Relevant bibliographies by topics / Secretory phenotype

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  4. Conference papers

Academic literature on the topic 'Secretory phenotype'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Secretory phenotype"

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Sukla, Krishna, Pooja Kunte, Rajashree Kamat, Deepa Raut, Dattatray Bhat, Akshay Dedaniya, Giriraj Chandak, Anand Chaphekar, and Chittaranjan Yajnik. "FUT Genotypes, Secretor Status, H.pylori Antibody Levels and Vitamin-B12 Concentrations in Indians." Current Developments in Nutrition 5, Supplement_2 (June 2021): 951. http://dx.doi.org/10.1093/cdn/nzab050_018.

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Abstract Objectives Background: The FUT2 gene is responsible for the secretion of ABO blood type antigens into the body fluids (saliva, mucous, urine, tears, breast milk, sweat, and semen). Those who secrete the antigens into body fluids are call secretors, those who do not are called non-secretors. Hypothesis: GWAS studies have reported FUT gene variants to be associated with circulating vitamin-B12 (Vit-B12) concentrations. Missense mutations in the FUT2 gene result in a non-secretor phenotype. Thus, the secretory status of an individual may affect circulating vitamin-B12 concentrations over and above the genotype. Methods Materials and Methods: We included 780 participants (271 children, 282 mothers, and 227 fathers) from Pune Maternal Nutrition Study (PMNS). We measured the secretor status of individuals in saliva by hemagglutination test. A total of eight genetic variants including six SNPs from the FUT2 gene (rs492602, rs681343, rs281377, rs601338, rs1800027, and rs602662) and two SNPs from the FUT6 gene (rs3760776 and rs3760775) from our previous GWAS study were correlated with circulating vitamin-B12 levels. We tested the associations of FUT gene variants with secretor status phenotype and of the secretor phenotype with circulating vit-B12, folate, and ferritin concentrations in addition to H.pylori antibody levels. Results Results and Discussion: We found 33% of participants were non-secretors compared to 20% reported in Western Caucasian populations. Non-secretors had higher vitamin-B12 concentrations but not of folate and ferritin, vitamin-B12 associations were over and above FUT genotypes. Non-secretors showed a higher response to Vit-B12 supplementation. We found a FUT2 haplotype () to be strongly associated with Vit-B12 concentrations and non-secretor status. Non-secretors had lower H.pylori antibody concentrations. FUT6 genotype and haplotype were associated with Vit-B12 concentrations but not with secretor status and H.pylori antibody levels. Conclusions Our data suggest that secretor status may influence Vit-B12 concentrations through susceptibility to H.pylori infection and possibly other gut microbiota. A higher frequency of non-secretors in Indians could offer a selective advantage against Vit-B12 deficiency. Funding Sources BBSRC, UK; MRC, UK; WELLCOME TRUST, UK; DBT, India; ICMR India
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Strzyz, Paulina. "Controlling the senescence-associated secretory phenotype." Nature Reviews Molecular Cell Biology 17, no. 12 (November 21, 2016): 740. http://dx.doi.org/10.1038/nrm.2016.157.

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Tamò, Luca, Kleanthis Fytianos, Fabienne Caldana, Cedric Simillion, Anis Feki, Izabela Nita, Manfred Heller, Thomas Geiser, and Amiq Gazdhar. "Interactome Analysis of iPSC Secretome and Its Effect on Macrophages In Vitro." International Journal of Molecular Sciences 22, no. 2 (January 19, 2021): 958. http://dx.doi.org/10.3390/ijms22020958.

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Induced pluripotent stem cell secretome (iPSC-CM) mitigate organ injury and help in repair. Macrophages play a critical role in tissue repair and regeneration and can be directed to promote tissue repair by iPSC-CM, although the exact mechanisms are not known. In the current investigative study, we evaluated the possible mechanism by which iPSC-CM regulates the phenotype and secretory pattern of macrophages in vitro. Macrophages were obtained from human peripheral blood mononuclear cells and differentiated to various subpopulations and treated with either iPSC-CM or control media in vitro. Macrophage phenotype was assessed by flow cytometry, gene expression changes by qRT PCR and secretory pattern by multiplex protein analysis. The protein and gene interaction network revealed the involvement of Amyloid precursor protein (APP) and ELAV-like protein 1 (ELAVL-1) both present in the iPSC-CM to play an important role in regulating the macrophage phenotype and their secretory pattern. This exploratory study reveals, in part, the possible mechanism and identifies two potential targets by which iPSC-CM regulate macrophages and help in repair and regeneration.
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Sokol, Ethan, Sophia Maund, Jeffrey Ross, and Timothy Wilson. "Abstract P3-09-10: NTRK1/2/3 fusions are observed in both secretory and non-secretory breast cancers." Cancer Research 82, no. 4_Supplement (February 15, 2022): P3–09–10—P3–09–10. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-09-10.

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Abstract Background NTRK1/2/3 kinase fusions are rare oncogenic drivers found in <1% of solid tumors. NTRK fusion-positive (NTRK+) solid tumors have shown meaningful clinical response to small molecule NTRK inhibitors such as entrectinib and larotrectinib, and broad genomic testing will help identify patients (pts) with these rare alterations. NTRK fusions occur more frequently in some cancers than others. For example, NTRK fusions are characteristic of secretory breast cancers (BCa), and it has been posited that non-secretory BCa lack druggable NTRK fusions (PMID: 30707464). However, these conclusions were drawn on limited patient populations. Here we show evidence of NTRK fusions in both secretory and non-secretory breast tumors in the largest real-world cohort of NTRK+ breast tumors reported to date. Methods Comprehensive genomic profiling of at least 324 cancer-related genes, including NTRK1/2/3, was done at Foundation Medicine on de-identified all-comer BCa pts during the course of routine clinical care. Pathology reports and hematoxylin and eosin (H&E) images of NTRK+ breast tumor tissue were examined by a board-certified pathologist for designation of secretory vs. non-secretory phenotype. Results NTRK fusions were identified in 23 BCa specimens. H&E images were available for review in 22 cases, and another was confirmed as secretory via the pathology report. Pathologist review of those 23 cases revealed that NTRK fusions were present in 11 with secretory phenotypes, 11 with non-secretory phenotypes, and 1 with a mixed secretory phenotype. Secretory cases most often harbored a ETV6-NTRK3 fusion (n=7) with additional recurrent fusions seen in TPM3-NTRK1 (n=2) and LMNA-NTRK1 (n=2). Non-secretory breast cancers also harbored ETV6-NTRK3 (n=2), TPM3-NTRK1 (n=1), and LMNA-NTRK1 (n=1) fusions, as well as several unique fusion events that retain the NTRK kinase domain. Conclusions While rare, NTRK fusions occur in a wide variety of tumor types. Within BCa, this includes both secretory and non-secretory phenotypes, with half of the identified alterations occurring in non-secretory BCa. Recurrent events, including ETV6-NTRK3, were observed in both populations. These data support NTRK fusion testing for all BCa pts with both secretory and non-secretory histologic subtypes. Citation Format: Ethan Sokol, Sophia Maund, Jeffrey Ross, Timothy Wilson. NTRK1/2/3 fusions are observed in both secretory and non-secretory breast cancers [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P3-09-10.
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Busarcevic, Ivan, Svetlana Vojvodic, and Una Vojvodic. "Association between secretor status and Lewis phenotype with seronegative spondyloarthritis as indicator of autoimmunity." Genetika 52, no. 1 (2020): 127–36. http://dx.doi.org/10.2298/gensr2001127b.

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The classical paradigm of autoimmune pathogenesis involving specific genetic makeup and exposure to environmental triggers has been challenged recently by the addition of a third element, the loss of intestinal barrier function. Regardless of HLA B27 phenotype or gastrointestinal symptoms, evidence of ileitis, ileocolitis or colitis exists in patients with spondyloarthropathy. The FUT2 secretory gene is a strong candidate for Crohn's susceptibility by shaping the functional states of mucosal microbiota and may thus have influence on the release of zonulin, the main regulator of gut permeability. Gram negative bacteria precipitate and may be involved in the pathogenesis of spondyloarthropathies. Susceptibility to many infectious agents is associated with ABO blood group or secretor state. Patients who cannot secrete ABO and Lewis blood group antigens into body fluids, an ability controlled by a single gene on chromosome 19, are known to be at increased risk of certain autoimmune diseases associated with human leukocyte antigen (HLA) markers. Lewis (Le) blood group phenotype can be used to infer secretor status. The objective of this study was to determine the distribution of secretor state and Lewis blood group phenotype in patients with seronegative spondyloarthropathies and healthy control subjects. Hundred and ten (110) patients with seronegative spondyloarthropathies (58 females and 52 males) and 103 control (74 males and 29 females) subjects participated in this study. Samples of saliva and blood were subjected to haemagglutination inhibition tests for determination of secretor status and Lewis phenotype. A total of 92(84%) patients and 92 (89%) control subjects were secretors while 18 (16%) patients and 11 (11%) control subjects were non-secretors. There was no statistically significant difference (?2 1,461 p<0,05 and degrees of freedom 1) in distribution of secretor status in comparison to seronegative spondyloarthropathies by comparing two observed populations. Seven patients had modified (reduced) expression of Lewis b antigen on their erythrocytes. Reduction of Lewis b antigen expression was not observed on erythrocytes of healthy subjects. Reduced expression of Lewis b antigen could be a consequence of the inflammatory process within the gut and it also suggests several pathogenic mechanisms which may be relevant to the synthesis of Lewis antigens inside the gut or its absorption on erythrocytes in patients with spondyloarthropathy.
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Salmina, Alla B., Yana V. Gorina, Alexander I. Erofeev, Pavel M. Balaban, Ilya B. Bezprozvanny, and Olga L. Vlasova. "Optogenetic and chemogenetic modulation of astroglial secretory phenotype." Reviews in the Neurosciences 32, no. 5 (February 8, 2021): 459–79. http://dx.doi.org/10.1515/revneuro-2020-0119.

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Abstract Astrocytes play a major role in brain function and alterations in astrocyte function that contribute to the pathogenesis of many brain disorders. The astrocytes are attractive cellular targets for neuroprotection and brain tissue regeneration. Development of novel approaches to monitor and to control astroglial function is of great importance for further progress in basic neurobiology and in clinical neurology, as well as psychiatry. Recently developed advanced optogenetic and chemogenetic techniques enable precise stimulation of astrocytes in vitro and in vivo, which can be achieved by the expression of light-sensitive channels and receptors, or by expression of receptors exclusively activated by designer drugs. Optogenetic stimulation of astrocytes leads to dramatic changes in intracellular calcium concentrations and causes the release of gliotransmitters. Optogenetic and chemogenetic protocols for astrocyte activation aid in extracting novel information regarding the function of brain’s neurovascular unit. This review summarizes current data obtained by this approach and discusses a potential mechanistic connection between astrocyte stimulation and changes in brain physiology.
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Tominaga-Yamanaka, Kumiko, Kotb Abdelmohsen, Jennifer L. Martindale, Xiaoling Yang, Dennis D. Taub, and Myriam Gorospe. "NF90 coordinately represses the senescence-associated secretory phenotype." Aging 4, no. 10 (October 31, 2012): 695–708. http://dx.doi.org/10.18632/aging.100497.

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Campisi, J. "Protumorigenic Effects of the Senescence-Associated Secretory Phenotype." AACR Education book 2008, no. 1 (April 12, 2008): 505–9. http://dx.doi.org/10.1158/aacr.edb-08-8139.

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Wang, Rong, Bharath Sunchu, and Viviana I. Perez. "Rapamycin and the inhibition of the secretory phenotype." Experimental Gerontology 94 (August 2017): 89–92. http://dx.doi.org/10.1016/j.exger.2017.01.026.

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Wildes, Tanya M., Jacob Paasch, Mark A. Fiala, Ling Chen, Ravi Vij, Keith E. Stockerl-Goldstein, Sheila Stewart, Graham A. Colditz, and Michael Tomasson. "The Senescence-Associated Secretory Phenotype In Multiple Myeloma." Blood 122, no. 21 (November 15, 2013): 5357. http://dx.doi.org/10.1182/blood.v122.21.5357.5357.

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Abstract Introduction The incidence of multiple myeloma (MM) increases with age, yet some cytogenetic changes are actually more common in younger patients with MM (Avet-Loiseau J Clin Oncol 2013). This suggests that a mechanism other than chromosomal changes underlies the increased incidence with age. Senescent cells secrete a number of proinflammatory cytokines, chemokines, growth factors and proteases resulting in the senescence-associated secretory phenotype (SASP), which can promote tumor growth. Preclinical data suggests that myeloma bone marrow stromal cells express the SASP (Andre PLOS ONE 2013). We hypothesized that SASP factors correlate with age in patients with MM. Methods Peripheral blood serum and matched bone marrow aspirate plasma from patients with multiple myeloma were evaluated for selected factors associated with the SASP using quantitative multiplex immunoassay (Rules Based Medicine, Austin TX USA). SASP factors with a known role in MM [interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-15 (IL-15), granulocyte-macrophage colony-stimulating factor (GMCSF), intercellular adhesion molecule 1(ICAM1), osteoprotegerin (OPG), hepatocyte growth factor (HGF), insulin-like growth factor-binding protein(IGFBP-1), interleukin-1 beta (IL1b), monocyte chemotactic protein 1(MCP-1), macrophage inflammatory protein-1 alpha(MIP-1a), angiogenin, leptin, vascular endothelial growth factor receptor 1(VEGFR1) and stem cell factor(SCF)] were selected. The relationship between age and SASP factors were analyzed using Kendall tau rank correlation coefficient. Results Samples from 25 patients (each with peripheral blood serum and matched bone marrow aspirate plasma) were analyzed. The median age was 62 (range 47 - 74). Disease states were as follows: 36% newly diagnosed/untreated, 24% pretransplant and 40% relapsed. ISS stage included 40% stage I, 28% stage II and 32% stage III. Three of the selected SASP factors in the peripheral blood correlated with age: IL-8 (Kendall Tau 0.334, p=0.027), OPG (Kendall Tau 0.289, p=0.046) and MCP-1 (Kendall Tau 0.332, p=0.022). No SASP factors tested in the bone marrow plasma were significantly correlated with age. Conclusions We demonstrated age-associated differences in the SASP factors IL-8, OPG and MCP-1 in the peripheral blood of myeloma patients. Future research will examine differences between patients with myeloma and age-matched controls without cancer. Disclosures: Vij: Celgene : Honoraria, Research Funding, Speakers Bureau; Millennium: Honoraria, Speakers Bureau; Onyx: Honoraria, Research Funding, Speakers Bureau. Stockerl-Goldstein:Celgene : Speakers Bureau; Celgene : Speakers Bureau; Millennium: Speakers Bureau; Millennium: Speakers Bureau.
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Dissertations / Theses on the topic "Secretory phenotype"

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Roeske, Cassandra. "Role of the Heterotrimeric Go Protein Alpha-subunit on the Cardiac Secretory Phenotype." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24191.

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Atrial natriuretic factor (ANF) is a polypeptide hormone produced in heart atria, stored in atrial secretory granules and released into the circulation in response to various stimuli. Proper sorting of ANF at the level of the trans-Golgi network (TGN) is required for the storage of ANF in these specific granules, and this sorting of hormones has been found to be associated with G-proteins. Specifically, the Go protein alpha-subunit (Gαo) was established to participate in the stretch-secretion coupling of ANF, but may also be involved in the transporting of ANF from the TGN into atrial granules for storage and maturation. Based on knowledge of Gαo involvement in hormone production in other endocrine tissues, protein-protein interactions of Gαo and proANF and their immunochemical co-localization in granules, the direct involvement of these two proteins in atrial granule biogenesis is probable. In this study, mice were created using the Cre/lox recombination system with a conditional Gαo knockout in cardiocytes to study and characterize ANF production, secretion and granule formation. Deletion of this gene was successful following standard breeding protocols. Characterization and validation of cellular and molecular content of the knockout mice through mRNA levels, protein expression, peptide content, electron microscopy, and electrocardiography determined that a significant phenotypic difference was observed in the abundance of atrial granules. However, Gαo knockout mice did not significantly alter the production and secretion of ANF and only partially prevented granule biogenesis, likely due to incomplete Gαo knockout. These studies demonstrate an involvement of Gαo in specific atrial granule formation.
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Benyamini, Payam. "The mammalian ribosome receptor, p180, mediates RER membrane biogenesis and establishment of a secretory phenotype." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1324373401&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Kabir, T. D. "Micromanaging fibroblast senescence : the role of small non-coding RNAs in senescence associated secretory phenotype (SASP)." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9141/.

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Introduction: The molecular pathways that dictate the acquisition of senescence-associated secretory phenotype (SASP) by stromal fibroblast during ageing or in response to genotoxic insult have yet to be elucidated. In this thesis the ability of cisplatin-induced SASP of oral fibroblasts to stimulate pro-tumourigenic stromal tumour cross-talk in oral cancer has been studied. Moreover the miRNA expression profile associated with development of SASP in stress-induced premature senescent oral fibroblasts and senescent-CAFs of genetically unstable oral squamous cell carcinoma (GU OSCC) had been thoroughly investigated. Materials and methods: Oral fibroblasts were treated with sub-cyotoxic doses of H2O2 and cisplatin or allowed to undergo replicative exhaustion to induce senescence. Senescence was confirmed by measurement of SA-β-gal activity, cyclin dependent kinase inhibitors (CDKI): p21 and p16, and secreted cytokines and MMP-2 by human cytokine array, ELISA and zymography. MiRNA expression profile was determined by TaqMan miRNA TLDA and candidate miRNAs were validated by qRT-PCR. Transfection was used to study the functional effects of candidate miRNAs. Paracrine effects were assessed by proliferation, migration and invasion assays. pmiR-Reporter vector was used to identify novel functional gene target of miRNAs. Results: Senescent oral fibroblasts showed increased SA-β-Gal activity and higher levels of p21 and p16. They secreted more MMP-2, IL-6, MCP-1, Endothelin-1, PGE2. Inhibiting COX-2 activity and blockade of secreted MCP-1 diminished the stimulatory effect of senescent fibroblasts on oral cancer cells. Both senescent-normal oral fibroblasts and senescent-CAFs demonstrated differential expression of miRNAs. miR-335 and miR-148b were significantly elevated in senescent fibroblasts and was found to target PTEN. A COX-2 mediated inflammatory loop was identified in senescent oral fibroblasts that could be rescued by celecoxib treatment (selective COX-2 inhibitor) via up-regulation of PTEN. Conclusion: In this thesis a SASP-associated miRNA signature had been identified in oral fibroblasts, which may provide insight into the molecular pathways associated with chemotherapy resistance and cancer recurrences in elderly patients.
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Gonzalez, Meljem J. M. "The role of cytokine signalling, cellular senescence and its secretory phenotype in normal pituitary development and tumourigenesis." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1546237/.

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Oncogene-induced senescence (OIS) is classically described as a potent antitumourigenic barrier that restrains the proliferation of pre-malignant cells. Senescent cells can also promote immune clearance by secreting a plethora of chemokines and inflammatory factors, collectively known as the Senescence-Associated Secretory Phenotype (SASP). However, the SASP can also promote tumourigenesis paracrinally. In this study, OIS and the SASP were studied in mouse models for adamantinomatous craniopharyngioma (ACP), which express oncogenic β-catenin in pituitary progenitors/stem cells. Surprisingly, oncogenic β-catenin-targeted cells did not give rise to the tumour mass in the majority of cases and stopped dividing after a short burst of proliferation to form β-catenin-accumulating cell clusters. Here it is demonstrated that β-catenin clusters undergo OIS as determined by a lack of proliferation markers, activation of the p53/p21 and p16/Rb pathways, induction of the DNA damage response (DDR) and activation of the NF-κB pathway. Additionally, unbiased mRNA expression analysis shows enrichment of OIS and SASP genes in β-catenin clusters, while SASP gene expression is corroborated by qRT-PCR and ELISA assays. Of translational significance, these results are recapitulated in the β- catenin clusters of human ACP. Furthermore, evidence is presented indicating that the paracrine signals secreted by the β-catenin clusters are involved in non-cell autonomous tumourigenesis through modification of their microenvironment and the recruitment of endothelial progenitors displaying aberrant SOX9 expression. A genetic strategy demonstrated that induction of OIS and the SASP in the clusters is p53-independent, but that p53 is required to prevent a full bias for cell-autonomous tumourigenesis. Finally, a mouse line that also develops β-catenin clusters, albeit with a dampened SASP is described. These clusters do not appear to modify their microenvironment and tumours do not develop. Together, the mouse and human data suggest that senescence and SASP are likely to modify the tumour microenvironment resulting in cell transformation, tumour growth and survival.
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Buhl, Juliane [Verfasser], and Peter [Akademischer Betreuer] Angel. "The senescence-associated secretory phenotype regulates the growth behavior of pediatric pilocytic astrocytoma / Juliane Buhl ; Betreuer: Peter Angel." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1191760510/34.

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Hari, Priya. "Identification and study of a role for toll-like receptors in oncogene-induced senescence." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31443.

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Oncogene-induced senescence (OIS) is a fail-safe mechanism activated to halt the proliferation of cells at risk of malignant transformation. It is a cell cycle arrest program of biological changes to the cell comprising of the activation of tumour suppressor pathways, altered cellular metabolism, extensive chromatin remodelling and the activation of a senescence-associated secretory phenotype (SASP). The vast array of proteins secreted by the cells not only play a cell-autonomous role in reinforcing the senescence phenotype, but also modulate the cell's micro-environment by inducing senescence in neighbouring cells, promoting angiogenesis, and initiating an immune response through the recruitment of immune cells. To this end, senescence is a complex phenotype that has countless pathophysiological implications and understanding its molecular mechanisms of activation could prove to be fruitful for understanding its diverse functions. Components of the innate immune system have been shown to play an essential role in the development of the SASP through its processing and activation of Caspase 1 that in turn leads to activation of IL-1B. A gene set enrichment analysis of OIS cells showed significant upregulation in the Pattern Recognition Receptor (PRR) family, from the innate immune response. Hence, we explored the role of innate immune receptors in OIS. Methods and Materials IMR90 human diploid fibroblast cells, stably transfected with an oncogenic ER:RAS fusion protein undergo OIS upon treatment with 4-hydroxytamoxifen. A loss of function siRNA screen was conducted targeting components of the innate immune systems, including pattern recognition receptors. This served as a proof-of-principle screen for a larger screen of proteases and ubiquitin conjugation enzymes. Potential regulators of OIS were identified through siRNA that bypassed the proliferative arrest associated with OIS. We chose to focus on studying the role of TLR2 and TLR10 in senescence. A transcriptome analysis was carried out to identify genes regulated by these TLRs and further biological manipulation was used to confirm the mechanism through which these receptors control senescence. Results Toll-like receptor 2 (TLR2) and TLR10 have been identified as regulators of OIS. Their overexpression in IMR90 cells induces a premature form of senescence where the cells have significantly reduced proliferative activity and display senescence-associated β galactosidase activity. Moreover, the knockdown of TLR2 and TLR10 results in suppression of tumour suppressor pathway genes, reduced signaling through the pathway and blunting of the SASP. High TLR2 expression in patients with lung adenocarcinoma is associated with a higher survival rate. Concomitantly, the screening also identified Caspase 4, a critical component of non-canonical inflammasome signaling, to be regulated by TLR2 and TLR10 in OIS. A full transcriptome analysis of cells with TLR2 and TLR10 knockdown revealed serum amyloid amylase 1 (SAA1) and SAA2 are upregulated in OIS and were also confirmed to be activating ligands of TLR2. The activation of TLR2 by SAA, followed by the engagement of the non-canonical inflammasome by LPS electroporation induced senescence in proliferating IMR90 cells. Conclusion Our results suggest that the TLR2 and TLR10 act as potential tumour suppressor genes, signaling upstream of the inflammasome to initiate the production of inflammatory cytokines, and thereby the SASP. The production of the SASP develops a positive feedback loop, generating the damage-associated molecular pattern (DAMP) A-SAA that initiates an immune response signal cascade and subsequently activates senescence.
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Pungsrinont, Thanakorn [Verfasser], Aria [Gutachter] Baniahmad, Jörg [Gutachter] Müller, and Marcus V. [Gutachter] Cronauer. "Analysis of senescence-associated secretory phenotype induced by different androgen receptor ligands in human prostate cancer cells / Thanakorn Pungsrinont ; Gutachter: Aria Baniahmad, Jörg Müller, Marcus V. Cronauer." Jena : Friedrich-Schiller-Universität Jena, 2021. http://d-nb.info/1238141684/34.

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Perry, Elizabeth Holly. "Association of ABO, Lewis and Secretor phenotypes and genotypes with Neisseria gonorrhoeae thesis submitted in (partial) fulfilment of the Master of Applied Science, Auckland University of Technology, November 2003." Full thesis. Abstract, 2003. http://puka2.aut.ac.nz/ait/theses/PerryE.pdf.

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Vannier, Daphné. "Découverte d'une sénescence associée à un phénotype sécrétoire déclenchée par les défauts mécaniques de la cellule endothéliale lors de la perte de CCM2 dans un modèle de cavernome cérébral." Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV012.pdf.

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Les lésions CCM (Cerebral Cavernous Malformations) sont formées d’un empilement de vaisseaux capillaires tortueux, dilatés et hémorragiques situés dans le cerveau. Ces capillaires cérébraux sont dépourvus de cellules murales et sont formés d’une monocouche de cellules endothéliales (CE) peu jointives. La mutation perte de fonction de l’un des 3 gènes ccm (ccm1, ccm2 et ccm3) est suffisante pour induire la formation de lésions CCM chez l’Homme.Dans les différents modèles mutants ccm, les CE présentent une homéostasie tensionnelle défectueuse caractérisée par un défaut de coordination entre les forces d’adhésions cellule-matrice et cellule-cellule. Ceci se traduit par la formation de fibres contractiles d’actomyosine ancrées sur de nombreuses adhérences focales à intégrine B1 et par la perte des jonctions intercellulaires dépendantes de VE-cadhérine. L’association des protéines CCM1-3 forme une plateforme moléculaire qui contrôle, en aval de RhoA, l’activité des kinases ROCK1 et ROCK2 sur l’organisation du cytosquelette d’acto-myosine. Le complexe CCM recrute ROCK2 aux jonctions dépendantes de VE-cadhérine pour promouvoir un réseau d’actine cortical stabilisateur de ces jonctions intercellulaires alors que dans le même temps, il inhibe l’activité de ROCK1 pour réduire la formation de fibres de stress ventrales et ainsi limiter l’adhésion de la CE à la matrice extracellulaire. Il est connu que le microenvironnement de la lésion est remodelé notamment par des cellules immunitaires qui s’infiltrent pour déclencher une réponse inflammatoire chronique et favoriser l’expansion de la lésion. Il est également connu que les CE mutantes sécrètent des métalloprotéases et des cytokines, qu’elles surproduisent des ROS et qu’elles subissent une transition endothélio-mésenchymateuse (endoMT). Enfin, les lésions CCM sont des mosaïques de CE mutantes et sauvages qui sont recrutées au cours du temps dans la lésion. Néanmoins, le lien qui existe entre tous ces phénomènes favorables à la progression de la lésion CCM est encore mal compris et reste à élucider.Les travaux que j’ai effectués au cours de cette thèse m’ont permis de proposer un modèle qui unifie l’ensemble de ces comportements cellulaires. En effet, j’ai mis en lumière le vieillissement prématuré des cellules endothéliales déplétées en CCM2. J’ai montré que cette sénescence est associée à un comportement sécrétoire SASP (Senescence Associated with a Secretory Phenotype) qui confère à la CE la capacité de remodeler activement son environnement notamment en le dégradant de manière localisée, de l’envahir et d’attirer par chimio-attraction des CE sauvages et des cellules immunitaires. Le second apport majeur de mon travail a été de montré que cette SASP est due aux dérèglements dans la mécanique de la CE. En effet, j’ai montré que l’augmentation de la contractilité intracellulaire, associée à un défaut de coordination entre les activités de ROCK1 et ROCK2, est responsable de cette SASP. L’inhibition de la myosine II ou la déplétion préférentielle de ROCK1 ou de ROCK2, restaure l’expression de la moitié des gènes dérégulés par la perte de CCM2, bloque l’apparition des marqueurs de sénescence ainsi que les capacités invasives et chimio-attractantes des CE déplétées pour CCM2. Ces résultats ouvrent la voie vers l’identification de nouvelles cibles thérapeutiques pour bloquer les mécanismes à l’origine de l’apparition et de l’expansion des lésions CCM
CCM (Cerebral Cavernous Malformations) lesions are formed by stacks of tortuous, dilated and hemorrhagic capillaries located in the brain. These brain capillaries are devoid of mural cells and are formed of a monolayer of weakly joined endothelial cells (EC). The loss of function mutation in one of the 3 ccm genes (ccm1, ccm2 and ccm3) is sufficient to induce the formation of CCM lesions in humans.In the different ccm mutant models, the ECs present defective tensional homeostasis characterized by a lack of coordination between the cell-matrix and cell-cell forces. This results in the formation of contractile actomyosin fibers anchored on numerous focal adhesions containing B1 integrin and in the loss of VE-cadherin-dependent intercellular junctions. The association of CCM1-3 proteins forms a molecular scaffold that controls downstream of RhoA the activity of ROCK1 and ROCK2 on the organization of the acto-myosin cytoskeleton. The CCM complex recruits ROCK2 at the VE-cadherin dependent junctions to promote a network of cortical actin stabilizing these intercellular junctions while at the same time, it inhibits the activity of ROCK1 to reduce the formation of ventral stress fibers and thus limit the adhesion of the EC to the extracellular matrix. It is known that the microenvironment in the lesion is reshaped in particular by immune cells that infiltrate it to trigger a chronic inflammatory response and promote the expansion of the lesion. It is also known that mutant ECs secrete metalloproteases and cytokines, that they overproduce ROS and that they undergo an endothelio-mesenchymal transition (endoMT). Finally, CCM lesions are mosaics of mutant and wild-type ECs recruited into the lesion over time. However, whether a link exists between all these phenomena conducive to the progression of the CCM lesion is not known and remains to be elucidated.My work during this PhD allowed me to propose a model that unifies all these cellular behaviors. Indeed, I have highlighted a premature aging of endothelial cells depleted in CCM2. I have shown that this senescence is associated with a secretory behavior SASP (Senescence Associated with a Secretory Phenotype) which gives the EC the ability to actively reshape its environment, in particular by degrading it locally, to invade it and attract by chemo-attraction wild EC and immune cells. The second major contribution of my work has been to show that this SASP is due to the dysregulation of the mechanics of the EC. Indeed, I have shown that the increase in intracellular contractility, associated with the loss of balance between the activities of ROCK1 and ROCK2, is responsible for this SASP. Inhibiting myosin II or depleting ROCK1 or ROCK2 restores the expression of half of the genes dysregulated by the loss of CCM2, blocks the appearance of senescence markers as well as the invasive and chemo-attractive capacities of CCM2-depleted ECs. These results open the way to the identification of new therapeutic targets responsible for the appearance and expansion of CCM lesions
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Halkoum, Rym. "Rôle du glyoxal dans la sénescence cellulaire : implications dans le vieillissement de la peau." Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS016.pdf.

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La sénescence est une réponse cellulaire associée à des marqueurs spécifiques comme un arrêt irréversible du cycle cellulaire ainsi que la sécrétion d’un ensemble de facteurs comme les cytokines, chimiokines et protéases, constituant le SASP, pour Senescence-Associated Secretory Phenotype. Le SASP peut avoir des rôles autocrine et paracrine qui contribuent au renforcement et à la propagation du phénotype sénescent. La composition du SASP et par conséquent son rôle, dépendent notamment du type cellulaire et de la nature du stress inducteur de sénescence. Du fait de sa fonction de barrière avec l’environnement externe, la peau est particulièrement soumise à différents types de stress induisant la sénescence des cellules et un vieillissement prématuré. Le glyoxal, composé dicarbonylé formé au cours des réactions de glycation, d’auto-oxydation du glucose ou de la peroxydation lipidique, est un précurseur des produits avancés de glycation impliqués dans le vieillissement normal et pathologique. Mes travaux de thèse ont permis de montrer que le glyoxal induit la sénescence de kératinocytes humains normaux ainsi qu’une accumulation d’espèces réactives de l’oxygène et de produits avancés de glycation intracellulaires traduisant un état de stress oxydant. L’initiation de cette sénescence est due à l’activation de la voie d’arrêt du cycle cellulaire AKT/FOXO3a/p27KIP1 suivie d’une phase tardive caractérisée par l’activation de la voie p16INK4A/pRb. La caractérisation du phénotype sécrétoire associé à la phase précoce de cette sénescence, a été réalisée par spectrométrie de masse afin d’identifier des facteurs pouvant être ciblés par des ingrédients sénomorphiques
Senescence is a well-characterized cellular state associated with specific markers such as permanent cell proliferation arrest, and the secretion of messenger molecules by cells expressing the Senescence-Associated Secretory Phenotype (SASP). The SASP can display autocrine and paracrine effects which contribute to the senescent phenotype reinforcement and propagation. The SASP composition depends on many factors such as the cell type or the nature of the stress that induces senescence. Since the skin constitutes a barrier with the external environment, it is particularly subjected to different types of stresses, and consequently prone to premature cellular aging. Glyoxal, a dicarbonyl compound produced during glucose metabolism and lipid peroxidation, is a precursor of Advanced Glycation End-products (AGEs), whose presence marks normal and pathological aging. My thesis work showed that glyoxal treatment provokes oxidative stress by increasing reactive oxygen species and AGEs levels and induce senescence in human keratinocytes. Furthermore, glyoxal-induced senescence bears a unique molecular progression profile: an “early-stage” when AKT-FOXO3a-p27KIP1 pathway mediates cell-cycle arrest, and a “late-stage” senescence maintained by the p16INK4/pRb pathway. Moreover, we characterized the resulting secretory phenotype during early senescence by mass spectrometry in order to find new targets for senomorphic ingredients. Our study provides evidence that glyoxal can affect keratinocyte functions and act as a driver of human skin aging
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Book chapters on the topic "Secretory phenotype"

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Rodier, Francis. "Detection of the Senescence-Associated Secretory Phenotype (SASP)." In Methods in Molecular Biology, 165–73. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-239-1_10.

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Malaquin, Nicolas, Véronique Tu, and Francis Rodier. "Assessing Functional Roles of the Senescence-Associated Secretory Phenotype (SASP)." In Methods in Molecular Biology, 45–55. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8931-7_6.

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Velarde, Michael C., Marco Demaria, and Judith Campisi. "Senescent Cells and Their Secretory Phenotype as Targets for Cancer Therapy." In Cancer and Aging, 17–27. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000343572.

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Hari, Priya, and Juan Carlos Acosta. "Detecting the Senescence-Associated Secretory Phenotype (SASP) by High Content Microscopy Analysis." In Methods in Molecular Biology, 99–109. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_9.

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Frasca, Daniela. "The Senescence-Associated Secretory Phenotype: Induction, Regulation, Function and Therapeutic Interventions to Counteract the Negative Effects." In Cellular and Molecular Aspects of Ageing, 123–38. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-55022-5_9.

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Gerst, J. E. "SNC1 and SNC2." In Secretory Pathway, 172. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0107.

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Abstract SNC1 was isolated as a multicopy suppressor of the CAP null phenotype in yeast possessing an activated allele of RAS26The CAP gene in 5. cerevisiae encodes a 526-residue protein that co-purifies with a RAS-responsive adenylyl cyclase complex and is required for full cellular responsiveness to activated RAS proteins7,8. Deletion analysis of CAP has shown that the CAP protein is bifunctional: 168 amino acids at the N-terminus are required for the penetrance of phenotypes associated with activated RAS (e.g., heatshock sensitivity)8, while 160 amino acids at the (-terminal are required for suppression of growth and morphology defects not associated with the RAS pathway8
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Bankaitis, V. "SEC14." In Secretory Pathway, 156–57. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0095.

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Abstract Mutants harboring conditional-lethal mutations were isolated using a Ludox density enrichment method and found to exhibit a terminal phenotype of exaggerating intracellular toroid structures interpreted to represent dysfunctional yeast Golgi9 Indeed, within 15 min of shift to a restrictive temperature, sec14rs mutants display a secretory block and accumulate fully-glycosylated secretory proteins within the ce11.
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Marcusson, D., B. Horazdovsky,, and S. D. Emr. "VPS10." In Secretory Pathway, 234. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0137.

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Abstract vps10 mutant cells grow at wild-type rates1 and exhibit normal vacuolar morphology3A, but exhibit a differential vacuolar protein sorting phenotype. Approximately 95% of the CPY is secreted from the cell as its Golgi modified p2 precursor form while the majority of proteinase A, proteinase B, and alkaline phophatase are matured normally5, presumably reflecting delivery to the vacuole.
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Segev, N. "YPT1." In Secretory Pathway, 121–23. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0074.

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Abstract Analysis of the phenotype of several ypt1 mutants indicates that the Ypt1 protein plays an essential role in the secretory pathway3. First, null mutations, generated by gene disruption techniques, reveal that the YPT1 gene is essential for vegetative growth in yeast45. Second, analysis of conditional-lethal mutations suggests that the Ypt1 protein is involved in an early step of protein transport.
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és, F. K. ép. "SEC53." In Secretory Pathway, 52. Oxford University PressOxford, 1994. http://dx.doi.org/10.1093/oso/9780198599425.003.0033.

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Abstract Temperature-sensitive, conditionally-lethal sec53 mutants were selected on the basis of accumulation of inactive precursors of secreted proteins2. Temperature-sensitive a/g4 mutants were selected by their survival after a prolonged exposure to tritiated mannose. Cells that efficiently incorporated the labeled sugar were killed by self-irradiation. The best characterized sec53 allele, sec53-6, shows the strongest phenotype. At restrictive temperature, sec53-6, like alg4-9, accumulate inactive and incompletely glycosylated forms of secretory proteins within the lumen of the ER.
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Conference papers on the topic "Secretory phenotype"

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Schlegel, Julian, Sophie Domhan, Jürgen Debus, and Amir Abdollahi. "Abstract B63: Differences between replicative senescence- versus radiation- associated secretory phenotype." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b63.

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Singer, C. A., M. A. Ba, and J. Evasovic. "miR-106b∼25 Promotes a Secretory Airway Smooth Muscle Phenotype in Asthma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4412.

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Schaum, Nicholas, Christopher Wiley, Fatouma Almirah, Jose A. Lopez-Dominguez, Gary Scott, Christopher Benz, Judith Campisi, and Albert R. Davalos. "Abstract 4864: Small-molecule MDM2 antagonists attenuate the senescence-associated secretory phenotype." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4864.

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Santos, B., L. Gaspar, C. Carvalhas-Almeida, A. T. Barros-Viegas, S. Carmo-Silva, C. Santos, S. Carvalho, et al. "Unraveling the impact of obstructive sleep apnea on senescent associate secretory phenotype." In Sleep and Breathing 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.sleepandbreathing-2021.82.

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Patel, Rupesh S., Rodrigo Romero, Anthony C. Liang, Emma V. Watson, Megan Burger, Peter M. K. Westcott, Kim L. Mercer, et al. "Abstract IA17: The role of the senescence-associated secretory phenotype in cancer." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-ia17.

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Hohloch, J., F. Selt, T. Hielscher, F. Sahm, D. Capper, D. Usta, J. Ecker, et al. "Oncogene-induced senescence and the senescence-associated secretory phenotype in pilocytic astrocytoma." In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602221.

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Zhang, Jing, Lian Wu, Chunxue Bai, Mervyn J. Merrilees, and Peter N. Black. "Pulmonary Fibroblasts From Patients With COPD Have A Senescence-associated Secretory Phenotype." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4924.

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Woldhuis, R. R., I. H. Heijink, M. Van Den Berge, W. Timens, B. Oliver, M. De Vries, and C. Brandsma. "COPD-derived fibroblasts secrete higher levels of senescence associated secretory phenotype (SASP) proteins." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.28.

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Hassibi, Shyreen, Jonathan Baker, Louise Donnelly, and Peter Barnes. "The RNA binding protein HuR regulates the senescence-associated secretory phenotype under conditions of oxidative stress." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2374.

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Kenny, Sarah, Ziling Huang, Kiwhan Kim, Allyson Capili, Susan Carpenter, Diane Ward, and Suzanne Cloonan. "Mitochondrial iron regulates AEC2 dysfunction, senescence and senescent associated secretory phenotype in response to bleomycin challenge." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.222.

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