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Journal articles on the topic 'Secretory phenotype'

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Author: Grafiati

Published: 25 May 2024

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1

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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2

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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Hou, Jingang, Changhao Cui, Sunchang Kim, Changkeun Sung, and Chulhee Choi. "Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype." Chemico-Biological Interactions 283 (March 2018): 75–83. http://dx.doi.org/10.1016/j.cbi.2018.02.002.

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Lopes-Paciencia, Stéphane, Emmanuelle Saint-Germain, Marie-Camille Rowell, Ana Fernández Ruiz, Paloma Kalegari, and Gerardo Ferbeyre. "The senescence-associated secretory phenotype and its regulation." Cytokine 117 (May 2019): 15–22. http://dx.doi.org/10.1016/j.cyto.2019.01.013.

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Stödberg, Tommy, Måns Magnusson, Nicole Lesko, Anna Wredenberg, Daniel Martin Munoz, Henrik Stranneheim, and Anna Wedell. "SLC12A2 mutations cause NKCC1 deficiency with encephalopathy and impaired secretory epithelia." Neurology Genetics 6, no. 4 (July 2, 2020): e478. http://dx.doi.org/10.1212/nxg.0000000000000478.

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ObjectiveTo describe the phenotype in 2 sisters with a rare constellation of neurologic symptoms and secretory impairments and to identify the etiology by the use of whole-genome sequencing (WGS).MethodsAfter an extensive workup failed to reveal the cause of disease, in a girl with a previously not reported phenotype, WGS of the proband, her diseased older sister, an older healthy brother, and their parents was performed, and potentially pathogenic variants were analyzed.ResultsThe proband and her older sister both presented with neonatal Staphylococcus aureus parotitis, apneas, disappearance of the Moro reflex, and hypotonia. The proband survived. Her brain MRI showed white matter and basal ganglia abnormalities, and CSF damage biomarkers were increased. At age 8 years, she exhibits a constellation of symptoms including severe neurodevelopmental disorder, hearing impairment, gastrointestinal problems, and a striking lack of tear fluid, saliva, and sweat. Her respiratory mucosa is dry with potentially life-threatening mucus plugging. Through WGS, 2 loss-of-function variants in SLC12A2 were identified that follow an autosomal recessive inheritance pattern.ConclusionsTaken together with a single previously reported case and the close resemblance to the phenotypes of corresponding mouse models, our study firmly establishes biallelic variants in SLC12A2 as causing human disease and adds data regarding the neurologic phenotype.

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Malaquin, Nicolas, Aurélie Martinez, and Francis Rodier. "Keeping the senescence secretome under control: Molecular reins on the senescence-associated secretory phenotype." Experimental Gerontology 82 (September 2016): 39–49. http://dx.doi.org/10.1016/j.exger.2016.05.010.

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Peinado, J. R., R. Vazquez-Martinez, D. Cruz-García, A. Ruiz-Navarro, Y. Anouar, M. C. Tonon, H. Vaudry, F. Gracia-Navarro, J. P. Castano, and M. M. Malagón. "Differential Expression and Processing of Chromogranin A and Secretogranin II in Relation to the Secretory Status of Endocrine Cells." Endocrinology 147, no. 3 (March 1, 2006): 1408–18. http://dx.doi.org/10.1210/en.2005-0975.

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Chromogranin A (CgA) and secretogranin II (SgII) are neuroendocrine secretory proteins that participate in regulation of the secretory pathway and also serve as precursors of biologically active peptides. To investigate whether there is a relationship between the expression, distribution, and processing of CgA and SgII and the degree of secretory activity, we employed two melanotrope subpopulations of the pituitary intermediate lobe that exhibit opposite secretory phenotypes. Thus, although one of the melanotrope subtypes shows high secretory activity, the other exhibits characteristics of a hormone storage phenotype. Our data show that SgII expression levels were higher in secretory melanotropes, whereas CgA expression showed similar rates in both cell subsets. The use of various antibodies revealed the presence of the unprocessed proteins as well as three CgA-derived peptides (67, 45, and 30 kDa) and six SgII-derived peptides (81, 66, 55, 37, 32, and 30 kDa) in both subpopulations. However, the smallest molecular forms of both granins predominated in secretory melanotropes, whereas the largest SgII- and CgA-immunoreactive peptides were more abundant in storage melanotropes, which is suggestive of a more extensive processing of granins in the secretory subset. Confocal microscopy studies showed that CgA immunoreactivity was higher in storage cells, but SgII immunoreactivity was higher in secretory melanotropes. Taken together, our results indicate that SgII and CgA are differentially regulated in melanotrope subpopulations. Thus, SgII expression is strongly related to the secretory activity of melanotrope cells, whereas CgA expression may not be related to secretory rate, but, rather, to hormone storage in this endocrine cell type.

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Buj, Raquel, Kelly E. Leon, Marlyn A. Anguelov, and Katherine M. Aird. "Suppression of p16 alleviates the senescence-associated secretory phenotype." Aging 13, no. 3 (February 6, 2021): 3290–312. http://dx.doi.org/10.18632/aging.202640.

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Melino, Michelle. "Macrophage secretory products induce an inflammatory phenotype in hepatocytes." World Journal of Gastroenterology 18, no. 15 (2012): 1732. http://dx.doi.org/10.3748/wjg.v18.i15.1732.

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Tchkonia, Tamara, Yi Zhu, Jan van Deursen, Judith Campisi, and James L. Kirkland. "Cellular senescence and the senescent secretory phenotype: therapeutic opportunities." Journal of Clinical Investigation 123, no. 3 (March 1, 2013): 966–72. http://dx.doi.org/10.1172/jci64098.

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Pathipati, Praneeti, Sebastian Müller, Xiangning Jiang, and Donna Ferriero. "Phenotype and Secretory Responses to Oxidative Stress in Microglia." Developmental Neuroscience 35, no. 2-3 (2013): 241–54. http://dx.doi.org/10.1159/000346159.

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Capell, Brian C., Adam M. Drake, Jiajun Zhu, Parisha P. Shah, Zhixun Dou, Jean Dorsey, Daniel F. Simola, et al. "MLL1 is essential for the senescence-associated secretory phenotype." Genes & Development 30, no. 3 (February 1, 2016): 321–36. http://dx.doi.org/10.1101/gad.271882.115.

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McCarthy, Donald a., James McNeilan, Nicole L. Flaherty, and J. Andres Melendez. "Targeted Antioxidant Delivery Suppresses the Senescence Associated Secretory Phenotype." Free Radical Biology and Medicine 65 (November 2013): S129. http://dx.doi.org/10.1016/j.freeradbiomed.2013.10.718.

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Doubleday, Peter F., Luca Fornelli, and Neil L. Kelleher. "Elucidating Proteoform Dynamics Underlying the Senescence Associated Secretory Phenotype." Journal of Proteome Research 19, no. 2 (January 15, 2020): 938–48. http://dx.doi.org/10.1021/acs.jproteome.9b00739.

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Behnia, Fara, Brandie Taylor, Eryn Dutta, George Saade, and Ramkumar Menon. "579: Senescence associated secretory phenotype: a signal for parturition?" American Journal of Obstetrics and Gynecology 212, no. 1 (January 2015): S289. http://dx.doi.org/10.1016/j.ajog.2014.10.785.

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Wiley, Christopher D., Michael C. Velarde, Pacome Lecot, Su Liu, Ethan A. Sarnoski, Adam Freund, Kotaro Shirakawa, et al. "Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype." Cell Metabolism 23, no. 2 (February 2016): 303–14. http://dx.doi.org/10.1016/j.cmet.2015.11.011.

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Vital, Paz, Patricia Castro, Susan Tsang, and Michael Ittmann. "The Senescence-Associated Secretory Phenotype Promotes Benign Prostatic Hyperplasia." American Journal of Pathology 184, no. 3 (March 2014): 721–31. http://dx.doi.org/10.1016/j.ajpath.2013.11.015.

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Langhi Prata, Larissa G. P., Tamar Tchkonia, and James L. Kirkland. "Cell senescence, the senescence-associated secretory phenotype, and cancers." PLOS Biology 21, no. 9 (September 21, 2023): e3002326. http://dx.doi.org/10.1371/journal.pbio.3002326.

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Chopra, D. P., J. K. Sullivan, and S. Reece-Kooyer. "Regulation by calcium of proliferation and morphology of normal human tracheobronchial epithelial cell cultures." Journal of Cell Science 96, no. 3 (July 1, 1990): 509–17. http://dx.doi.org/10.1242/jcs.96.3.509.

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Human tracheobronchial epithelial cells have been serially passaged in serum-free medium. This serum-free model was employed to investigate the effects of different concentrations of Ca2+ (0.1, 1.0 and 2.0 mM) on multiplication and morphology of the cells. The responses were analysed in terms of growth kinetics, histochemical and ultrastructural alterations. Culturing of the cells in high Ca2+ (1.0-2.0 mM) medium stimulated cell multiplication characterized by increased colony forming efficiency, greater number of cells per colony and cell population doublings per day. Additionally, the high Ca2+ concentrations induced proliferation in cultures grown to confluency in low Ca2+ (0.1 mM) medium. Cells propagated in low Ca2+ medium consisted of relatively heterogeneous cell populations, with most cells staining positive with periodic acid-Schiff (PAS) reagent. Ultrastructurally the cells exhibited secretory vesicles and microvilli on their surfaces, small desmosomes and intercellular interdigitation between cells and numerous large secretory vesicles in the cytoplasm. The cells grown in high Ca2+ medium acquired characteristics of a highly proliferative phenotype. The cultures consisted of closely packed, relatively homogeneous cells that did not stain with PAS reagent. Their characteristic features were: absence of surface secretory vesicles, reductions of microvilli and intercellular interdigitations, and increases in size and number of desmosomal junctions. The results show that low Ca2+ in the culture medium inhibits cell multiplication and favors the secretory cell phenotype, while high Ca2+ levels stimulate cell multiplication and inhibit the secretory cell phenotype.

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Hernaez-Estrada, Beatriz, Lindsay Steele, and Kara Spiller. "756 Effects of Bioengineered Allogeneic Cellular Constructs on Macrophage Phenotype in the Context of Burns." Journal of Burn Care & Research 44, Supplement_2 (May 1, 2023): S162. http://dx.doi.org/10.1093/jbcr/irad045.231.

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Abstract Introduction The persistent inflammatory and stress responses generate in burn patients have a strong effect on the immune system. Macrophages that are activated in response to burn injuries polarize towards an immunosuppressive phenotype commonly known as M2b. Furthermore, due to sepsis, the chronic exposure to the pro-inflammatory environment also leads to an exhausted macrophage phenotype. Together these effects compromise macrophage behavior that influences the healing outcome. In clinical trials, bioengineered allogeneic cellular constructs (BACCs) have shown potential in promoting healing in patients with deep partial thickness burns. However, the mechanism(s) behind these successful effects are not totally understood yet. For this reason, the aim of this study is to investigate how the crosstalk with the BACC influence different burn-related macrophage phenotype. Methods Primary human macrophages (N=4 healthy donors) were co-cultured with the BACC or collagen controls. Macrophages were isolated over 6 days of co-culture and their RNA was extracted for gene expression analysis, and conditioned media was collected to analyze the secretion of proteins. To assess phenotype changes, we performed gene set analysis using single sample gene set enrichment. To investigate changes in the phenotype of macrophages relevant to burn wounds macrophages were polarized to the immune suppressive M2b phenotype or LPS-exhausted phenotypes before co-culturing them with the BACC. Undifferentiated macrophages (M0) were used as controls. Results Gene expression analysis revealed a shift in undifferentiated macrophage phenotype towards an M2 phenotype by day 3 and 6 in co-culture as demonstrated by an increase in the expression of multiple M2 genes, including MRC1 and CCL18. Secretory analysis revealed a decrease in the secretory of inflammatory proteins, like interleukin 6. Conclusions Collectively these results demonstrate that BACCs promote the transition of macrophage phenotype towards a pro-reparative M2 phenotype which may contribute to the construct’s pro-healing capabilities. Applicability of Research to Practice This study provides insight into the mechanism by which BACCs promote healing in the burn wound environment.

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Thyberg, Johan, Karin Blomgren, Joy Roy, Phan Kiet Tran, and Ulf Hedin. "Phenotypic Modulation of Smooth Muscle Cells after Arterial Injury Is Associated with Changes in the Distribution of Laminin and Fibronectin." Journal of Histochemistry & Cytochemistry 45, no. 6 (June 1997): 837–46. http://dx.doi.org/10.1177/002215549704500608.

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Earlier in vitro studies suggest opposing roles of laminin and fibronectin in regulation of differentiated properties of vascular smooth muscle cells. To find out if this may also be the case in vivo, we used immunoelectron microscopy to study the distribution of these proteins during formation of intimal thickening after arterial injury. In parallel, cell structure and content of smooth muscle α-actin was analyzed. The results indicate that the cells in the normal media are in a contractile phenotype with abundant α-actin filaments and an incomplete basement membrane. Within 1 week after endothelial denudation, most cells in the innermost layer of the media convert into a synthetic phenotype, as judged by loss of actin filaments, construction of a large secretory apparatus, and destruction of the basement membrane. Some of these cells migrate through fenestrae in the internal elastic lamina and invade a fibronectin-rich network deposited on its luminal surface. Within another few weeks a thick neointima forms, newly produced matrix components replace the strands of fibronectin, and a basement membrane reappears. Simultaneously, the cells resume a contractile phenotype, recognized by disappearance of secretory organelles and restoration of α-actin filaments. These findings support the notion that laminin and other basement membrane components promote the expression of a differentiated smooth muscle phenotype, whereas fibronectin stimulates the cells to adopt a proliferative and secretory phenotype.

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Lui-Roberts, Winnie W. Y., Francesco Ferraro, Thomas D. Nightingale, and Daniel F. Cutler. "Aftiphilin and γ-Synergin Are Required for Secretagogue Sensitivity of Weibel-Palade Bodies in Endothelial Cells." Molecular Biology of the Cell 19, no. 12 (December 2008): 5072–81. http://dx.doi.org/10.1091/mbc.e08-03-0301.

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Formation of secretory organelles requires the coupling of cargo selection to targeting into the correct exocytic pathway. Although the assembly of regulated secretory granules is driven in part by selective aggregation and retention of content, we recently reported that adaptor protein-1 (AP-1) recruitment of clathrin is essential to the initial formation of Weibel-Palade bodies (WPBs) at the trans-Golgi network. A selective co-aggregation process might include recruitment of components required for targeting to the regulated secretory pathway. However, we find that acquisition of the regulated secretory phenotype by WPBs in endothelial cells is coupled to but can be separated from formation of the distinctive granule core by ablation of the AP-1 effectors aftiphilin and γ-synergin. Their depletion by small interfering RNA leads to WPBs that fail to respond to secretagogue and release their content in an unregulated manner. We find that these non-responsive WPBs have density, markers of maturation, and highly multimerized von Willebrand factor similar to those of wild-type granules. Thus, by also recruiting aftiphilin/γ-synergin in addition to clathrin, AP-1 coordinates formation of WPBs with their acquisition of a regulated secretory phenotype.

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Dessì, Angelica, Despina Briana, Sara Corbu, Stavroula Gavrili, Flaminia Cesare Marincola, Sofia Georgantzi, Roberta Pintus, Vassilios Fanos, and Ariadne Malamitsi-Puchner. "Metabolomics of Breast Milk: The Importance of Phenotypes." Metabolites 8, no. 4 (November 20, 2018): 79. http://dx.doi.org/10.3390/metabo8040079.

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Breast milk is the gold standard of nutrition for newborns. Its composition is tailored to the nutritional needs of the infant and varies between mothers. In recent years, several bioactive molecules have been discovered in addition to the main nutrients, such as multipotent stem cells, hormones, immunoglobulins, and bacteria. Furthermore, the human milk oligosaccharides (HMOs) seem to exert several important protective biological functions. According to the HMOs’ composition, breast milk can be classified as a secretory or non-secretory phenotype. In our study, we investigated the metabolome of milk collected from 58 mothers that delivered neonates at term, that were appropriate, small or large for gestational age, by performing nuclear magnetic resonance spectroscopy (1H-NMR). From the data analysis, two groups were distinguished based on their different types of oligosaccharides, and classified according the mother phenotype: secretory and non-secretory. This information is of major importance given the different biological function of the different HMOs, such as immune-modulation and protection against disease. This would allow us to predict whether the neonate would be, for instance, more prone to developing certain diseases, and to tailor her or his nutrition to fit their needs perfectly and pave the way to a personalized nutrition.

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Ramírez, Rafael, Noemi Ceprian, Andrea Figuer, Gemma Valera, Guillermo Bodega, Matilde Alique, and Julia Carracedo. "Endothelial Senescence and the Chronic Vascular Diseases: Challenges and Therapeutic Opportunities in Atherosclerosis." Journal of Personalized Medicine 12, no. 2 (February 4, 2022): 215. http://dx.doi.org/10.3390/jpm12020215.

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Atherosclerosis is probably one of the paradigms of disease linked to aging. Underlying the physiopathology of atherosclerosis are cellular senescence, oxidative stress, and inflammation. These factors are increased in the elderly and from chronic disease patients. Elevated levels of oxidative stress affect cellular function and metabolism, inducing senescence. This senescence modifies the cell phenotype into a senescent secretory phenotype. This phenotype activates immune cells, leading to chronic systemic inflammation. Moreover, due to their secretory phenotype, senescence cells present an increased release of highlighted extracellular vesicles that will change nearby/neighborhood cells and paracrine signaling. For this reason, searching for specific senescent cell biomarkers and therapies against the development/killing of senescent cells has become relevant. Recently, senomorphic and senolityc drugs have become relevant in slowing down or eliminating senescence cells. However, even though they have shown promising results in experimental studies, their clinical use is still yet to be determined.

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Li, Zhenwei, Yinzi Wu, Guannan He, Renzhi Wang, and Xinjie Bao. "Phenotype Transformation of PitNETs." Cancers 16, no. 9 (April 29, 2024): 1731. http://dx.doi.org/10.3390/cancers16091731.

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Phenotype transformation in pituitary neuroendocrine tumors is a little-known and unpredictable clinical phenomenon. Previous studies have not clearly defined and systematically concluded on the causes of this rare phenomenon. Additionally, the mechanisms of phenotype transformation are not well known. We reviewed cases reported in the literature with the aim of defining phenotype transformation in pituitary neuroendocrine tumors. We present an overview of the wide spectrum of phenotype transformation and its clinical features. We also discuss findings on the potential mechanism of this rare transformation, which may be related to PC1/3, the bioactivity of secretory hormones, gene mutations and the plasticity of pituitary neuroendocrine tumors. Clinicians should be aware of this rare phenomenon and more studies on the underlying mechanisms are required.

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Benyamini, Payam, Paul Webster, and David I. Meyer. "Knockdown of p180 Eliminates the Terminal Differentiation of a Secretory Cell Line." Molecular Biology of the Cell 20, no. 2 (January 15, 2009): 732–44. http://dx.doi.org/10.1091/mbc.e08-07-0682.

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We have previously reported that the expression in yeast of an integral membrane protein (p180) of the endoplasmic reticulum (ER), isolated for its ability to mediate ribosome binding, is capable of inducing new membrane biogenesis and an increase in secretory capacity. To demonstrate that p180 is necessary and sufficient for terminal differentiation and acquisition of a secretory phenotype in mammalian cells, we studied the differentiation of a secretory cell line where p180 levels had been significantly reduced using RNAi technology and by transiently expressing p180 in nonsecretory cells. A human monocytic (THP-1) cell line, that can acquire macrophage-like properties, failed to proliferate rough ER when p180 levels were lowered. The Golgi compartment and the secretion of apolipoprotein E (Apo E) were dramatically affected in cells expressing reduced p180 levels. On the other hand, expression of p180 in a human embryonic kidney nonsecretory cell line (HEK293) showed a significant increase in proliferation of rough ER membranes and Golgi complexes. The results obtained from knockdown and overexpression experiments demonstrate that p180 is both necessary and sufficient to induce a secretory phenotype in mammalian cells. These findings support a central role for p180 in the terminal differentiation of secretory cells and tissues.

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Xi, Chenxiang, Jiatong Sun, Xiaocui Xu, You Wu, Xiaochen Kou, Yanhong Zhao, Jiacheng Shen, et al. "Mettl14-driven senescence-associated secretory phenotype facilitates somatic cell reprogramming." Stem Cell Reports 17, no. 8 (August 2022): 1799–809. http://dx.doi.org/10.1016/j.stemcr.2022.06.012.

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Wang, Wen-Juan, Guang-Yan Cai, and Xiang-Mei Chen. "Cellular senescence, senescence-associated secretory phenotype, and chronic kidney disease." Oncotarget 8, no. 38 (April 21, 2017): 64520–33. http://dx.doi.org/10.18632/oncotarget.17327.

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Guerrero, Ana, and Jesús Gil. "HMGB2 holds the key to the senescence-associated secretory phenotype." Journal of Cell Biology 215, no. 3 (October 31, 2016): 297–99. http://dx.doi.org/10.1083/jcb.201610044.

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The senescence-associated secretory phenotype (SASP) is a hallmark of senescence with an important physiological impact, but how it is established is unclear. In this issue, Aird et al. (2016. J. Cell Biol. https://doi.org/10.1083/jcb.201608026) describe how chromatin-bound HMGB2 fine tunes SASP expression by avoiding heterochromatin spreading.

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38

Di Marco Vieira, Bruno, Rowan A. W. Radford, Junna Hayashi, Emma D. Eaton, Ben Greenaway, Mark Jambas, Eugen B. Petcu, Roger S. Chung, and Dean L. Pountney. "Extracellular Alpha-Synuclein Promotes a Neuroinhibitory Secretory Phenotype in Astrocytes." Life 10, no. 9 (September 8, 2020): 183. http://dx.doi.org/10.3390/life10090183.

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Multiple system atrophy (MSA) and dementia with Lewy bodies (DLB) are α-synucleinopathies that exhibit widespread astrogliosis as a component of the neuroinflammatory response. Munc18, a protein critical to vesicle exocytosis, was previously found to strongly mark morphologically activated astrocytes in brain tissue of MSA patients. Immunofluorescence of MSA, DLB and normal brain tissue sections was combined with cell culture and co-culture experiments to investigate the relationship between extracellular α-synuclein and the transition to a secretory astrocyte phenotype. Increased Munc18-positive vesicles were resolved in activated astrocytes in MSA and DLB tissue compared to controls, and they were also significantly upregulated in the human 1321N1 astrocytoma cell line upon treatment with α-synuclein, with parallel increases in GFAP expression and IL-6 secretion. In co-culture experiments, rat primary astrocytes pretreated with α-synuclein inhibited the growth of neurites of co-cultured primary rat neurons and upregulated chondroitin sulphate proteoglycan. Taken together, these results indicate that the secretory machinery is significantly upregulated in the astrocyte response to extracellular α-synuclein and may participate in the release of neuroinhibitory and proinflammatory factors in α-synucleinopathies.

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Marx, Hans, Michael Sauer, David Resina, Marina Vai, Danilo Porro, Francisco Valero, Pau Ferrer, and Diethard Mattanovich. "Cloning, disruption and protein secretory phenotype of theGAS1homologue ofPichia pastoris." FEMS Microbiology Letters 264, no. 1 (November 2006): 40–47. http://dx.doi.org/10.1111/j.1574-6968.2006.00427.x.

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40

Oubaha, M., K. Miloudi, A. Dejda, V. Guber, G. Mawambo, M. A. Germain, G. Bourdel, et al. "Senescence-associated secretory phenotype contributes to pathological angiogenesis in retinopathy." Science Translational Medicine 8, no. 362 (October 26, 2016): 362ra144. http://dx.doi.org/10.1126/scitranslmed.aaf9440.

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Laberge, Remi-Martin, Lili Zhou, Melissa R. Sarantos, Francis Rodier, Adam Freund, Peter L. J. de Keizer, Su Liu, et al. "Glucocorticoids suppress selected components of the senescence-associated secretory phenotype." Aging Cell 11, no. 4 (April 17, 2012): 569–78. http://dx.doi.org/10.1111/j.1474-9726.2012.00818.x.

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Meyer, P., P. Maity, A. Burkovski, K. Singh, F. Ferreira, L. Krug, M. Wlaschek, T. Wirth, H. A. Kestler, and K. Scharffetter-Kochanek. "397 In-silico modeling of the senescence associated secretory phenotype." Journal of Investigative Dermatology 136, no. 5 (May 2016): S70. http://dx.doi.org/10.1016/j.jid.2016.02.431.

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Lee, Sangim. "Expression of Senescence-Associated Secretory Phenotype in Senescent Gingival Fibroblasts." Journal of Dental Hygiene Science 23, no. 2 (June 30, 2023): 169–75. http://dx.doi.org/10.17135/jdhs.2023.23.2.169.

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Jeon, Hee-Young, Jun-Kyum Kim, Seok Won Ham, Se-Yeong Oh, Jaebong Kim, Jae-Bong Park, Jae-Yong Lee, Sung-Chan Kim, and Hyunggee Kim. "Irradiation induces glioblastoma cell senescence and senescence-associated secretory phenotype." Tumor Biology 37, no. 5 (November 19, 2015): 5857–67. http://dx.doi.org/10.1007/s13277-015-4439-2.

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45

Ionescu-Tîrgovişte, C., Elena Nicoleta Tudorică, and Nicoleta Toma. "What is behind genetics of diabetes?" Romanian Medical Journal 62, no. 3 (September 30, 2015): 237–42. http://dx.doi.org/10.37897/rmj.2015.3.4.

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The modern era of diabetes, which began in the early nineteenth century, continues until now, despite the hopes that the genetic revolution will bring major clarifications, both in terms of defining diabetes, the classification of its different phenotypes, the pathogenetic mechanisms and especially the finding of effective therapeutic solutions or even their prevention. Despite the useful information brought by genetic revolution, which refers primarily to identify structural or functional molecules associated with the various phenotypes, most of them expresed in pancreatic β-cell, the pancreatic genetic risk score, failed to improve prediction of diabetes. In the authors’ concept, the primary cause of diabetes, regardless of phenotype analyzed can be identified in β-cell secretory dysfunction, in turn, secondary to pancreatic β-cell inability to produce mature secretory vesicles, the only one able to respond promptly and efficiently to its physiological stimuli. The authors propose as indicator for the β-cell dysfunction, the increas of serum proinsulin, or better yet the ratio proinsulin / adiponectin.

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Xie, Zhigang, Min Fang, and Vytas A. Bankaitis. "Evidence for an Intrinsic Toxicity of Phosphatidylcholine to Sec14p-dependent Protein Transport from the Yeast Golgi Complex." Molecular Biology of the Cell 12, no. 4 (April 2001): 1117–29. http://dx.doi.org/10.1091/mbc.12.4.1117.

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Yeast phosphatidylinositol-transfer protein (Sec14p) is essential for Golgi secretory function and cell viability. This requirement of Sec14p is relieved by genetic inactivation of the cytidine diphosphate-choline pathway for phosphatidycholine (PtdCho) biosynthesis. Standard phenotypic analyses indicate that inactivation of the phosphatidylethanolamine (PtdEtn) pathway for PtdCho biosynthesis, however, does not rescue the growth and secretory defects associated with Sec14p deficiency. We now report inhibition of choline uptake from the media reveals an efficient “bypass Sec14p” phenotype associated with PtdEtn-methylation pathway defects. We further show that the bypass Sec14p phenotype associated with PtdEtn-methylation pathway defects resembles other bypass Sec14p mutations in its dependence on phospholipase D activity. Finally, we find that increased dosage of enzymes that catalyze phospholipase D-independent turnover of PtdCho, via mechanisms that do not result in a direct production of phosphatidic acid or diacylglycerol, effect a partial rescue of sec14-1ts-associated growth defects. Taken together, these data support the idea that PtdCho is intrinsically toxic to yeast Golgi secretory function.

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Lai, Zhennan, Hongen Yin, Javier Cabrera-Pérez, Maria C. Guimaro, Sandra Afione, Drew G. Michael, Patricia Glenton, et al. "Aquaporin gene therapy corrects Sjögren’s syndrome phenotype in mice." Proceedings of the National Academy of Sciences 113, no. 20 (May 2, 2016): 5694–99. http://dx.doi.org/10.1073/pnas.1601992113.

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Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease that is estimated to affect 35 million people worldwide. Currently, no effective treatments exist for Sjögren’s syndrome, and there is a limited understanding of the physiological mechanisms associated with xerostomia and hyposalivation. The present work revealed that aquaporin 5 expression, a water channel critical for salivary gland fluid secretion, is regulated by bone morphogenetic protein 6. Increased expression of this cytokine is strongly associated with the most common symptom of primary Sjögren’s syndrome, the loss of salivary gland function. This finding led us to develop a therapy in the treatment of Sjögren’s syndrome by increasing the water permeability of the gland to restore saliva flow. Our study demonstrates that the targeted increase of gland permeability not only resulted in the restoration of secretory gland function but also resolved the hallmark salivary gland inflammation and systemic inflammation associated with disease. Secretory function also increased in the lacrimal gland, suggesting this local therapy could treat the systemic symptoms associated with primary Sjögren’s syndrome.

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Tiemann, Janina, Thomas Wagner, Christopher Lindenkamp, Ricarda Plümers, Isabel Faust, Cornelius Knabbe, and Doris Hendig. "Linking ABCC6 Deficiency in Primary Human Dermal Fibroblasts of PXE Patients to p21-Mediated Premature Cellular Senescence and the Development of a Proinflammatory Secretory Phenotype." International Journal of Molecular Sciences 21, no. 24 (December 18, 2020): 9665. http://dx.doi.org/10.3390/ijms21249665.

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Pseudoxanthoma elasticum (PXE) is a rare autosomal-recessive disorder that is mainly caused by mutations in the ATP-binding cassette sub-family C member 6 (ABCC6) gene. Clinically PXE is characterized by a loss of skin elasticity, arteriosclerosis or visual impairments. It also shares some molecular characteristics with known premature aging syndromes like the Hutchinson–Gilford progeria syndrome (HGPS). However, little is known about accelerated aging processes, especially on a cellular level for PXE now. Therefore, this study was performed to reveal a potential connection between premature cellular aging and PXE pathogenesis by analyzing cellular senescence, a corresponding secretory phenotype and relevant factors of the cell cycle control in primary human dermal fibroblasts of PXE patients. Here, we could show an increased senescence-associated β-galactosidase (SA-β-Gal) activity as well as an increased expression of proinflammatory factors of a senescence-associated secretory phenotype (SASP) like interleukin 6 (IL6) and monocyte chemoattractant protein-1 (MCP1). We further observed an increased gene expression of the cyclin-dependent kinase inhibitor (CDKI) p21, but no simultaneous induction of p53 gene expression. These data indicate that PXE is associated with premature cellular senescence, which is possibly triggered by a p53-independent p21-mediated mechanism leading to a proinflammatory secretory phenotype.

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Alhaddad, Lina, Andreyan N. Osipov, and Sergey Leonov. "Radiation-Induced Premature Senescence of Tumor Cells." MEDICAL RADIOLOGY AND RADIATION SAFETY 68, no. 2 (March 2023): 5–10. http://dx.doi.org/10.33266/1024-6177-2023-68-2-5-10.

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CONTENTS Introduction Factors and mechanisms of Stress-Associated Secretory Phenotype (SASP) Morphological and transcriptional signatures of SASP Radiation-induced signaling pathways associated with premature senescence Conclusion

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Clover, Todd, Amrou Abdelkader, and Guru Subramanian Guru Murthy. "Transformation of a non-secretory neuroendocrine tumor to insulinoma after treatment with Sunitinib: A case report and review of the literature." Journal of Oncology Pharmacy Practice 25, no. 6 (August 8, 2018): 1516–19. http://dx.doi.org/10.1177/1078155218791309.

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We report a case of a non-secretory neuroendocrine tumor which transformed into an insulin secreting tumor after treatment with Sunitinib. To our knowledge, this has only been described in three other cases worldwide. Previously reported case series find transformation of non-secretory neuroendocrine cancers into secretory lesions occurs in 3.4–6.8% of cases. Sunitinib is known to have the potential to lower blood glucose and induce epigenetic changes in cells of various types. We hypothesize that the mechanism for Sunitinib-induced transformation in cancer phenotype is through epigenetic changes in DNA expression within the tumor cells.

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