Caveolin‐1 deficiency induces premature senescence with mitochondrial dysfunction

Dong, Yu; Jung, Sun Ho; An, Hyoung Tae; Lee, Sungsoo; Hong, Jin Hee; Park, Jun Sub; Lee, Hyun; Lee, Hwayeon; Bahn, Myeong Suk; Lee, Hyung Chul; Han, Namshik; Ko, Jesang; Lee, Jae Seon; Ko, Young Gyu

doi:10.1111/acel.12606

Cited by 54 publications

(42 citation statements)

References 45 publications

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“…In addition to the markers mentioned above, recent studies have uncovered new players and their role in the field of cellular senescence. Mitochondria can be affected by cellular senescence in several aspects such as caveolin-1 deficiency, which has been shown to induce cellular senescence by affecting the functionality of the mitochondria [ 93 ]. The other aspect is mitochondrial DNA hypomethylation, which is a feature of induced senenscence in human fetal heart mesenchymal stem cells and can be induced by reactive oxidative species [ 94 ].…”

Section: New Players In the Field Of Senescence?mentioning

confidence: 99%

Markers of T Cell Senescence in Humans

Larbi

2017

IJMS

176

157

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Many countries are facing the aging of their population, and many more will face a similar obstacle in the near future, which could be a burden to many healthcare systems. Increased susceptibility to infections, cardiovascular and neurodegenerative disease, cancer as well as reduced efficacy of vaccination are important matters for researchers in the field of aging. As older adults show higher prevalence for a variety of diseases, this also implies higher risk of complications, including nosocomial infections, slower recovery and sequels that may reduce the autonomy and overall quality of life of older adults. The age-related effects on the immune system termed as "immunosenescence" can be exemplified by the reported hypo-responsiveness to influenza vaccination of the elderly. T cells, which belong to the adaptive arm of the immune system, have been extensively studied and the knowledge gathered enables a better understanding of how the immune system may be affected after acute/chronic infections and how this matters in the long run. In this review, we will focus on T cells and discuss the surface and molecular markers that are associated with T cell senescence. We will also look at the implications that senescent T cells could have on human health and diseases. Finally, we will discuss the benefits of having these markers for investigators and the future work that is needed to advance the field of T cell senescence markers.

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Section: New Players In the Field Of Senescence?mentioning

confidence: 99%

Markers of T Cell Senescence in Humans

Larbi

2017

IJMS

176

157

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“…Several previous studies using in vitro senescent cells [18] and in vivo aged tissues [17,37] have suggested that cav-1 expression is increased with aging. Additionally, cav-1 overexpression displays senescence phenotypes [20,38,39], suggesting that increased cav-1 expression may play an important role in aging at the cellular level, although there have been con icting observations that cav-1 knockout accelerates premature senescence in MEFs [40] and loss of cav-1 accelerates neurodegeneration and aging [41].…”

Section: Discussionmentioning

confidence: 99%

Age-Related Increase in Caveolin-1 Expression Facilitates Cell-To-Cell Transmission of α-Synuclein in Neurons

Choi

Noh

et al. 2020

Preprint

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Background: Parkinson's disease (PD) is the second most prevalent neurodegenerative disease, with aging being considered the greatest risk factor for developing PD. Caveolin-1 (Cav-1) is known to participate in the aging process. Recent evidence indicates that prion-like propagation of misfolded α-synuclein (α-syn) released from neurons to neighboring neurons plays an important role in PD progression. In the present study, we explored the association between cav-1 and cell-to-cell transmission of α-syn.Methods: Using SH-SY5Y cells and primary neurons overexpressing WT and Y14A cav-1, we investigated the effect of cav-1 expression on the uptake of α-syn using a dual chamber system. Additionally, we investigated the effect of cav-1 expression on the formation of Lewy body-like inclusions using co-culture assay and microfluidic chamber assay.Results: We demonstrated that cav-1 expression in the brain increased with age, and considerably increased in the brain of A53T α-syn transgenic mice. Cav-1 overexpression facilitated the uptake of α-syn into neurons and formation of additional Lewy body-like inclusion bodies, phosphorylation of cav-1 at tyrosine 14 was found to be crucial for this process. Conclusions: This study demonstrates the relationship between age and α-syn spread and will facilitate our understanding of the molecular mechanism of the cell-to-cell transmission of α-syn.

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“…In addition, caveolin-1 and integrins play critical roles in determining senescent cell morphology [48]. Recently, it was also reported that premature senescence induced by cavelin-1-deficiency is mediated by inhibition of mitochondrial respiration and oxidative phosphorylation complex I, a reduction in the NAD+/NADH ratio, and SIRT1 inactivation [49]. Activation of focal adhesion signaling induces PI3K-AKT signaling.…”

Section: Discussionmentioning

confidence: 99%

Proteomics profiling and pathway analysis of hippocampal aging in rhesus monkeys

Meng

Xia

Pan

et al. 2019

Preprint

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Background: Aged rhesus monkeys exhibit deficits in memory mediated by the hippocampus. Although extensive research has been carried out on the characteristics of human hippocampal aging, there is still very little scientific understanding of the changes associated with hippocampal aging in rhesus monkeys. To explore the proteomics profiling and pathway-related changes in the rhesus hippocampus during the aging process, we conducted a high throughput quantitative proteomics analysis of hippocampal samples from two groups of rhesus macaques aged 6 years and 20 years, using 2-plex tandem mass tag (TMT) labeling. In addition, we used a comprehensive bioinformatics analysis approach to investigate the enriched signaling pathways of differentially expressed proteins (the ratios of 20-y vs. 6-y, ≥1.20 or ≤ 0.83). Results: In total, 3,260 proteins were identified with a high level of confidence in rhesus hippocampus. We found 367 differentially expressed proteins related to rhesus hippocampus aging. Based on biological pathway analysis, we found these aging-related proteins were predominantly enriched in the electron transport chain, NRF2 pathway, focal adhesion-PI3K-AKT-mTOR signaling pathway and cytoplasmic ribosome proteins. Data are available via ProteomeXchange with identifier PXD011398. Conclusion: This study provides a detail description of the proteomics profile related to rhesus hippocampal aging. These findings should make an important contribution to further mechanistic studies, marker selection and drug development for the prevention and treatment of aging or age-related neurodegeneration.

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Caveolin‐1 deficiency induces premature senescence with mitochondrial dysfunction

Cited by 54 publications

References 45 publications

Markers of T Cell Senescence in Humans

Markers of T Cell Senescence in Humans

Age-Related Increase in Caveolin-1 Expression Facilitates Cell-To-Cell Transmission of α-Synuclein in Neurons

Proteomics profiling and pathway analysis of hippocampal aging in rhesus monkeys

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