Regulation of replicative senescence by insulin‐like growth factor‐binding protein 3 in human umbilical vein endothelial cells

Kim, Kwang Seok; Kim, Min-Sun; Seu, Young‐Bae; Chung, Hae Young; Kim, Jung Hye; Kim, Jae‐Ryong

doi:10.1111/j.1474-9726.2007.00315.x

Cited by 77 publications

(60 citation statements)

References 55 publications

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“…IGFBP3 and IGFBP5 were upregulated in endothelial cells made senescent by serial culture in vitro (Shelton et al 1999, Grillari et al 2000. IGFBP3 overexpression increased aspects of the senescent phenotype in human umbilical vein endothelial cells, whereas IGFBP3 knockdown impaired this phenotype (Kim et al 2007a). Some effects of IGFBP3 on senescence varied in cells from different donors (Muck et al 2008).…”

Section: Igf Actions In Endothelial Cellsmentioning

confidence: 99%

Endothelial cells and the IGF system

Bach¹

2014

Journal of Molecular Endocrinology

156

118

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Endothelial cells line blood vessels and modulate vascular tone, thrombosis, inflammatory responses and new vessel formation. They are implicated in many disease processes including atherosclerosis and cancer. IGFs play a significant role in the physiology of endothelial cells by promoting migration, tube formation and production of the vasodilator nitric oxide. These actions are mediated by the IGF1 and IGF2/mannose 6-phosphate receptors and are modulated by a family of high-affinity IGF binding proteins. IGFs also increase the number and function of endothelial progenitor cells, which may contribute to protection from atherosclerosis. IGFs promote angiogenesis, and dysregulation of the IGF system may contribute to this process in cancer and eye diseases including retinopathy of prematurity and diabetic retinopathy. In some situations, IGF deficiency appears to contribute to endothelial dysfunction, whereas IGF may be deleterious in others. These differences may be due to tissue-specific endothelial cell phenotypes or IGFs having distinct roles in different phases of vascular disease. Further studies are therefore required to delineate the therapeutic potential of IGF system modulation in pathogenic processes.

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Section: Igf Actions In Endothelial Cellsmentioning

confidence: 99%

Endothelial cells and the IGF system

Bach¹

2014

Journal of Molecular Endocrinology

156

118

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“…HUVECs in EGM-2 media were cultured as previously described. 39 For the experiments, cells were used at either passage 7 (PDo28) or passage 15 (PD450). These are referred to as 'young' and 'old' cells, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…The cell cycle profiles were measured by staining with propidium iodide. 39 The intracellular propidium iodide fluorescence intensity of each population of 10 000 cells was measured in each sample using a Becton-Dickinson FACS Canto II flow cytometer (BD Bioscience, San Jose, CA, USA).…”

Section: Discussionmentioning

confidence: 99%

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POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) inhibits endothelial cell senescence through a p53 dependent pathway

Cho

Kim

et al. 2011

Cell Death Differ

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Vascular cell senescence, induced by the DNA damage response or inflammatory stress, contributes to age-associated vascular disease. Using complementary DNA microarray technology, we found that the level of POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is downregulated during endothelial cell (EC) senescence. PATZ1 may have an important role as a transcriptional repressor in chromatin remodeling and transcription regulation; however, the role of PATZ1 in EC senescence and vascular aging remains unidentified. Knockdown of PATZ1 in young cells accelerated premature EC senescence, which was confirmed by growth arrest, increased p53 protein level and senescence-associated b-galactosidase (SA-b-gal) activity, and repression of EC tube formation. In contrast, overexpression of PATZ1 in senescent cells reversed senescent phenotypes. Cellular senescence induced by PATZ1 knockdown in young cells was rescued by knockdown of p53, but not by knockdown of p16 INK4a . PATZ1 knockdown increased ROS levels, and pretreatment with N-acetylcysteine abolished EC senescence induced by PATZ1 knockdown. Notably, PATZ1 immunoreactivity was lower in ECs of atherosclerotic tissues than those of normal arteries in LDLR À/À mice, and immunoreactivity also decreased in ECs of old human arteries. These results suggest that PATZ1 may have an important role in the regulation of EC senescence through an ROS-mediated p53-dependent pathway and contribute to vascular diseases associated with aging.

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“…By cDNA microarray technology, Kim et al found that IGFBP3 increased in dermal fibroblasts in the aged human [40]. The mRNA and protein of IGFBP3 increase in human umbilical vein endothelial cells (HUVECs) in the aged human.…”

Section: Ibfbp3mentioning

confidence: 99%

Insulin-like Growth Factor System and Aging

Li¹,

Sun²,

Cai³

et al. 2017

J Aging Sci

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IGF (insulin-like growth factor, IGF) system is composed of three ligands (insulin, IGF-1, IGF-2), three cell surface binding receptors (Ins R, IGF-1R, IGF-2 R), and Insulin-like growth factor binding proteins (IGF binding proteins, IGFBPs) and IGFBP protease. Delaying aging and exploring the molecular mechanism of aging have always been important research topics. IGF system plays an important role in the life processes by binding with the receptor or activating multiple intracellular signaling cascades. The researches have showed IGF system plays an important role in regulating signal pathways about senescence and aging related diseases such as cardiovascular disease, osteoporosis and vertebral aging.

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Regulation of replicative senescence by insulin‐like growth factor‐binding protein 3 in human umbilical vein endothelial cells

Cited by 77 publications

References 55 publications

Endothelial cells and the IGF system

Endothelial cells and the IGF system

POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) inhibits endothelial cell senescence through a p53 dependent pathway

Insulin-like Growth Factor System and Aging

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