scholarly journals Cilia Control Vascular Mural Cell Recruitment in Vertebrates

Cell Reports ◽  
2017 ◽  
Vol 18 (4) ◽  
pp. 1033-1047 ◽  
Author(s):  
Xiaowen Chen ◽  
Dafne Gays ◽  
Carlo Milia ◽  
Massimo M. Santoro
Keyword(s):  
Mural Cell ◽  
Cell Recruitment

scholarly journals Analysis of Mural Cell Recruitment to Tumor Vessels

Circulation ◽  
2002 ◽  
Vol 105 (1) ◽  
pp. 112-117 ◽  
Author(s):  
Alexandra Abramsson ◽  
Örjan Berlin ◽  
Hayk Papayan ◽  
Denise Paulin ◽  
Moshe Shani ◽  
...  
Keyword(s):  
Mural Cell ◽  
Tumor Vessels ◽  
Cell Recruitment

scholarly journals Inhibition of Cyclooxygenase-2 Disrupts Tumor Vascular Mural Cell Recruitment and Survival Signaling

2006 ◽  
Vol 66 (8) ◽  
pp. 4378-4384 ◽  
Author(s):  
Alice Lee ◽  
Jason Frischer ◽  
Anna Serur ◽  
Jianzhong Huang ◽  
Jae-O Bae ◽  
...  
Keyword(s):  
Cyclooxygenase 2 ◽  
Mural Cell ◽  
Cell Recruitment ◽  
Survival Signaling

Abstract TMP118: Alk1 Deficiency Impairs Mural Cell Recruitment During Brain Angiogenesis

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Wanqiu Chen ◽  
Yi Guo ◽  
Kristine Jun ◽  
Mamta Wankhede ◽  
Hua Su ◽  
...  
Keyword(s):  
Growth Factor ◽  
Viral Vector ◽  
Lentiviral Vector ◽  
Mural Cell ◽  
Cell Recruitment ◽  
Vascular Dysplasia ◽  
Highly Correlated ◽  
Endothelial Growth Factor ◽  
Brain Angiogenesis

Background and Purpose: VEGF stimulation induced dysplasia vessel formation in the Alk1 -deficient brain. The dysplastic vessels had less mural cell coverage associated with increased extravasation of blood contents. Platelet-derived growth factor B (PDGFB) signaling is important in mural cell recruitment during angiogenesis. Notch signaling is upstream of PDGFB. We hypothesized that Alk1 deletion impairs pericyte recruitment through downregulation of DLL4/PDGFB signaling. Thalidomide can increase PDGFB expression and was used to test our hypothesis in vivo. Methods: Human brain microvascular endothelial cells (HBMECs) were infected with a lentiviral vector carrying ALK1 shRNA. Cells with 80% reduction of ALK1 gene expression were treated with vascular endothelial growth factor (VEGF; 0, 10, 50, and 100 ng/ml) for 18 hours. DLL4 and PDGFB mRNA were measured using real-time PCR. Pericyte-recruitment was evaluated by co-culturing pericytes with HBMECs. Cerebrovascular dysplasia was induced by co-injection of an adenoviral vector expressing cre-recombinase and an adeno-associated viral vector expressing VEGF into the basal ganglia of Alk1 -floxed mice. Two weeks later, thalidomide (75 mg/kg, i.p.) or DMSO was administered twice per week for six weeks. Results: Knockdown of ALK1 attenuated the increase of DLL4 and PDGFB in HBMECs following VEGF stimulation. DLL4 and PDGFB expression was highly correlated (R 2 = 0.93). ALK1 knockdown reduced the ability of HBMEC to recruit pericytes (P = 0.014). In vivo, thalidomide treatment significantly reduced vascular dysplasia (dysplastic vessels: thalidomide vs. DMSO, 3.4±1.2/200 vessels vs. 1.0±0.5, P = 0.003), without affecting vessel density (P = 0.11). Smooth muscle-negative dysplastic vessels decreased in thalidomide-treated mice, compared to DMSO-treated mice (21%±6 vs 47±9, P = 0.0002). Prussian blue-positive area was reduced in the thalidomide group, compared to the DMSO group (P = 0.0011). Conclusions: Our findings suggest that Alk1 regulates pericyte recruitment through DLL4/PDGFB signaling during brain angiogenesis.

Regulation of angiogenesis, mural cell recruitment and adventitial macrophage behavior by Toll-like receptors

Angiogenesis ◽  
2013 ◽  
Vol 17 (1) ◽  
pp. 147-161 ◽  
Author(s):  
Alfred C. Aplin ◽  
Giovanni Ligresti ◽  
Eric Fogel ◽  
Penelope Zorzi ◽  
Kelly Smith ◽  
...  
Keyword(s):  
Toll Like Receptors ◽  
Mural Cell ◽  
Cell Recruitment

scholarly journals Aberrant mural cell recruitment to lymphatic vessels and impaired lymphatic drainage in a murine model of pulmonary fibrosis

Blood ◽  
2012 ◽  
Vol 119 (24) ◽  
pp. 5931-5942 ◽  
Author(s):  
Anna-Katharina Meinecke ◽  
Nadine Nagy ◽  
Gabriela D'Amico Lago ◽  
Santina Kirmse ◽  
Ralph Klose ◽  
...  
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Murine Model ◽  
Lymphatic Vessels ◽  
Lymphatic Drainage ◽  
Platelet Derived Growth Factor ◽  
Mural Cell ◽  
Cell Recruitment ◽  
Mural Cells ◽  
Perilymphatic Space

Abstract Pulmonary fibrosis is a progressive disease with unknown etiology that is characterized by extensive remodeling of the lung parenchyma, ultimately resulting in respiratory failure. Lymphatic vessels have been implicated with the development of pulmonary fibrosis, but the role of the lymphatic vasculature in the pathogenesis of pulmonary fibrosis remains enigmatic. Here we show in a murine model of pulmonary fibrosis that lymphatic vessels exhibit ectopic mural coverage and that this occurs early during the disease. The abnormal lymphatic vascular patterning in fibrotic lungs was driven by expression of platelet-derived growth factor B (PDGF-B) in lymphatic endothelial cells and signaling through platelet-derived growth factor receptor (PDGFR)–β in associated mural cells. Because of impaired lymphatic drainage, aberrant mural cell coverage fostered the accumulation of fibrogenic molecules and the attraction of fibroblasts to the perilymphatic space. Pharmacologic inhibition of the PDGF-B/PDGFR-β signaling axis disrupted the association of mural cells and lymphatic vessels, improved lymphatic drainage of the lung, and prevented the attraction of fibroblasts to the perilymphatic space. Our results implicate aberrant mural cell recruitment to lymphatic vessels in the pathogenesis of pulmonary fibrosis and that the drainage capacity of pulmonary lymphatics is a critical mediator of fibroproliferative changes.

Defective valves and abnormal mural cell recruitment underlie lymphatic vascular failure in lymphedema distichiasis

2004 ◽  
Vol 10 (9) ◽  
pp. 974-981 ◽  
Author(s):  
Tatiana V Petrova ◽  
Terhi Karpanen ◽  
Camilla Norrmén ◽  
Russell Mellor ◽  
Tomoki Tamakoshi ◽  
...  
Keyword(s):  
Mural Cell ◽  
Cell Recruitment

scholarly journals α-parvin controls vascular mural cell recruitment to vessel wall by regulating RhoA/ROCK signalling

2009 ◽  
Vol 28 (20) ◽  
pp. 3132-3144 ◽  
Author(s):  
Eloi Montanez ◽  
Sara A Wickström ◽  
Johannes Altstätter ◽  
Haiyan Chu ◽  
Reinhard Fässler
Keyword(s):  
Vessel Wall ◽  
Mural Cell ◽  
Cell Recruitment

239. Hormonal control of vascular mural cell recruitment in the mouse endometrium

2005 ◽  
Vol 17 (9) ◽  
pp. 94
Author(s):  
J. E. Girling ◽  
L. M. Walter ◽  
P. A. W. Rogers
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Hormonal Control ◽  
Specific Marker ◽  
Mural Cell ◽  
Physiological Basis ◽  
Oestrogen Treatment ◽  
Cell Recruitment ◽  
Progesterone Treatment ◽  
Vehicle Injection

The human endometrium undergoes regular periods of growth and regression, including concomitant changes in the vasculature, and is one of the few adult tissues where significant angiogenesis (new blood vessel formation) and arteriogenesis (recruitment of vascular smooth muscle cells (VSMC) and pericytes) occurs on a routine, physiological basis. In this study, mouse models were used to investigate the effects of oestrogen and progesterone on endometrial vascular mural cell recruitment. The aim was to quantify changes in the proportion of vessels covered by α-smooth muscle actin (α-SMA, a marker of VSMC and pericytes) in hormone-treated ovariectomised mice. We hypothesised that relative vessel α-SMA coverage would increase following progesterone treatment (in conjunction with endothelial cell (EC) proliferation), but not following oestrogen treatment (when EC proliferation also occurs). Ovariectomised mice were given a single oestradiol (100 ng) or vehicle injection, before dissection 24 h later, or three consecutive daily injections of progesterone (1 mg) or vehicle. The percentage of vessel profiles with no, minimal, extensive or complete α-SMA coverage were quantified after CD31/α-SMA double immunostaining. There was a significant decrease in the percentage of vessel profiles with no α-SMA coverage following progesterone treatment (20±4.3 % [mean±SE] v. 57±4.6 %, t(7)=12.5, P<0.001), and a significant increase in the percentage of vessels with minimal or extensive α-SMA coverage (44±3.4 % v. 27±3.7%, t(7)=4.7, P<0.001 and 27±4.3% v. 5±0.5%, t(7)=5.8, P<0.001, respectively), in comparison to vehicle-treated mice. The percentage of vessels with complete α-SMA coverage, representing vessels with a coat of VSMC, did not change significantly in comparison to vehicle-treated mice (8±2.3% v. 10±1.2%, t(7)=0.6, P=0.55). There were no significant changes in the percentage of vessels with differing α-SMA coverage in oestrogen-treated mice. In continuing studies, we will quantify the proportion of proliferating α-SMA positive cells and examine mouse endometrial tissues using a pericyte-specific marker.

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