Enrichment of Lymphatic Vessel Endothelial Hyaluronan Receptor 1 (LYVE1)-Positive Macrophages Around Blood Vessels in the Normal Human Sclera

Schlereth, Simona L.; Neuser, Barbara; Caramoy, Albert; Grajewski, Rafael S.; Koch, Konrad R.; Schrödl, Falk; Cursiefen, Claus; Heindl, Ludwig M.

doi:10.1167/iovs.13-13453

Cited by 32 publications

(27 citation statements)

References 37 publications

(39 reference statements)

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“…Macrophages are often observed in histological sections, being interspersed among lymphatic endothelial cells, especially in tumor-associated lymphatic vessels. A subpopulation of LYVE-1-positive macrophages is reported to be closely related to blood (Schlereth et al 2014) and lymphatic vessels (Gordon et al 2010). All these data should support macrophages as a potential source of lymphatic progenitor cells, but other experimental data showed that LYVE-1-positive macrophages do not express Prox 1 and, thus, are unlikely to be underwent trans-differentiation into lymphatic endothelial cells (Gordon et al 2010).…”

Section: Macrophagesmentioning

confidence: 99%

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Cimpean

Raica

2015

Arch. Immunol. Ther. Exp.

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Several papers about lymphangiogenesis and inflammation focused on the detailed and complicated descriptions of the molecular pathways accompanying both non-tumor and tumor inflammatory-induced lymphatic vessel development. Many authors are tempted to present inflammatory-induced lymphangiogenesis in pathologic conditions neglecting the role of inflammatory cells during embryonic lymphatic vessel development. Some of the inflammatory cells are largely characterized in inflammatory-induced lymphangiogenesis, while others as mast cells, eosinophils, or plasma cells are less studied. No phenotypic characterization of inflammation-activated lymphatic endothelial cell is available in this moment. Another paradox is related to the existence of few papers regarding lymphangiogenesis inside lymphoid organs and for their related pathology. There are still several "missing pieces of such a big puzzle" of lymphangiogenesis and inflammation, with a direct impact on the ineffectiveness of the anti-inflammatory therapy as lymphangiogenesis inhibitors. The present paper will focus on the controversial issues of lymphangiogenesis and inflammation.

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Section: Macrophagesmentioning

confidence: 99%

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Cimpean

Raica

2015

Arch. Immunol. Ther. Exp.

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“…10 Vascular vessel formation is impaired in T1DM mice. CD31 is a specific marker widely used for vascular vessel identification (15). In the following experiments, CD31 protein levels were detected in the wounded skin of control and T1DM mice.…”

Section: Resultsmentioning

confidence: 86%

Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model

Jing

2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the mechanisms for impaired skin wound healing in subjects with diabetes. Type 1 diabetes (T1DM) was induced in BALB/c mice using streptozotocin. One month after the establishment of the T1DM mouse model, a wound was formed on the back of the mice, and tissues from the wounds and the margins were collected on days 0, 3, 7 and 10. Protein levels of cluster of differentiation 31 (CD31) were detected using immunohistochemistry, and the mRNA levels of Akt, hypoxia-inducible factor-1α (Hif-1α), vascular endothelial growth factor (Vegf ), VEGF receptor 2 (Vegfr2), stromal cell-derived growth factor-1α (Sdf-1α) and CXC chemokine receptor 4 (Cxcr4) were determined using reverse transcription-quantitative polymerase chain reaction analysis. The corresponding protein levels were determined using western blotting. The skin wound healing rate in the T1DM mice was significantly lower than that in the control mice, and the protein level of CD31 in the wounded skin of the T1DM mice was significantly decreased. Furthermore, the overall mRNA levels of Akt, Vegf, Vegfr2, and Cxcr4 in the T1DM mice were significantly lower than those in the control mice, and similar trends were observed in the protein levels. In conclusion, skin wound healing was impaired in the T1DM mice, and this may have been caused by a deficiency of Akt/HIF-1α and downstream signaling, as well as delayed angiogenesis. IntroductionDiabetes mellitus is a chronic disease threatening the health of individuals worldwide (1). There are multiple, often serious, complications associated with diabetes mellitus, one of which is impaired healing, which can lead to a reduction in physical activity and, in certain cases, chronic wounds and limb amputation (1,2). An imbalance between the pro-and anti-inflammatory mediators accentuates diabetic vascular complications and impedes proper wound healing (3). Other factors that contribute to deficient healing in patients with diabetes include altered host responses; attenuated antibacterial defenses; prolonged inflammation; changes in protease activity; insufficient cell production for rapid and robust healing; angiogenic disorders; decreased production of growth factors; inadequate extracellular matrix production; and changes in apoptosis (1-5).Wound healing is a complex process involving inflammation, granulation tissue formation, the production of new structures and tissue remodeling (2). The process is dependent upon a series of interactions between a variety of cell types, cytokine mediators and the extracellular matrix (1). In order for wound healing to be successful, a sufficient number of cells must be generated to participate in the repair (2,6,7). Processes that have a negative effect on the generation of an adequate cell number, such as inappropriately high levels of fibroblast apoptosis, may limit healing (6,7).Hypoxia-inducible factor (HIF)-1 is a master regulator of oxygen homeostasis and is comprised of HIF-1α, a finely regulated subunit, and HIF-1β (also ...

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“…Similar to the cornea, the sclera and the inner eye are also physiologically devoid of lymphatic vessels, although in direct neighborhood to lymphvascularized tissues [4,31,32]. Lymphatic vessels accompany the extraocular muscles, which insert into the sclera, but lymphatic vessel growth abruptly stops when approaching the sclera.…”

Section: The Lymphatic Vascular Anatomy Of the Eyementioning

confidence: 99%

“…Lymphatic vessels accompany the extraocular muscles, which insert into the sclera, but lymphatic vessel growth abruptly stops when approaching the sclera. The most outer layer of the sclera, the episclera, contains a tight network of blood vessels, which is surrounded by LYVE1+ macrophages [32]. The fetal sclera is also alymphatic but, in contrast to the adult sclera, contains only few macrophages [33].…”

Section: The Lymphatic Vascular Anatomy Of the Eyementioning

confidence: 99%

Antilymphangiogenic therapy to promote transplant survival and to reduce cancer metastasis: What can we learn from the eye?

Hos

Schlereth

Bock

et al. 2015

Seminars in Cell & Developmental Biology

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Enrichment of Lymphatic Vessel Endothelial Hyaluronan Receptor 1 (LYVE1)-Positive Macrophages Around Blood Vessels in the Normal Human Sclera

Cited by 32 publications

References 37 publications

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Lymphangiogenesis and Inflammation—Looking for the “Missing Pieces” of the Puzzle

Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse model

Antilymphangiogenic therapy to promote transplant survival and to reduce cancer metastasis: What can we learn from the eye?

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