Academic literature on the topic 'Adipose tissue, senescence, aging, oxidative stress'
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Journal articles on the topic "Adipose tissue, senescence, aging, oxidative stress"
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Gorwood, Jennifer, Tina Ejlalmanesh, Christine Bourgeois, Matthieu Mantecon, Cindy Rose, Michael Atlan, Delphine Desjardins, et al. "SIV Infection and the HIV Proteins Tat and Nef Induce Senescence in Adipose Tissue and Human Adipose Stem Cells, Resulting in Adipocyte Dysfunction." Cells 9, no. 4 (April 1, 2020): 854. http://dx.doi.org/10.3390/cells9040854.
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Background: Aging is characterized by adipose tissue senescence, inflammation, and fibrosis, with trunk fat accumulation. Aging HIV-infected patients have a higher risk of trunk fat accumulation than uninfected individuals—suggesting that viral infection has a role in adipose tissue aging. We previously demonstrated that HIV/SIV infection and the Tat and Nef viral proteins were responsible for adipose tissue fibrosis and impaired adipogenesis. We hypothesized that SIV/HIV infection and viral proteins could induce adipose tissue senescence and thus lead to adipocyte dysfunctions. Methods: Features of tissue senescence were evaluated in subcutaneous and visceral adipose tissues of SIV-infected macaques and in human adipose stem cells (ASCs) exposed to Tat or Nef for up to 30 days. Results: p16 expression and p53 activation were higher in adipose tissue of SIV-infected macaques than in control macaques, indicating adipose tissue senescence. Tat and Nef induced higher senescence in ASCs, characterized by higher levels of senescence-associated beta-galactosidase activity, p16 expression, and p53 activation vs. control cells. Treatment with Tat and Nef also induced oxidative stress and mitochondrial dysfunction. Prevention of oxidative stress (using N-acetyl-cysteine) reduced senescence in ASCs. Adipocytes having differentiated from Nef-treated ASCs displayed alterations in adipogenesis with lower levels of triglyceride accumulation and adipocyte marker expression and secretion, and insulin resistance. Conclusion: HIV/SIV promotes adipose tissue senescence, which in turn may alter adipocyte function and contribute to insulin resistance.
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Schosserer, Markus, Johannes Grillari, Christian Wolfrum, and Marcel Scheideler. "Age-Induced Changes in White, Brite, and Brown Adipose Depots: A Mini-Review." Gerontology 64, no. 3 (December 7, 2017): 229–36. http://dx.doi.org/10.1159/000485183.
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Aging is a time-related process of functional decline at organelle, cellular, tissue, and organismal level that ultimately limits life. Cellular senescence is a state of permanent growth arrest in response to stress and one of the major drivers of aging and age-related disorders. Senescent cells accumulate with age, and removal of these cells delays age-related disorders in different tissues and prolongs healthy lifespan. One of the most studied aging mechanisms is the accumulation of reactive oxygen species damage in cells, organs, and organisms over time. Elevated oxidative stress is also found in metabolic diseases such as obesity, metabolic syndrome and associated disorders. Moreover, dysregulation of the energy homeostasis is also associated with aging, and many age-related genes also control energy metabolism, with the adipose organ, comprising white, brite, and brown adipocytes, as an important metabolic player in the regulation of whole-body energy homeostasis. This review summarizes transformations in the adipose organ upon aging and cellular senescence and sheds light on the reallocation of fat mass between adipose depots, on the metabolism of white and brown adipose tissue, on the regenerative potential and adipogenic differentiation capacity of preadipocytes, and on alterations in mitochondria and bioenergetics. In conclusion, the aging process is a lifelong, creeping process with gradual decline in (pre-)adipocyte function over time. Thus, slowing down the accumulation of (pre-)adipocyte damage and dysfunction, removal of senescent preadipocytes as well as blocking deleterious compounds of the senescent secretome are protective measures to maintain a lasting state of health at old age.
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Caron, Martine, Martine Auclair, Anais Vissian, Corinne Vigouroux, and Jacqueline Capeau. "Contribution of Mitochondrial Dysfunction and Oxidative Stress to Cellular Premature Senescence Induced by Antiretroviral Thymidine Analogues." Antiviral Therapy 13, no. 1 (January 2008): 27–38. http://dx.doi.org/10.1177/135965350801300103.
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Objectives Treatment of HIV-infected patients is associated with early onset of aging-related comorbidities. Some of the adverse effects of antiretroviral therapy have been attributed to the mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI), and it is of note that mitochondrial dysfunction and oxidative stress are involved in the aging processes. In this regard, we examined whether NRTIs could accelerate the senescence of cultured cells. Methods Human fibroblasts were exposed to NRTIs from culture passage 1 to 14. Cytochrome c-oxidase (COX) subunits 2 and 4, mitochondrial potential and mass, and reactive oxygen species (ROS) were quantified at each passage. Proliferation, cell-cycle arrest, senescence-associated β-galactosidase activity, and morphology were assessed in parallel. Mitochondrial and senescence markers were assessed in cultured murine preadipocytes and in fat samples from lipodystrophic HIV-infected patients. Results Stavudine and zidovudine induced mitochondrial dysfunction and increased ROS levels in fibroblasts at early culture passages, while cell division gradually slowed. At passages 8–12, fibroblasts exposed to stavudine or zidovudine but not abacavir, didanosine, lamivudine and tenofovir were senescent, on the basis of p16INK4 and p21WAF-1 protein expression, cell morphology and senescence-associated-β-galactosidase activity. Senescence markers and COX2 underexpression were also found in 3T3-F442A preadipocytes exposed for 7 weeks to stavudine or zidovudine, but not lamivudine, and in adipose tissue samples from lipodystrophic HIV-infected patients on antiretroviral regimens containing stavudine or zidovudine. Conclusions Mitochondrial changes and oxidative damage could partly explain the premature senescence of fibroblasts and adipose cells induced by stavudine and zidovudine. This suggests that thymidine analogues might be involved in the early aging-related diseases observed in some HIV-infected patients taking antiretroviral drugs.
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Kornicka, K., R. Walczak, A. Mucha, and K. Marycz. "Released from ZrO2/SiO2 coating resveratrol inhibits senescence and oxidative stress of human adipose-derived stem cells (ASC)." Open Chemistry 16, no. 1 (May 23, 2018): 481–95. http://dx.doi.org/10.1515/chem-2018-0039.
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AbstractThe rapid aging of the population results in increased number of metabolic and degenerative disorders, especially in the elderly.Thus, a novel approach in the fields of orthopedic and reconstructive surgery for bone regeneration is strongly desirable. A new perspective in the therapy of bone fractures is tissue engineering which combines living cells with biomaterials to develop modern substitutes that can restore tissue functions. Metallic biomaterials, including stainless steel and pure titanium, have been extensively used for the fabrication of surgical implants over decades. Chemical modification of material surface for example incorporation of chemotactic factors may significantly improve the therapeutic effect. In this paper we describe titanium substrate modifications with ZrO2/SiO2 coating functionalized with resveratrol using a sol – gel, dip-coating technique. Moreover, we established the effects of fabricated scaffolds on adipose stem cells isolated from elderly patients. Using fluorescence imaging, polymerase chain reaction (PCR)and cytotoxicity tests, we established that 0.5 Res_ZrO2/SiO2 significantly reduced apoptosis and accumulation of oxidative stress factors in adipose derived stem cells (ASC). Thus exploitation of fabricated biomaterials in regenerative medicine as a strategy for rejuvenate ASC from elderly patients in vivo, seems fully justified.
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Wang, Xiujuan, Rui Liu, Chan Wei, Meihong Xu, and Yong Li. "Exogenous Nucleotides Improved the Oxidative Stress and Sirt-1 Protein Level of Brown Adipose Tissue on Senescence-Accelerated Mouse Prone-8 (SAMP8) Mice." Nutrients 14, no. 14 (July 7, 2022): 2796. http://dx.doi.org/10.3390/nu14142796.
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Brown adipose tissue (BAT) is of great importance in rodents for maintaining their core temperature via non-shivering thermogenesis in the mitochondria. BAT′s thermogenic function has been shown to decline with age. The activation of adenosine 5′-monophosphate (AMP)-activated protein kinase/sirtuin-1 (AMPK/Sirt-1) is effective in regulating mitochondrial function. Exogenous nucleotides (NTs) are regulatory factors in many biological processes. Nicotinamide mononucleotide (NMN), which is a derivative of NTs, is widely known as a Sirt-1 activator in liver and muscle, but the effect of NMN and NTs on aging BAT has not been studied before. The purpose of this study was to investigate the effect of NTs on aging senescence-accelerated mouse prone-8 (SAMP8) mice. Senescence-accelerated mouse resistant 1 (SAMR1) mice were set as the model control group and NMN was used as the positive control. Male, 3 month old SAMP8 mice were divided into the SAMP8-normal chow (SAMP8-NC), SAMP8-young-normal chow (SAMP8-young-NC), NMN, NTs-free, NTs-low, NTs-medium, and NTs-high groups for long-term feeding. After 9 months of intervention, interscapular BAT was collected for experiments. Compared to the SAMP8-NC, the body weight and BAT mass were significantly improved in the NT-treated aging SAMP8 mice. NT supplementation had effects on oxidative stress in BAT. The concentration of malondialdehyde (MDA) was reduced and that of superoxide dismutase (SOD) increased significantly. Meanwhile, the expression of the brown adipocyte markers uncoupling protein-1 (UCP-1), peroxisome proliferator-activated receptor-γ coactlvator-1α (PGC-1α), and PR domain zinc finger protein 16 (PRDM16) were upregulated. The upregulated proteins may be activated via the Sirt-1 pathway. Thus, NT supplementation may be helpful to improve the thermogenesis of BAT by reducing oxidative stress and activating the Sirt-1 pathway.
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Kornicka, Katarzyna, Krzysztof Marycz, Krzysztof Andrzej Tomaszewski, Monika Marędziak, and Agnieszka Śmieszek. "The Effect of Age on Osteogenic and Adipogenic Differentiation Potential of Human Adipose Derived Stromal Stem Cells (hASCs) and the Impact of Stress Factors in the Course of the Differentiation Process." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–20. http://dx.doi.org/10.1155/2015/309169.
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Human adipose tissue is a great source of autologous mesenchymal stem cells (hASCs), which are recognized for their vast therapeutic applications. Their ability to self-renew and differentiate into several lineages makes them a promising tool for cell-based therapies in different types of degenerative diseases. Thus it is crucial to evaluate age-related changes in hASCs, as the elderly are a group that will benefit most from their considerable potential. In this study we investigated the effect of donor age on growth kinetics, cellular senescence marker levels, and osteogenic and adipogenic potential of hASCs. It also has been known that, during life, organisms accumulate oxidative damage that negatively affects cell metabolism. Taking this into consideration, we evaluated the levels of nitric oxide, reactive oxygen species, and superoxide dismutase activity. We observed that ROS and NO increase with aging, while SOD activity is significantly reduced. Moreover cells obtained from older patients displayed senescence associated features, for example,β-galactosidase activity, enlarged morphology, and p53 protein upregulation. All of those characteristics seem to contribute to decreased proliferation potential of those cells. Our results suggest that due to aging some cellular modification may be required before applying aged cells efficiently in therapies such as tissue engineering and regenerative medicine.
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Lefranc, Clara, Malou Friederich-Persson, Fabienne Foufelle, Aurélie Nguyen Dinh Cat, and Frédéric Jaisser. "Adipocyte-Mineralocorticoid Receptor Alters Mitochondrial Quality Control Leading to Mitochondrial Dysfunction and Senescence of Visceral Adipose Tissue." International Journal of Molecular Sciences 22, no. 6 (March 12, 2021): 2881. http://dx.doi.org/10.3390/ijms22062881.
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Mineralocorticoid receptor (MR) expression is increased in the adipose tissue (AT) of obese patients and animals. We previously demonstrated that adipocyte-MR overexpression in mice (Adipo-MROE mice) is associated with metabolic alterations. Moreover, we showed that MR regulates mitochondrial dysfunction and cellular senescence in the visceral AT of obese db/db mice. Our hypothesis is that adipocyte-MR overactivation triggers mitochondrial dysfunction and cellular senescence, through increased mitochondrial oxidative stress (OS). Using the Adipo-MROE mice with conditional adipocyte-MR expression, we evaluated the specific effects of adipocyte-MR on global and mitochondrial OS, as well as on OS-induced damage. Mitochondrial function was assessed by high throughput respirometry. Molecular mechanisms were probed in AT focusing on mitochondrial quality control and senescence markers. Adipo-MROE mice exhibited increased mitochondrial OS and altered mitochondrial respiration, associated with reduced biogenesis and increased fission. This was associated with OS-induced DNA-damage and AT premature senescence. In conclusion, targeted adipocyte-MR overexpression leads to an imbalance in mitochondrial dynamics and regeneration, to mitochondrial dysfunction and to ageing in visceral AT. These data bring new insights into the MR-dependent AT dysfunction in obesity.
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Park, Jeong Seop, Jiyuan Piao, Gabee Park, and Hyun Sook Hong. "Substance-P Restores Cellular Activity of ADSC Impaired by Oxidative Stress." Antioxidants 9, no. 10 (October 12, 2020): 978. http://dx.doi.org/10.3390/antiox9100978.
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Oxidative stress induces cellular damage, which accelerates aging and promotes the development of serious illnesses. Adipose-derived stem cells (ADSCs) are novel cellular therapeutic tools and have been applied for tissue regeneration. However, ADSCs from aged and diseased individuals may be affected in vivo by the accumulation of free radicals, which can impair their therapeutic efficacy. Substance-P (SP) is a neuropeptide that is known to rescue stem cells from senescence and inflammatory attack, and this study explored the restorative effect of SP on ADSCs under oxidative stress. ADSCs were transiently exposed to H2O2, and then treated with SP. H2O2 treatment decreased ADSC cell viability, proliferation, and cytokine production and this activity was not recovered even after the removal of H2O2. However, the addition of SP increased cell viability and restored paracrine potential, leading to the accelerated repopulation of ADSCs injured by H2O2. Furthermore, SP was capable of activating Akt/GSK-3β signaling, which was found to be downregulated following H2O2 treatment. This might contribute to the restorative effect of SP on injured ADSCs. Collectively, SP can protect ADSCs from oxidant-induced cell damage, possibly by activating Akt/GSK-3β signaling in ADSCs. This study supports the possibility that SP can recover cell activity from oxidative stress-induced dysfunction.
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Valverde, Mahara, and Aarón Sánchez-Brito. "Sustained Activation of TNFα-Induced DNA Damage Response in Newly Differentiated Adipocytes." International Journal of Molecular Sciences 22, no. 19 (September 29, 2021): 10548. http://dx.doi.org/10.3390/ijms221910548.
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The response to DNA damage is the mechanism that allows the interaction between stress signals, inflammatory secretions, DNA repair, and maintenance of cell and tissue homeostasis. Adipocyte dysfunction is the cellular trigger for various disease states such as insulin resistance, diabetes, and obesity, among many others. Previously, our group demonstrated that adipogenesis per se, from mesenchymal/stromal stem cells derived from human adipose tissue (hASCs), involves an accumulation of DNA damage and a gradual loss of the repair capacity of oxidative DNA damage. Therefore, our objective was to identify whether healthy adipocytes differentiated for the first time from hASCs, when receiving inflammatory signals induced with TNFα, were able to persistently activate the DNA Damage Response and thus trigger adipocyte dysfunction. We found that TNFα at similar levels circulating in obese humans induce a sustained response to DNA damage response as part of the Senescence-Associated Secretory Phenotype. This mechanism shows the impact of inflammatory environment early affect adipocyte function, independently of aging.
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Marycz, Krzysztof, Katarzyna Kornicka, Katarzyna Basinska, and Aleksandra Czyrek. "Equine Metabolic Syndrome Affects Viability, Senescence, and Stress Factors of Equine Adipose-Derived Mesenchymal Stromal Stem Cells: New Insight into EqASCs Isolated from EMS Horses in the Context of Their Aging." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–17. http://dx.doi.org/10.1155/2016/4710326.
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Currently, equine metabolic syndrome (EMS), an endocrine disease linked to insulin resistance, affects an increasing number of horses. However, little is known about the effect of EMS on mesenchymal stem cells that reside in adipose tissue (ASC). Thus it is crucial to evaluate the viability and growth kinetics of these cells, particularly in terms of their application in regenerative medicine. In this study, we investigated the proliferative capacity, morphological features, and accumulation of oxidative stress factors in mesenchymal stem cells isolated from healthy animals (ASCN) and horses suffering from EMS (ASCEMS).ASCEMSdisplayed senescent phenotype associated withβ-galactosidase accumulation, enlarged cell bodies and nuclei, increased apoptosis, and reduced heterochromatin architecture. Moreover, we observed increased amounts of nitric oxide (NO) and reactive oxygen species (ROS) in these cells, accompanied by reduced superoxide dismutase (SOD) activity. We also found inASCEMSan elevated number of impaired mitochondria, characterized by membrane raptures, disarrayed cristae, and vacuole formation. Our results suggest that the toxic compounds, accumulating in the mitochondria under oxidative stress, lead to alternations in their morphology and may be partially responsible for the senescent phenotype and decreased proliferation potential ofASCEMS.
Dissertations / Theses on the topic "Adipose tissue, senescence, aging, oxidative stress"
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TEBON, MAELA, Mauro Zamboni, and E. Zoico. "MODULAZIONE DEI FENOMENI DI SENESCENZA CELLULARE DI ADIPOCITI E PREADIPOCITI IN VITRO." Doctoral thesis, 2019. http://hdl.handle.net/11562/995191.
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L’invecchiamento è accompagnato da una complessa rete di processi biologici caratterizzati da uno stato infiammatorio cronico basale, a sua volta correlato allo sviluppo di patologie età-associate come: aterosclerosi, osteoartriti, Alzheimer, diabete di tipo 2. Una sempre più approfondita analisi del processo di senescenza tessutospecifico potrebbe consentire l’individuazione di target terapeutici utili a modulare il processo complessivo dell’invecchiamento stesso. L’invecchiamento è causa di declino delle funzionalità sistemiche e il tessuto adiposo è uno degli organi maggiormente colpiti in quanto subisce cambiamenti significativi che riguardano la quantità, la distribuzione, la composizione cellulare e l’attività endocrina, giocando un ruolo chiave nell’insorgenza di insulino-resistenza, di disfunzioni metaboliche e infiammazione sistemica. L’abbondanza del tessuto adiposo e le diverse funzioni da esso esercitate lo rendono un organo fondamentale per la comprensione della fisiologia dell’intero organismo. Tuttavia, i cambiamenti a cui è sottoposto durante il processo di invecchiamento sono solo in parte noti e oggetto di studio negli ultimi anni. È quindi fondamentale conoscere i processi molecolari che stanno alla base della fisiopatologia del tessuto adiposo e del suo invecchiamento in modo da poter individuare strategie terapeutiche per le malattie correlate all’invecchiamento. In questo studio, è stato messo a punto un modello cellulare di senescenza in vitro attraverso il trattamento con perossido di idrogeno (H2O2) in adipociti e preadipociti 3T3-L1 murini. Successivamente è stata valutata la potenziale attività senolitica della quercetina esaminandone l’effetto antiossidante e antinfiammatorio, cercando di individuarne il target molecolare.Aging is associated with pathological age-related processes as inflammatory low-grade state, atherosclerosis, Alzheimer's disease, type II diabetes and osteoarthritis diseases. A deep analysis of the tissue-specific senescence process could allow the identification of therapeutic targets to modulate the aging process itself. In this study, premature senescence model was developed in vitro through treatment with oxygen peroxide (H2O2) in murine 3T3-L1 preadipocytes before and after induction to mature adipocytes. H2O2 treated cells showed characteristic senescence-associated features including senescence-associated beta-galactosidase activity (SA-ß-gal), activation of reactive oxygen species (ROS) development of senescence-associated secretory phenotype (SASP), induction of cell cycle inhibitors P-21 as well as induction of pro-inflammatory transduction factor NFκB and a downregulation of deacetylase SIRT1. We found that stimulation with H2O2 results in an induction of miR-155-5p expression in preadipocytes and in mature adipocytes. The treatment with quercetin (20 μM) showed significant decrease in the number of ß-galactosidase positive cell along with the suppression of ROS, NFκB and SASP factor in both cell models. In addition, quercetin treatment also upregulated protein expression of SIRT1 and decreased miR-155-5p expression. These results suggest that quercetin acts as a potential senolytic agent in both preadipocytes and adipocytes cell models, inhibiting ROS production and proinflammatory miR-155-5p.
Book chapters on the topic "Adipose tissue, senescence, aging, oxidative stress"
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Jay Sarkar, Tapash, Maiko Hermsmeier, Jessica L. Ross, and G. Scott Herron. "Genetic and Epigenetic Influences on Cutaneous Cellular Senescence." In Senescence [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101152.
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Skin is the largest human organ system, and its protective function is critical to survival. The epithelial, dermal, and subcutaneous compartments are heterogeneous mixtures of cell types, yet they all display age-related skin dysfunction through the accumulation of an altered phenotypic cellular state called senescence. Cellular senescence is triggered by complex and dynamic genetic and epigenetic processes. A senescence steady state is achieved in different cell types under various and overlapping conditions of chronological age, toxic injury, oxidative stress, replicative exhaustion, DNA damage, metabolic dysfunction, and chromosomal structural changes. These inputs lead to outputs of cell-cycle withdrawal and the appearance of a senescence-associated secretory phenotype, both of which accumulate as tissue pathology observed clinically in aged skin. This review details the influence of genetic and epigenetic factors that converge on normal cutaneous cellular processes to create the senescent state, thereby dictating the response of the skin to the forces of both intrinsic and extrinsic aging. From this work, it is clear that no single biomarker or process leads to senescence, but that it is a convergence of factors resulting in an overt aging phenotype.