Expression of Vascular Endothelial Growth Factor in Human Umbilical Vein Endothelial Cells Stimulated with Interleukin-1α

Imaizumi, Tadaatsu; Itaya, Hiroyuki; Nasu, Satoki; Yoshida, Hidemi; Matsubara, Yuki; Fujimoto, Koji; Matsumiya, Tomoh; Kimura, Hiroto; Satoh, Kei

doi:10.1055/s-0037-1613948

Cited by 46 publications

(1 citation statement)

References 42 publications

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“…Interestingly, we found that PAR2 increases production of VEGF in endothelial cells. Based on the literature, endothelial VEGF protects itself by autocrine/paracrine manner 40,41 , which supports the protective role of PAR2 in our model. A lack of PAR2 did not affect glomerular macrophage infiltration, another source of VEGF 42 , in anti-VEGF Ab-treated mice.…”

Section: Discussionsupporting

confidence: 88%

Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury

Fushima

Sato

et al. 2019

Sci Rep

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Vascular endothelial growth factor (VEGF) inhibitors cause glomerular injury. We have recently shown that activation of protease-activated receptor 2 (PAR2) by factor Xa exacerbated diabetic kidney disease. However, the role of PAR2 in glomerular injury induced by VEGF blockade is not known. Herein, we investigated the effect of the lack of PAR2 on VEGF inhibitor-induced glomerular injury. Although administering an anti-VEGF antibody by itself did not show renal phenotype in wild type mice, its administration to mice lacking endothelial nitric oxide synthase (eNOS) caused glomerular injury. Different from what we expected, administration of an anti-VEGF antibody in mice lacking PAR2 and eNOS exacerbated albuminuria and reduced the expression levels of CD31, pro-angiogenic VEGF, and angiogenesis-related chemokines in their kidneys. Podocyte injury was also evident in this model of mice lacking PAR2. Our results suggest that PAR2 is protective against VEGF inhibitor-induced glomerular endothelial and podocyte injury.

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Section: Discussionsupporting

confidence: 88%

Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury

Fushima

Sato

et al. 2019

Sci Rep

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An intracrine view of angiogenesis

Ré

Cook

2006

BioEssays

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Angiogenesis, the generation of new blood vessels from pre-existing vessels, is an integral component of wound healing, responses to inflammation and other physiologic processes. It is also an essential part of tumor growth; in the absence of new vessel formation, tumors cannot expand beyond a small volume. Although much is known about angiogenesis and its regulation, there is no overall theory that describes or explains this process. It is here suggested that the intracrine hypothesis, which ascribes to certain extracellular signaling peptides (whether hormones, growth factors, DNA-binding proteins or enzymes) a role in both intracellular biology and extracellular signaling, can contribute to a more general understanding of angiogenesis. Intracrine factors participate in angiogenesis in the following ways: (1) they can act within the cells that synthesized them (type I intracrine action), (2) they can be secreted and then taken up by their cell of synthesis to act intracellularly (type II intracrine action ), or (3) they can be secreted and internalized by a distant target cell (type III intracrine action). The parallels between the intracrine growth factor mechanisms cancer cells employ in stimulating their own growth and the mechanisms operative in endothelial cell proliferation during angiogenesis ("intracrine reciprocity") are discussed. Collectively, these explorations lead to testable hypotheses regarding the regulation of normal and pathological angiogenesis, and point to similarities between tumor-induced angiogenesis and tissue differentiation.

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Hybrid cardiovascular sourced extracellular matrix scaffolds as possible platforms for vascular tissue engineering

Reid

Callanan

2019

J Biomed Mater Res

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The aim when designing a scaffold is to provide a supportive microenvironment for the native cells, which is generally achieved by structurally and biochemically imitating the native tissue. Decellularized extracellular matrix (ECM) possesses the mechanical and biochemical cues designed to promote native cell survival. However, when decellularized and reprocessed, the ECM loses its cell supporting mechanical integrity and architecture. Herein, we propose dissolving the ECM into a polymer/solvent solution and electrospinning it into a fibrous sheet, thus harnessing the biochemical cues from the ECM and the mechanical integrity of the polymer. Bovine aorta and myocardium were selected as ECM sources. Decellularization was achieved using sodium dodecyl sulfate (SDS), and the ECM was combined with polycaprolactone and hexafluoro‐2‐propanol for electrospinning. The scaffolds were seeded with human umbilical vein endothelial cells (HUVECs). The study found that the inclusion of aorta ECM increased the scaffold's wettability and subsequently lead to increased HUVEC adherence and proliferation. Interestingly, the inclusion of myocardium ECM had no effect on wettability or cell viability. Furthermore, gene expression and mechanical changes were noted with the addition of ECM. The results from this study show the vast potential of electrospun ECM/polymer bioscaffolds and their use in tissue engineering.

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Expression of Vascular Endothelial Growth Factor in Human Umbilical Vein Endothelial Cells Stimulated with Interleukin-1α

Cited by 46 publications

References 42 publications

Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury

Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury

An intracrine view of angiogenesis

Hybrid cardiovascular sourced extracellular matrix scaffolds as possible platforms for vascular tissue engineering

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