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Marie Toutfaire, Elise Dumortier, Antoine Fattaccioli, Martine Van Steenbrugge, Charlotte M Proby, Florence Debacq-Chainiaux
Cutaneous Squamous Cell Carcinoma (cSCC) is the second most common type of non-melanoma skin cancer in white-skinned populations. cSCC is associated with sun exposure and aging, which is concomitant with an accumulation of senescent cells in the skin. The involvement of senescent cells in carcinogenesis has been highlighted in several cancer types and an interaction between cSCC cells and senescent cells is proposed, but still little explored. Tumor-associated effects are mostly attributed to the senescence-associated secretory phenotype (SASP)...
March 14, 2018: International Journal of Biochemistry & Cell Biology
Stephen Capone, Kwasi M Connor, Anthony Colombo, Xin Li, Tim J Triche, Giridharan Ramsingh
Genomic transposable elements (TEs) constitute majority of the genome. Expression of TEs is known to activate the double-stranded RNA recognition pathway ("viral mimicry") leading to the activation of interferon-stimulated genes, inflammation and immune mediated cell death. We recently showed that the expression of TEs is suppressed along with immune pathways in leukemic stem cells (LSC) in acute myeloid leukemia, suggesting a potential mechanism for immune escape of LSC. This indicated that during oncogenesis, where there is escape from senescence, expression of TEs is suppressed...
March 13, 2018: Experimental Hematology
Sung Eun Kim, Jae Yong Lee, Kyu-Sik Shim, Sunghee Lee, Kyoengwoo Min, Ji-Hoon Bae, Hak-Jun Kim, Kyeongsoon Park, Hae-Ryong Song
The aim of this study was to investigate the effects of a sulfasalazine-containing hyaluronic acid (SASP/HA) systems on in vitro anti-inflammation and the alleviation of cartilage degradation in both lipopolysaccharide (LPS)-stimulated synoviocytes and a rat model of monosodium iodoacetate (MIA)-induced osteoarthritis (OA). The SASP/HA resulted in long-term release of SASP from the SASP/HA for up to 60 days in a sustained manner. In vitro studies performed using real-time polymerase chain reaction (PCR) assay revealed that the SASP/HA was able to effectively and dose-dependently inhibit the mRNA expression levels of pro-inflammatory cytokines such as matrix metalloproteinases-3 (MMP-3), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in LPS-stimulated synoviocytes...
March 13, 2018: International Journal of Biological Macromolecules
Adam D Hudgins, Cagdas Tazearslan, Archana Tare, Yizhou Zhu, Derek Huffman, Yousin Suh
Cellular senescence is a state of irreversible cellular growth arrest accompanied by distinct changes in gene expression and the acquisition of a complex proinflammatory secretory profile termed the senescence-associated secretory phenotype (SASP). Senescent cells accumulate in aged tissues and contribute to age-related disease in mice. Increasing evidence that selective removal of senescent cells can ameliorate diseases of late life and extend lifespan in mice has given rise to the development of senolytics that target senescent cells as anti-aging therapeutics...
2018: Frontiers in Genetics
S O Osawe, E O Farombi
Certain dietary flavonoids exhibit protective potentials against drug-induced male reproductive toxicities. We investigated the protective effects of quercetin and rutin on sulphasalazine-induced alterations in steroidogenic enzyme activity, hormone profile and spermiotoxicity in rats. Sulphasalazine (SASP, 600 mg/kg bw) was administered alone or in combination with quercetin (20 mg/kg bw) or rutin (10 mg/kg bw) for 14 days. SASP treatment significantly increased relative weights of the epididymis and seminal vesicles...
March 7, 2018: Andrologia
Alina Wiesemann, Julia Ketteler, Alexis Slama, Florian Wirsdörfer, Thomas Hager, Katharina Roeck, Daniel Engel, Jens Fischer, Clemens Aigner, Verena Jendrossek, Diana Klein
AIMS: Radiation-induced normal tissue toxicity often precludes the application of curative radiation doses. Here we investigated the therapeutic potential of Ccl2 signaling inhibition to protect normal lung tissue from radiotherapy (RT)-induced injury. RESULTS: RT-induced vascular dysfunction and associated adverse effects can be efficiently antagonized by inhibition of Ccl2 signaling using either the selective Ccl2 inhibitor bindarit (BIN) or mice deficient for the main Ccl2 receptor CCR2 (KO)...
February 20, 2018: Antioxidants & Redox Signaling
Siew-Min Ong, Eva Hadadi, Truong-Minh Dang, Wei-Hseun Yeap, Crystal Tze-Ying Tan, Tze-Pin Ng, Anis Larbi, Siew-Cheng Wong
Human primary monocytes comprise a heterogeneous population that can be classified into three subsets based on CD14 and CD16 expression: classical (CD14 high /CD16 - ), intermediate (CD14 high /CD16 + ), and non-classical (CD14 low /CD16 + ). The non-classical monocytes are the most pro-inflammatory in response to TLR stimulation in vitro, yet they express a remarkably high basal level of miR-146a, a microRNA known to negatively regulate the TLR pathway. This concurrence of a pro-inflammatory status and a high miR-146a level has been associated with cellular senescence in other cell types...
February 15, 2018: Cell Death & Disease
Xuerong Sun, Benyan Shi, Huiling Zheng, Ling Min, Jie Yang, Xiaoyi Li, Xiaoxin Liao, Weixing Huang, Mingmeng Zhang, Shun Xu, Zhe Zhu, Hongjing Cui, Xinguang Liu
Although targeted therapy and immunotherapy greatly improve the outcome of melanoma, drug resistance and low response rates still maintain the unsubstitutability of traditional chemotherapy. Cisplatin (CDDP) is widely used in different types of tumours with high response rates, but it generally has low efficiency in melanoma. The mechanisms underpinning the phenomena are not sufficiently understood. Here we demonstrated that various melanoma cell lines adopted senescence phenotype after CDDP treatment in contrast to the other types of tumour cells...
February 15, 2018: Cell Death & Disease
Isaac K Sundar, Kahkashan Rashid, Janice Gerloff, Dongmei Li, Irfan Rahman
Cigarette smoke (CS) affects DNA damage and cellular senescence signaling pathways in the pathogenesis of chronic obstructive pulmonary disease (COPD). p16(INK4a) (p16: a cyclin-dependent kinase inhibitor) is a key marker of cellular senescence, which is induced by CS in lung cells. It is thought that removal of p16 attenuates premature aging by removing senesced cells. However, the role of p16 in CS-induced stress induce premature senescence (SIPS) and senescence-associated secretory phenotype (SASP during the development of COPD/emphysema is not known...
February 15, 2018: American Journal of Respiratory Cell and Molecular Biology
Kotomi Seno, Nao Tanikawa, Hironori Takahashi, Akihide Ohkuchi, Hirotada Suzuki, Shigeki Matsubara, Hisataka Iwata, Takehito Kuwayama, Koumei Shirasuna
PROBLEM: We investigated the effect of oxygen concentrations on cellular senescence and autophagy and examined the role of autophagy in human trophoblast cells. METHOD OF STUDY: Human first-trimester trophoblast cells (Sw.71) were incubated under 21%, 5%, or 1% O 2 concentrations for 24 hours. We examined the extent of senescence caused using senescence-associated β-galactosidase (SA-β-Gal) and senescence-associated secretory phenotype (SASP) as markers. Moreover, we examined the role of autophagy in causing cellular senescence using an autophagy inhibitor (3-methyladenine, 3MA)...
February 15, 2018: American Journal of Reproductive Immunology: AJRI
Yuanyuan Su, Pengfeng Wang, Hong Shen, Zhaomeng Sun, Chenzhong Xu, Guodong Li, Tanjun Tong, Jun Chen
Senescent cells develop senescence-associated secretory phenotype (SASP) which possesses multiple biological functions via autocrine or paracrine manner. However, the status of the protein kinase D1 (PKD1)-mediated classical protein secretory pathway from trans-Golgi network (TGN) to cell surface during cellular senescence and its role in cellular senescent response remain unknown. Here, we show that the activities or quantities of the critical components of this pathway including PKD1, ADP-ribosylation factor 1 (ARF1), and phosphatidylinositol 4-kinase IIIβ (PI4KIIIβ) at TGN are increased in senescent cells...
February 2, 2018: Journal of Cell Science
Kevin C Flanagan, Elise Alspach, Ermira Pazolli, Shankar Parajuli, Qihao Ren, Laura L Arthur, Roberto Tapia, Sheila A Stewart
Tumorigenesis results from the convergence of cell autonomous mutations and corresponding stromal changes that promote tumor cell growth. Senescent cells, which secrete a plethora of pro-tumorigenic factors termed the senescence-associated secretory phenotype (SASP), play an important role in tumor formation. Investigation into SASP regulation revealed that many but not all SASP factors are subject to NF-kB and p38MAPK regulation. However, many pro-tumorigenic SASP factors, including osteopontin (OPN), are not responsive to these canonical pathways leaving the regulation of these factors an open question...
January 2, 2018: Oncotarget
Jing Wang, Yiji Feng, Peng Han, Fenghua Wang, Xueting Luo, Jian Liang, Xiangjun Sun, Jing Ye, Yiming Lu, Xiaodong Sun
Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in elderly people. AMD is classified as early, intermediate, advanced non-neovascular, and advanced neovascular forms depending on the clinical features. However, the exact pathogenesis remains unclear. Retinal pigment epithelium (RPE) cells degeneration is a hallmark of AMD. With aging, lipofuscin accumulates in RPE cells. N-retinylidene-N-retinylethanolamine (named A2E), a well-known fluorophore of lipofuscin, may contribute to RPE cells degeneration...
February 7, 2018: Cell Death & Disease
Jingang Hou, Changhao Cui, Sunchang Kim, Changkeun Sung, Chulhee Choi
Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by D-galactose via suppressing p38MAPK-dependent NF-κB activity...
February 2, 2018: Chemico-biological Interactions
Christopher D Wiley, Nicholas Schaum, Fatouma Alimirah, Jose Alberto Lopez-Dominguez, Arturo V Orjalo, Gary Scott, Pierre-Yves Desprez, Christopher Benz, Albert R Davalos, Judith Campisi
Processes that have been linked to aging and cancer include an inflammatory milieu driven by senescent cells. Senescent cells lose the ability to divide, essentially irreversibly, and secrete numerous proteases, cytokines and growth factors, termed the senescence-associated secretory phenotype (SASP). Senescent cells that lack p53 tumor suppressor function show an exaggerated SASP, suggesting the SASP is negatively controlled by p53. Here, we show that increased p53 activity caused by small molecule inhibitors of MDM2, which promotes p53 degradation, reduces inflammatory cytokine production by senescent cells...
February 5, 2018: Scientific Reports
Shankar J Chinta, Georgia Woods, Marco Demaria, Anand Rane, Ying Zou, Amanda McQuade, Subramanian Rajagopalan, Chandani Limbad, David T Madden, Judith Campisi, Julie K Andersen
Exposure to the herbicide paraquat (PQ) is associated with an increased risk of idiopathic Parkinson's disease (PD). Therapies based on PQ's presumed mechanisms of action have not, however, yielded effective disease therapies. Cellular senescence is an anticancer mechanism that arrests proliferation of replication-competent cells and results in a pro-inflammatory senescence-associated secretory phenotype (SASP) capable of damaging neighboring tissues. Here, we demonstrate that senescent cell markers are preferentially present within astrocytes in PD brain tissues...
January 23, 2018: Cell Reports
Marissa J Schafer, Andrew J Haak, Daniel J Tschumperlin, Nathan K LeBrasseur
PURPOSE OF THE REVIEW: Senescent cells have the capacity to both effect and limit fibrosis. Senotherapeutics target senescent cells to improve aging conditions. Here, we review the contexts in which senescent cells mediate wound healing and fibrotic pathology and the potential utility of senotherapeutic drugs for treatment of fibrotic disease. RECENT FINDINGS: Multi-action and temporal considerations influence deleterious versus beneficial actions of senescent cells...
January 26, 2018: Current Rheumatology Reports
Anna Strzeszewska, Olga Alster, Grażyna Mosieniak, Agata Ciolko, Ewa Sikora
Senescence of cancer cells is an important outcome of treatment of many cancer types. Cell senescence is a permanent cell cycle arrest induced by stress conditions, including DNA damage. DNA damage activates DNA damage response (DDR), which involves members of the phosphatidylinositol 3-kinase-related kinase (PIKK) superfamily: protein kinases ATM, ATR, and DNA-PKcs. The so-far collected data indicate that ATM, with its downstream targets CHK2, p53, and p21, is the key protein involved in DDR-dependent senescence...
January 19, 2018: Cell Death & Disease
Jianshuang Li, Di Lu, Hong Dou, Huadie Liu, Kevin Weaver, Wenjun Wang, Jiada Li, Edward T H Yeh, Bart O Williams, Tao Yang, Ling Zheng
The development, growth, and renewal of skeletal tissues rely on the function of osteochondroprogenitors (OCPs). Protein sumoylation/desumoylation has emerged as a pivotal mechanism for stem cell/progenitor homeostasis, and excessive sumoylation has been associated with cell senescence and tissue aging, but its role in regulating OCP function is unclear. Here we show that postnatal loss of the desumoylase SUMO1/sentrin-specific peptidase 6 (SENP6) causes premature aging. OCP-specific SENP6 knockout mice exhibit smaller skeletons, with elevated apoptosis and cell senescence in OCPs and chondrocytes...
January 10, 2018: Nature Communications
Simona di Martino, Carla Azzurra Amoreo, Barbara Nuvoli, Rossella Galati, Sabrina Strano, Francesco Facciolo, Gabriele Alessandrini, Harvey I Pass, Gennaro Ciliberto, Giovanni Blandino, Ruggero De Maria, Mario Cioce
Adaptive resistance to therapy is a hallmark of cancer progression. To date, it is not entirely clear how microenvironmental stimuli would mediate emergence of therapy-resistant cell subpopulations, although a rearrangement of the cancer cell secretome following therapy-induced stress can be pivotal for such a process. Here, by using the highly chemoresistant malignant pleural mesothelioma (MPM) as an experimental model, we unveiled a key contribution of the chaperone HSP90 at assisting a chemotherapy-instigated Senescence-Associated-Secretory-Phenotype (SASP)...
January 9, 2018: Oncogene
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