhao; Shi, Lianghui; Zhao, Guo‐Hai; Zhou, Wenbin; Ding, Qiang; Wang, Ming‑Hai; Zhang, Yisheng

doi:10.3892/mco.2017.1356

Cited by 56 publications

(52 citation statements)

References 69 publications

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“…CD31 is a traditional marker of blood vessels that is weakly expressed on lymphatics [110]. However, podoplanin is a more specific marker of lymphatic endothelium since it is absent from blood vessel endothelium [111]. Conversely, LYVE-1 has been found to be expressed in some macrophages and blood vessels, including liver sinusoids [110].…”

Section: After Transplantationmentioning

confidence: 99%

Variable Responses to Corneal Grafts: Insights from Immunology and Systems Biology

Zazzo

Lee

Sung

et al. 2020

JCM

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Corneal grafts interact with their hosts via complex immunobiological processes that sometimes lead to graft failure. Prediction of graft failure is often a tedious task due to the genetic and nongenetic heterogeneity of patients. As in other areas of medicine, a reliable prediction method would impact therapeutic decision-making in corneal transplantation. Valuable insights into the clinically observed heterogeneity of host responses to corneal grafts have emerged from multidisciplinary approaches, including genomics analyses, mechanical studies, immunobiology, and theoretical modeling. Here, we review the emerging concepts, tools, and new biomarkers that may allow for the prediction of graft survival.

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Section: After Transplantationmentioning

confidence: 99%

Variable Responses to Corneal Grafts: Insights from Immunology and Systems Biology

Zazzo

Lee

Sung

et al. 2020

JCM

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“…(1:200, catalog number 14044380, Thermo Fisher Scientific) and podoplanin (1:300, catalog number 127408, BioLegend, San Diego, CA) to label the lymphatic vasculature (14). To visualize the immune cell response after injury in tendon, tissues were fixed in ice cold acetone for ten minutes, blocked with 5% goat serum for one hour, and stained with biotinylated antibodies against CD11b to identify myeloid cells ( Invitrogen) were used to detect primary antibodies that were not already conjugated to a fluorophore.…”

Section: Surgeriesmentioning

confidence: 99%

Adaptive and Innate Immune Cell Responses in Tendons and Lymph Nodes After Tendon Injury and Repair

Noah

Martinez

et al. 2019

Preprint

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Tendon injuries are a common clinical condition with limited treatment options. The cellular components of the innate system, such as neutrophils and macrophages, have been well studied in tendon injuries. However the adaptive immune system, comprised of specialized lymphocytes, plays an important role in orchestrating the healing of numerous tissues but less is known about these cells in tendon healing. To gain a greater understanding of the biological processes that regulate tendon healing, we sought to determine how the cellular components of the adaptive and innate immune system respond to a tendon injury using two-month old male mice. We determined that the lymphatic vasculature is present in the epitenon and superficial regions of Achilles tendons. We then created an acute Achilles tenotomy followed by repair, and collected tendons and draining lymph nodes one, two, and four weeks after injury. Using flow cytometry and histology, after tendon injury we observed a robust adaptive immune cell response that followed an initial innate immune cell response. There was an accumulation of monocytes, neutrophils, and macrophages one week after injury that declined thereafter. Dendritic cells and CD4 + T cells peaked two weeks after injury, while B cells and CD8 + T cells progressively increased over time. In parallel, immune cells of the draining popliteal lymph node demonstrated a similarly coordinated response to the injury. These results suggest that there is an adaptive immune response to tendon injury and adaptive immune cells may play a role in regulating tendon healing.

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“…4 b). After purification, > 95% of the cells expressed the arteriovenous EC marker CXCR4 [ 33 , 34 ] and the arterial marker DLL4 [ 33 , 35 – 37 ], while ~ 16% expressed the venous marker EphB4 [ 38 , 39 ], but expression of the lymphatic EC marker podoplanin [ 40 , 41 ] was undetectable (Fig. 4 c).…”

Section: Resultsmentioning

confidence: 99%

“…Three cell lines were reprogrammed from the cells of patients with diseases or disease symptoms that are associated with endothelial dysfunction: T2DM (two lines) [ 23 ] and Hutchinson-Gilford progeria syndrome (one line) [ 24 , 25 ]. Analysis of the expression of markers for arterial (DLL4 and CXCR4) [ 33 – 37 ], venous (EphB4 and CXCR4) [ 33 , 34 , 38 , 39 ], and lymphatic (podoplanin) [ 40 , 41 ] ECs indicated that the population of differentiated cells contained only arteriovenous ECs. hiPSC-ECs formed tubular structures and EC lumens in vitro and restore perfusion and improve vascularity in a murine HLI model after transplantation in vivo.…”

Section: Discussionmentioning

confidence: 99%

The prostaglandin H2 analog U-46619 improves the differentiation efficiency of human induced pluripotent stem cells into endothelial cells by activating both p38MAPK and ERK1/2 signaling pathways

Kong

Lim

et al. 2018

Stem Cell Res Ther

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BackgroundWe have shown that the differentiation of human-induced pluripotent stem cells (hiPSCs) into endothelial cells (ECs) is more efficient when performed with a 3-dimensional (3D) scaffold of biomaterial than in monolayers. The current study aims to further increase hiPSC-EC differentiation efficiency by deciphering the signaling pathways in 3D scaffolds.Methods and resultsWe modified our 3D protocol by using U-46619 to upregulate both p38 mitogen-activated protein kinase (p38MAPK) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, which increased the differentiation efficiency (as measured by CD31 expression) to as high as 89% in two established hiPSC lines. The differentiated cells expressed arteriovenous, but not lymphatic, markers; formed tubular structures and EC lumen in vitro; had significantly shorter population-doubling times than monolayer-differentiated hiPSC-ECs; and restored perfusion and vascularity in a murine hind limb ischemia model. The differentiation efficiency was also > 85% in three hiPSC lines that had been derived from patients with diseases or disease symptoms that have been linked to endothelial dysfunction.ConclusionsThese observations demonstrate that activating both p38MAPK and ERK1/2 signaling pathways with U-46619 improves the efficiency of arteriovenous hiPSC-EC differentiation and produces cells with greater proliferative capacity.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-1061-4) contains supplementary material, which is available to authorized users.

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The optimum marker for the detection of lymphatic vessels

Cited by 56 publications

References 69 publications

Variable Responses to Corneal Grafts: Insights from Immunology and Systems Biology

Variable Responses to Corneal Grafts: Insights from Immunology and Systems Biology

Adaptive and Innate Immune Cell Responses in Tendons and Lymph Nodes After Tendon Injury and Repair

The prostaglandin H2 analog U-46619 improves the differentiation efficiency of human induced pluripotent stem cells into endothelial cells by activating both p38MAPK and ERK1/2 signaling pathways

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