scholarly journals Differences in bovine placentome blood vessel density and transcriptomics in a mid to late-gestating maternal nutrient restriction model

Placenta ◽  
2022 ◽  
Vol 117 ◽  
pp. 122-130
Author(s):  
Dana S. Reid ◽  
Derris D. Burnett ◽  
Zully E. Contreras-Correa ◽  
Caleb O. Lemley
Angiogenesis ◽  
2021 ◽  
Author(s):  
Delphine M. Lees ◽  
Louise E. Reynolds ◽  
Ana Rita Pedrosa ◽  
Marina Roy-Luzarraga ◽  
Kairbaan M. Hodivala-Dilke

AbstractFocal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis. Pericytes also play a vital role in regulating tumour blood vessel stabilisation, but the specific involvement of pericyte FAK-Y397 and FAK-Y861 phosphorylation in tumour blood vessels is unknown. Using PdgfrβCre + ;FAKWT/WT, PdgfrβCre + ;FAKY397F/Y397F and PdgfrβCre + ;FAKY861F/Y861F mice, our data demonstrate that tumour growth, tumour blood vessel density, blood vessel perfusion and pericyte coverage were affected only in late stage tumours in PdgfrβCre + ;FAKY861F/Y861F but not PdgfrβCre + ;FAKY397F/Y397F mice. Further examination indicates a dual role for pericyte FAK-Y861 phosphorylation in the regulation of tumour vessel regression and also in the control of pericyte derived signals that influence apoptosis in cancer cells. Overall this study identifies the role of pericyte FAK-Y861 in the regulation of tumour vessel regression and tumour growth control and that non-phosphorylatable FAK-Y861F in pericytes reduces tumour growth and blood vessel density.


2013 ◽  
Vol 12 (1) ◽  
pp. 4-11 ◽  
Author(s):  
Ana Tellechea ◽  
Antonios Kafanas ◽  
Ermelindo C. Leal ◽  
Francesco Tecilazich ◽  
Sarada Kuchibhotla ◽  
...  

Systemic inflammation is associated with impaired wound healing in diabetes mellitus (DM) patients. Using immunohistochemistry techniques, the authors investigated changes in skin inflammation and skin blood vessels in human and experimental diabetes. Comparing to the non-DM human subjects, the total number of inflammatory cells per biopsy and the number of inflammatory cells around blood vessels, a strong indication of inflammation, were higher in DM subjects irrespective of their risk for developing diabetic foot ulcer. Inflammatory cell infiltration was robustly increased in all DM animal models compared with their non-DM controls. The number and density of blood vessels and CD31 positive proliferating endothelial cells around preexisting skin vessels was also higher in the DM patients. However, there were no differences in the skin blood flow between the non-DM and DM subjects. The number of skin blood vessels was also increased in the DM animals; however, these differences were less obvious than the ones observed for inflammatory cells. We conclude that skin inflammation and skin blood vessel density is increased in diabetic human subjects and in rodent and rabbit models of diabetes.


The Lancet ◽  
1993 ◽  
Vol 342 (8873) ◽  
pp. 742 ◽  
Author(s):  
J. Krupinski ◽  
J. Kaluza ◽  
P. Kumar ◽  
M. Wang ◽  
S. Kumar

2008 ◽  
Vol 129 (4) ◽  
pp. 578-586 ◽  
Author(s):  
Yasser M. El-Gohary ◽  
Ghada Metwally ◽  
Reda S. Saad ◽  
Morton J. Robinson ◽  
Thomas Mesko ◽  
...  

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