scholarly journals IL-27 Inhibits Lymphatic Endothelial Cell Proliferation by STAT1-Regulated Gene Expression

2013 ◽  
Vol 20 (6) ◽  
pp. 555-564 ◽  
Author(s):  
Sebastian Rune Nielsen ◽  
Troels Hammer ◽  
Josefine Gibson ◽  
Michael S. Pepper ◽  
Riccardo E. Nisato ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Lymphatic Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Regulated Gene Expression

scholarly journals Macrophages define dermal lymphatic vessel calibre during development by regulating lymphatic endothelial cell proliferation

Development ◽  
2010 ◽  
Vol 137 (22) ◽  
pp. 3899-3910 ◽  
Author(s):  
E. J. Gordon ◽  
S. Rao ◽  
J. W. Pollard ◽  
S. L. Nutt ◽  
R. A. Lang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Lymphatic Vessel ◽  
Lymphatic Endothelial Cell ◽  
Endothelial Cell Proliferation

Hypoxia induces different genes in the lungs of rats compared with mice

2003 ◽  
Vol 12 (3) ◽  
pp. 209-219 ◽  
Author(s):  
Yasushi Hoshikawa ◽  
Patrick Nana-Sinkam ◽  
Mark D. Moore ◽  
Sylk Sotto-Santiago ◽  
Tzulip Phang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Vascular Remodeling ◽  
Chronic Hypoxia ◽  
Gene Expression Pattern ◽  
Endothelial Cell Proliferation ◽  
Pulmonary Vascular Remodeling ◽  
Hypoxic Conditions ◽  
Expression Of Genes

Different animal species have a varying response to hypoxia. Mice develop less pulmonary artery thickening after chronic hypoxia exposure than rats. We hypothesized that the lung tissue gene expression pattern displayed in hypoxic rats would differ from that of hypoxic mice. We exposed Sprague-Dawley rats and C57BL/6 mice to both 1 and 3 wk of hypobaric hypoxia. Although both species developed pulmonary hypertension, mice showed less pulmonary vascular remodeling than rats. Microarray gene analysis demonstrated a distinct pattern of gene expression between mice and rats when exposed to hypoxic conditions. In addition, some genes appeared to be more responsive at an earlier time point of 1 wk of hypoxia. Hypoxic conditions in the rat induce genes involved in endothelial cell proliferation, repression of apoptosis, and vasodilation. Mice exposed to hypoxic conditions decrease the expression of genes involved in vasodilation and in endothelial cell proliferation. Although we cannot determine whether the differential expression of genes during chronic hypoxia is cause or consequence of the differential pulmonary vascular remodeling, we propose that a balance between over- and under-expression of a selective group of genes may be responsible for lung vascular remodeling and vascular tone control.

scholarly journals Sonic hedgehog selectively promotes lymphangiogenesis after kidney injury through noncanonical pathway

2019 ◽  
Vol 317 (4) ◽  
pp. F1022-F1033 ◽  
Author(s):  
Hui Zhuo ◽  
Dong Zhou ◽  
Yuanyuan Wang ◽  
Hongyan Mo ◽  
Ying Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Sonic Hedgehog ◽  
Lymphatic Vessels ◽  
Kidney Injury ◽  
Lymphatic Endothelial Cell ◽  
Cell Counting ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial

Kidney fibrosis is associated with an increased lymphangiogenesis, characterized by the formation and expansion of new lymphatic vessels. However, the trigger and underlying mechanism responsible for the growth of lymphatic vessels in diseased kidney remain poorly defined. Here, we report that tubule-derived sonic hedgehog (Shh) ligand is a novel lymphangiogenic factor that plays a crucial role in mediating lymphatic endothelial cell proliferation and expansion. Shh was induced in renal tubular epithelium in various models of fibrotic chronic kidney disease, and this was accompanied by an expansion of lymphatic vessels in adjacent areas. In vitro, Shh selectively promoted the proliferation of human dermal lymphatic endothelial cells (HDLECs) but not human umbilical vein endothelial cells, as assessed by cell counting, MTT assay, and bromodeoxyuridine incorporation. Shh also induced the expression of vascular endothelial growth factor receptor-3, cyclin D1, and proliferating cell nuclear antigen in HDLECs. Shh did not affect the expression of Gli1, the downstream target and readout of canonical hedgehog signaling, but activated ERK-1/2 in HDLECs. Inhibition of Smoothened with small-molecule inhibitor or blockade of ERK-1/2 activation abolished the lymphatic endothelial cell proliferation induced by Shh. In vivo, inhibition of Smoothened also repressed lymphangiogenesis and attenuated renal fibrosis. This study identifies Shh as a novel mitogen that selectively promotes lymphatic, but not vascular, endothelial cell proliferation and suggests that tubule-derived Shh plays an essential role in mediating lymphangiogenesis after kidney injury.

scholarly journals Androgen stimulates endothelial cell proliferation via an androgen receptor/VEGF/cyclin A-mediated mechanism

2011 ◽  
Vol 300 (4) ◽  
pp. H1210-H1221 ◽  
Author(s):  
Jingjing Cai ◽  
Yuan Hong ◽  
Chunyan Weng ◽  
Chen Tan ◽  
Julianne Imperato-McGinley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Endothelial Cell ◽  
Cyclin D1 ◽  
Cyclin A ◽  
Endothelial Cell Proliferation ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Cardiovascular Functions

Growing evidences support that androgen displays beneficial effects on cardiovascular functions although the mechanism of androgen actions remains to be elucidated. Modulation of endothelial cell growth and function is a potential mechanism of androgen actions. We demonstrated in the present study that androgens [dihydrotestosterone (DHT) and testosterone], but not 17β-estradiol, produced a time- and dose-dependent induction of cell proliferation in primary human aortic endothelial cells (HAECs) as evident by increases in viable cell number and DNA biosynthesis. Real-time qRT-PCR analysis showed that DHT induced androgen receptor (AR), cyclin A, cyclin D1, and vascular endothelial growth factor (VEGF) gene expression in a dose- and time-dependent manner. The addition of casodex, a specific AR antagonist, or transfection of a specific AR siRNA blocked DHT-induced cell proliferation and target gene expression, indicating that the DHT effects are mediated via AR. Moreover, coadministration of SU5416 to block VEGF receptors, or transfection of a specific VEGF-A siRNA to knockdown VEGF expression, produced a dose-dependent blockade of DHT induction of cell proliferation and cyclin A gene expression. Interestingly, roscovitine, a selective cyclin-dependent kinase inhibitor, also blocked the DHT stimulation of cell proliferation with a selective inhibition of DHT-induced VEGF-A expression. These results indicate that androgens acting on AR stimulate cell proliferation through upregulation of VEGF-A, cyclin A, and cyclin D1 in HAECs, which may be beneficial to cardiovascular functions since endothelial cell proliferation could assist the repair of endothelial injury/damage in cardiovascular system.

scholarly journals Macrophages define dermal lymphatic vessel calibre during development by regulating lymphatic endothelial cell proliferation

Development ◽  
2011 ◽  
Vol 138 (4) ◽  
pp. 797-797
Author(s):  
E. J. Gordon ◽  
S. Rao ◽  
J. W. Pollard ◽  
S. L. Nutt ◽  
R. A. Lang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Lymphatic Vessel ◽  
Lymphatic Endothelial Cell ◽  
Endothelial Cell Proliferation
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