Aging reduces susceptibility of vascular smooth muscle cells to H2O2-induced apoptosis through the down-regulation of Jagged1 expression in endothelial cells

Qian, Dehui; Wu, Xiaojing; Jiang, Haowei; Gao, Pan; Kuang, Chunyan; Wang, Kui; Huang, Lan

doi:10.3892/ijmm.2011.671

Cited by 4 publications

(5 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…mJagged1 is directly associated with multiple Notch receptors and is involved in the mediating Notch signaling [ 36 – 38 ]. The decrease mJagged1 can promote proliferation of vascular smooth muscle cells (VSMCs) through Notch signaling pathway[ 39 ] and then lead to vascular diseases. We observed a decrease in Jagged1 expression in our D-galactose mice which could potentially promote proliferation of vascular smooth muscle cells (VSMCs) through Notch signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

“…The Jagged1 protein mediates Notch signaling and its potential effect on vascular diseases by associating directly with multiple Notch receptors [ 36 , 37 ]. In D-galactose mice, the decrease in mJagged1 could promote the proliferation of vascular smooth muscle cells (VSMCs) through the Notch signaling pathway [ 39 ]. On the other hand, kallikrein 1-related petidase b26(KLK1b26), a member of the kallikrein 1-related petidases (KLK1), has the opposite effect on the proliferation of VSMCs.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Gene Transcriptional and Metabolic Profile Changes in Mimetic Aging Mice Induced by D-Galactose

Zhou

et al. 2015

PLoS ONE

View full text Add to dashboard Cite

D-galactose injection has been shown to induce many changes in mice that represent accelerated aging. This mouse model has been widely used for pharmacological studies of anti-aging agents. The underlying mechanism of D-galactose induced aging remains unclear, however, it appears to relate to glucose and 1ipid metabolic disorders. Currently, there has yet to be a study that focuses on investigating gene expression changes in D-galactose aging mice. In this study, integrated analysis of gas chromatography/mass spectrometry-based metabonomics and gene expression profiles was used to investigate the changes in transcriptional and metabolic profiles in mimetic aging mice injected with D-galactose. Our findings demonstrated that 48 mRNAs were differentially expressed between control and D-galactose mice, and 51 potential biomarkers were identified at the metabolic level. The effects of D-galactose on aging could be attributed to glucose and 1ipid metabolic disorders, oxidative damage, accumulation of advanced glycation end products (AGEs), reduction in abnormal substance elimination, cell apoptosis, and insulin resistance.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gene Transcriptional and Metabolic Profile Changes in Mimetic Aging Mice Induced by D-Galactose

Zhou

et al. 2015

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…This response is greater in older patients due in part to the excessive proliferation and reduced apoptosis of vascular smooth muscle cells (VSMCs), and the same result is observed in aging mice (Vazquez-Padron et al, 2004). Interestingly, the reduced apoptosis in the VSMCs during aging may involve reduced signaling from adjacent endothelial cells (Qian et al, 2011). …”

Section: Pcd In Normal Tissue Development Adult Homeostasisand Agingmentioning

confidence: 99%

Programmed cell death in aging

Tower

2015

Ageing Research Reviews

331

208

View full text Add to dashboard Cite

Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.

show abstract

“…The Notch signaling pathway mediates the interaction between adjacent endothelial cells (ECs) to regulate differentiation, embryonic development, and proliferation [ 20 ]. Mammalian cells express four transmembrane Notch receptors (Notch 1–4) and five transmembrane ligands [Jagged (JAG) 1, 2 and Delta-like canonical notch ligand (DLL) 1, 3, and 4], that are abundantly expressed in ECs [ 20 , 21 ]. The Notch ligands JAG1 and DLL4 are antagonistic.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, overexpression of JAG1 in tumors can promote angiogenesis [ 23 ]. Regarding cellular senescence, it has been reported that JAG1 expression decreases with aging in ECs [ 20 ], and inhibition of Notch signaling induces premature senescence via a p16-dependent pathway [ 20 , 24 ]. However, the mechanism of JAG1 downregulation during cellular senescence has not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA miR-214-5p induces senescence of microvascular endothelial cells by targeting the JAG1/Notch signaling pathway

Hwang

Jeong

2023

Non-coding RNA Research

View full text Add to dashboard Cite

Aging reduces susceptibility of vascular smooth muscle cells to H2O2-induced apoptosis through the down-regulation of Jagged1 expression in endothelial cells

Cited by 4 publications

References 23 publications

Gene Transcriptional and Metabolic Profile Changes in Mimetic Aging Mice Induced by D-Galactose

Gene Transcriptional and Metabolic Profile Changes in Mimetic Aging Mice Induced by D-Galactose

Programmed cell death in aging

MicroRNA miR-214-5p induces senescence of microvascular endothelial cells by targeting the JAG1/Notch signaling pathway

Contact Info

Product

Resources

About