Endothelial cells and the IGF system

Bach, Leon Ashley

doi:10.1530/jme-14-0215

Cited by 147 publications

(122 citation statements)

References 115 publications

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“…Expressions of IGF1 and CTGF in cPCs were drastically altered by the expression of Ninj1. IGF1 promotes migration and tube formation in ECs, 28 and stabilizes neovessels generated from ECs through extracellular signal-regulated kinase activation. 29 CTGF plays a central role in diseases in which tissue Inhibiting Ninj1 expression in cECs had no effect on their ability to form tube-like structures; however, Ninj1 overexpression decreased EC tube formation.…”

Section: Discussionmentioning

confidence: 99%

Ninjurin1 Is a Novel Factor to Regulate Angiogenesis Through the Function of Pericytes

Matsuki

Kabara

Saito

et al. 2015

Circ J

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Background: Capillary pericytes (cPCs), the mural cells of microvessels, play an important role in the formation and maintenance of microvessels; however, little is known about the mechanisms of how cPCs regulate angiogenesis. To identify factors that modulate cPC function, genes whose levels were altered in cPCs during neovessel formation were identified through a microarray screen. Methods and Results:Ninjurin1 (nerve injury-induced protein, Ninj1) was selected as a candidate factor for angiogenesis regulation. Ninj1 was expressed in capillary cells including endothelial cells (cECs) and was expressed at a higher level in cPCs. Hypoxia induced the gene expression of Ninj1 in addition of vascular endothelial growth factor (VEGF) in cPCs. When cPCs were co-incubated with a thoracic aorta in a three-dimensional Matrigel system, the length of the EC-tubes sprouting from the aorta was increased. Small interfering RNA-mediated downregulation of Ninj1 in cPCs enhanced these cPCs-mediated angiogenic effects, whereas overexpression of Ninj1 attenuated their effects. The production of angiogenic growth factors, such as VEGF and angiopoietin 1, by cPCs was enhanced by the downregulation of Ninj1, and reduced by the overexpression of Ninj1. also determined. EC Tube Formation Angiogenesis AssayThe EC tube formation assay was performed as previously described. 14 A 40-μl volume of growth factor-reduced Matirgel was added to each well of a 96-well plate at room temperature. The gel was solidified at 37°C for at least 30 min and then seeded with 1×10 4 cells/well in 100 μl medium (EBM2 with 2% FBS and 10 ng/ml VEGF). The assay was performed in a CO2 incubator, with plates incubated at 37°C for 24 h. Images were obtained by phase contrast microscopy and the length of the tube-like structure in each well was measured at 40× magnification. Hind Limb Ischmia Surgery and ImmunocytochemistryMale C57BL/6 mice 12 weeks of age were used for experiments. All animal protocols were approved by the Animal Care and Use Committee of Asahikawa Medical University. Unilateral hindlimb ischemia (HLI) models were established by ligation and excision of the femoral artery/vein as previously described. 16 At predetermined time points, mice were sacrificed by overdose with a pentobarbital-based euthanasia solution (200 mg/kg by intraperitoneal injection). Gastrocnemius muscle samples were collected and stored at −80°C for quantitative polymerase chain reaction (qPCR) analysis. The histological assessment of ischemic limb tissue was performed 14 days after hindlimb surgery. Functional vessels were stained by injecting 300 μl phosphate-buffered saline (PBS) containing rhodamine-labeled G. simplicifolia lectin I (100 μg/ml, Vector Laboratories) via the tail vein. After 5 min, mice were sacrificed and perfused through the heart with PBS followed by 4% paraformaldehyde in PBS, and the gastrocnemius muscle was dissected and embedded in Tissue-Tek OCT medium. Ninj1 expression in 10-μm cross-sections was detected by immunocytochemistry using an anti-Ninj1 ...

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Section: Discussionmentioning

confidence: 99%

Ninjurin1 Is a Novel Factor to Regulate Angiogenesis Through the Function of Pericytes

Matsuki

Kabara

Saito

et al. 2015

Circ J

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“…In addition, many reports are highly contradictory, perhaps reflecting the importance of the precise context of the studies and the pleiotropic nature of the growth factor and its receptor. 18,19 IGF1 is an effective FDA-approved therapy for children with short stature as it has a beneficial effect upon the entire musculoskeletal system. In addition to its anabolic properties, IGF1 enhances tissue repair by promoting angiogenesis and attenuating inflammation, necrosis, and apoptosis.…”

Section: Vascular Endothelial Growth Factor (Vegf) a And Fibroblast mentioning

confidence: 99%

Enhancing engineered vascular networks in vitro and in vivo: The effects of IGF1 on vascular development and durability

et al. 2017

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Objectives: Creation of functional, durable vasculature remains an important goal within the field of regenerative medicine. Engineered biological vasculature has the potential to restore or improve human tissue function. We hypothesized that the pleotropic effects of insulin-like growth factor 1 (IGF1) would enhance the engineering of capillary-like vasculature. Results: IGF1 supplementation significantly enhanced de novo vasculogenesis both in vitro and in vivo. Effects were long-term as they lasted the duration of the study period, and included network density, vessel length, and diameter. Bifurcation density was not affected. However, the highest concentrations of IGF1 tested were either ineffective or even deleterious. Sustained IGF1 delivery was required in vivo as the inclusion of recombinant IGF1 protein had minimal impact.Conclusion: IGF1 supplementation can be used to produce neovasculature with significantly enhanced network density and durability. Its use is a promising methodology for engineering de novo vasculature to support regeneration of functional tissue.

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“…To date, the only identified substrate for MASP-3 is insulin-like growth factor-binding protein-5, 36 which regulates the activity of insulin-like growth factor. Insulin-like growth factor is increasingly implicated in endothelial function, 37 which might potentially explain our observations. Future research may clarify the functions of MASP-3 and MAp44 in lectinpathway regulation and potentially identify noncomplement substrates of MASP-3.…”

Section: Discussionmentioning

confidence: 63%

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Hertle

Arts

Kallen

et al. 2016

ATVB

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12associations with future CVD. When the effect of MBL on complications of established CVD was investigated, low MBL was in fact protective in most studies. [13][14][15] Thus, considerable discrepancy remains in the literature on whether MBL has beneficial or adverse effects in CVD.This reported discrepancy might be explained by a dual role of MBL in different etiologic aspects of CVD. Objective-Previous studies suggested that the lectin-complement pathway plays a complex role in cardiovascular disease (CVD). To date, no prospective human studies have investigated the relationship between the initiating factor of the lectin pathway, that is, mannose-binding lectin (MBL), and low-grade inflammation, endothelial dysfunction, or carotid intima-media thickness (cIMT). Moreover, MBL-associated proteases (MASPs) and MBL-associated proteins (MAps), which mediate downstream complement activation, have not been studied in the development of CVD. Approach and Results-In a prospective cohort (n=574; age 60±7 years; 7-year follow-up), we investigated longitudinal associations of plasma MBL, MASP-1, MASP-2, MASP-3, and MAp44 with biomarker scores that reflect low-grade inflammation and endothelial dysfunction, respectively, and with cIMT. We also investigated their associations with incident CVD (n=73). In adjusted analyses, low-grade inflammation was lowest in the middle tertile (T Middle )

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Endothelial cells and the IGF system

Cited by 147 publications

References 115 publications

Ninjurin1 Is a Novel Factor to Regulate Angiogenesis Through the Function of Pericytes

Ninjurin1 Is a Novel Factor to Regulate Angiogenesis Through the Function of Pericytes

Enhancing engineered vascular networks in vitro and in vivo: The effects of IGF1 on vascular development and durability

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

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