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Relevant bibliographies by topics / Paracrine

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Academic literature on the topic 'Paracrine'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 June 2025

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Journal articles on the topic "Paracrine"

1

Ash, C. "Paracrine Parable." Science 325, no. 5941 (2009): 656. http://dx.doi.org/10.1126/science.325_656d.

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Mueller, K. L. "Paracrine Pass-Through." Science 325, no. 5944 (2009): 1049. http://dx.doi.org/10.1126/science.325_1049c.

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Legg, Katrin. "PTEN goes paracrine." Nature Cell Biology 15, no. 8 (2013): 894. http://dx.doi.org/10.1038/ncb2825.

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Lever, A. F. "Renin: Endocrine, Paracrine, or Part-Paracrine Control of Blood Pressure?" American Journal of Hypertension 2, no. 4 (1989): 276–85. http://dx.doi.org/10.1093/ajh/2.4.276.

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Leipziger, Jens, and Helle Praetorius. "Renal Autocrine and Paracrine Signaling: A Story of Self-protection." Physiological Reviews 100, no. 3 (2020): 1229–89. http://dx.doi.org/10.1152/physrev.00014.2019.

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Autocrine and paracrine signaling in the kidney adds an extra level of diversity and complexity to renal physiology. The extensive scientific production on the topic precludes easy understanding of the fundamental purpose of the vast number of molecules and systems that influence the renal function. This systematic review provides the broader pen strokes for a collected image of renal paracrine signaling. First, we recapitulate the essence of each paracrine system one by one. Thereafter the single components are merged into an overarching physiological concept. The presented survey shows that despite the diversity in the web of paracrine factors, the collected effect on renal function may not be complicated after all. In essence, paracrine activation provides an intelligent system that perceives minor perturbations and reacts with a coordinated and integrated tissue response that relieves the work load from the renal epithelia and favors diuresis and natriuresis. We suggest that the overall function of paracrine signaling is reno-protection and argue that renal paracrine signaling and self-regulation are two sides of the same coin. Thus local paracrine signaling is an intrinsic function of the kidney, and the overall renal effect of changes in blood pressure, volume load, and systemic hormones will always be tinted by its paracrine status.

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Iliodromiti, Zoe, Nikolaos Antonakopoulos, Stavros Sifakis, et al. "Endocrine, paracrine, and autocrine placental mediators in labor." HORMONES 11, no. 4 (2012): 397–409. http://dx.doi.org/10.14310/horm.2002.1371.

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Weinbauer, G. F., and J. Wessels. "'Paracrine' control of spermatogenesis." Andrologia 31, no. 5 (1999): 249–62. http://dx.doi.org/10.1046/j.1439-0272.1999.00295.x.

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Yuan, X. H., and Z. H. Jin. "Paracrine regulation of melanogenesis." British Journal of Dermatology 178, no. 3 (2018): 632–39. http://dx.doi.org/10.1111/bjd.15651.

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Yuan, X. H., and Z. H. Jin. "Paracrine regulation of melanogenesis." British Journal of Dermatology 178, no. 3 (2018): e234-e234. http://dx.doi.org/10.1111/bjd.16387.

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Dominguez, F., A. Pellicer, and C. Simón. "Paracrine dialogue in implantation." Molecular and Cellular Endocrinology 186, no. 2 (2002): 175–81. http://dx.doi.org/10.1016/s0303-7207(01)00659-1.

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Dissertations / Theses on the topic "Paracrine"

1

Petersen, Cecilia. "Paracrine regulation of Sertoli cell proliferation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-443-7/.

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Renshaw, Derek. "Paracrine regulation of the rat adrenal gland." Thesis, Queen Mary, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251614.

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Luke, Garry A. "Paracrine signals of the endometrium and trophoblast." Thesis, University of Aberdeen, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327971.

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Both the endometrium and the trophoblast secrete a number of proteins. Some of these, e.g. human chorionic gonadotrophin (hCG) from the trophoblast and pregnancy-associated endometrial α2-globulin (α2-PEG) from the endometrium, are secreted into the bloodstream and may act as endocrines. Moreover, they may also function as paracrines, signalling to adjacent tissues. Several models have been developed, by which the paracrine activity of the endometrium and the trophoblast might be examined <i>in vitro</i>. These include, cultures of endometrium and trophoblast, dual chamber superfusion of membranes and dual perfusion of individual placental cotyledons. The purpose of the present study was to examine some aspects of experimental design on the results from these models and consider the factors that might govern the rate of release. A good many trophoblast proteins have been characterised and methods devised for their quantitative measurement, however, the study of endometrial proteins is less advanced. As a first step, a method was developed for the measurement of α2-PEG, the major secretory protein of the secretory endometrium during the first trimester of pregnancy. This thesis describes the development of a competitive ELISA for measuring α2-PEG. This assay was employed for measuring α2-PEG in the medium from decidual cultures. In this thesis, release of protein <i>in vitro</i> has been examined as a mode of basal unstimulated secretion <i>in vivo</i>. The release is compounded of at least two simultaneous processes, biosynthesis and the transport of formed material to the outside of the cell. The concept is put forward that protein release is determined by a dynamic balance between biosynthesis of new protein and diffusion of protein down the concentration gradient between cell cytoplasm and the surrounding medium.

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Smith, Katherine Sue. "Autocrine/paracrine regulation of ATP citrate lyase /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487683401444039.

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Rajapakse, Niwanthi W. "Paracrine factors and regulation of regional kidney perfusion." Monash University, Dept. of Physiology, 2004. http://arrow.monash.edu.au/hdl/1959.1/9589.

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Renlund, Nina. "Hormonal and paracrine influences on Leydig cell steroidogenesis /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-842-8/.

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Tamiya, Shigeo. "Autocrine and paracrine signalling mechanisms in lens cells." Thesis, University of East Anglia, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365025.

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Bent, Eric Huttenlocher. "Mechanisms of microenvironmental paracrine signaling in cancer chemoresistance." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104167.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>Chemoresistance remains a major barrier to the effective treatment of cancer. Cancer therapy occurs in the context of a tissue environment, with cancer cells surrounded by many non-malignant cells that contribute to tumor growth and resistance to therapy. Yet much remains unknown about the tumor microenvironment and its impact on therapeutic response. The specific cell types and microenvironment factors that influence chemoresistance, how therapy induced damage of the microenvironment changes these factors and the mechanisms by which the microenvironment contributes to therapy failure remain incompletely understood. To study microenvironment signaling and its impact on therapy response, I have used mouse models of B-cell leukemia and lymphoma. I find that the chemotherapeutic doxorubicin promotes endothelial IL-6 release through reactive oxygen species-mediated p38 signaling and use tissue specific knockout mice to demonstrate that endothelial-specific production of IL-6 promotes lymphoma chemoresistance in vivo. Doxorubicin induces endothelial-cell senescence, an irreversible growth arrest typically accompanied by a robust secretory response. I show that P13K/AKT/mTOR signaling is repressed in senescent endothelial cells and serves as switch, turning off chronic senescence-associated IL-6 production. These data implicate endothelial paracrine signaling in the promotion of chemoresistance and elucidates the molecular control of acute vs. chronic therapy-induced cytokine secretion. Conventional chemotherapeutics such as doxorubicin can induce anti-cancer immune responses through the promotion of an immunogenic form of cell death. However, these responses are normally repressed by the microenvironment, impairing therapeutic response. I demonstrate that microenvironment IL-6 inhibits the generation of anti-leukemia immunity after immunogenic chemotherapy and find that CD8+ T-cell responses cure the majority of IL-6-/- mice treated with immunogenic chemotherapy. IL-6 also inhibits the efficacy of immune checkpoint blocking agents, implicating it as a promising target to improve the generation of anti-cancer immunity. Thus, the work in this thesis identifies the molecular control of therapy induced endothelial paracrine signaling and identifies a key role for IL-6 in suppressing anti-cancer immune responses induced by therapy.<br>by Eric Huttenlocher Bent.<br>Ph. D.

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Smyth, Christopher David. "Paracrine mechanisms of gonadotrophin action on the ovary." Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/20805.

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This thesis describes a study of the role of local regulators in the modulation of gonadotrophin action. It was found that <I>in vivo</I> FSH stimulated granulosa cell proliferation and increased ovarian weight, but was incapable of stimulating granulosa cells to proliferate <I>in vitro</I>. This suggests that the action of FSH <I>in vivo</I> is mediated through another factor. However, in the presence of LH, FSH also stimulated the expression of differentiated functions (progesterone and oestradiol production) both <I>in vivo</I> and <I>in vitro</I> demonstrating a direct effect of FSH. In the absence of LH or aromatase substrate, FSH induced the potential for aromatisation but did not increase uterine weight, a marker of oestradiol production. Therefore it is concluded that FSH is the primary stimulus for follicular development but that LH is also required for co-ordinated follicular development. There is a growing body of indirect evidence to suggest that factors of FSH-stimulated granulosa cell origin may regulate adjacent thecal/interstitial cells. Cytochrome P45017α (17-hydroxylase/C<SUB>17-20</SUB> lyase) in thecal/interstitial cells is a LH-responsive steroidogenic enzyme vital for androgen production. To obtain direct evidence for FSH-stimulated paracrine signalling in the ovary a rat thecal/interstitial cell culture system was validated for the study of the control of androgen production. Using this system and Northern hybridisation the control of androgen production by gonadotrophins and granulosa cell derived factors was studied. The 2.0 kb P45017α mRNA signal in ovarian total RNA from intact animals was dose-dependently increased by treatment with recombinant human FSH (rh-FSH). Treatment of hypophysectomised animals with rh-FSH did not consistently alter ovarian P45017α mRNA levels, though in the presence of low levels of LH, FSH increased P45017α mRNA expression.

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Sjöblom, Tobias. "Paracrine and autocrine functions of PDGF in malignant disease." Doctoral thesis, Uppsala University, Ludwig Institute for Cancer Research, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2678.

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<p>Growth factors and their receptors are frequently activated by mutations in human cancer. Platelet-derived growth factor (PDGF)-B and its tyrosine kinase receptor, the PDGF β-receptor, have been implicated in autocrine transformation as well as paracrine stimulation of tumor growth. The availability of clinically useful antagonists motivates evaluation of PDGF inhibition in these diseases.</p><p>In chronic myelomonocytic leukemia with t(5;12), parts of the transcription factor TEL and the PDGF β-receptor are fused, generating a constitutively signaling protein. Oligomerization and unique phosphorylation pattern of TEL-PDGFβR was demonstrated, as well as the transforming activity of TEL-PDGFβR, which was sensitive to PDGF β-receptor kinase inhibition.</p><p>Dermatofibrosarcoma protuberans (DFSP) is characterized by a translocation involving the collagen Iα1 and PDGF B-chain genes. The COLIA1-PDGFB fusion protein was processed to mature PDGF-BB and transformed fibroblasts in culture. The PDGF antagonist STI571 inhibited growth of <i>COLIA1-PDGFB</i> transfected cells and primary DFSP cells <i>in vitro</i> and <i>in vivo</i> through induction of apoptosis.</p><p>Paracrine effects of PDGF-DD, a ligand for the PDGF β-receptor, were evaluated in a murine model of malignant melanoma. PDGF-DD production accelerated tumor growth and altered the vascular morphology in experimental melanomas.</p><p>A validated immunohistochemical procedure for PDGF β-receptor detection was established and applied to normal tissues and more than 280 tumor biopsies. Perivascular and stromal expression was detected in 90% and 50%, respectively, of human tumors.</p><p>Recently, non-transformed cells in the tumor microenvironment have emerged as targets in cancer therapy. Selective sensitization of tumor fibroblasts to paclitaxel by STI571 was evaluated <i>in vitro</i> and in a xenograft model. Whereas neither drug alone caused growth inhibition, combination of the two significantly reduced tumor growth, suggesting anti-stromal therapy as a possible treatment modality in solid tumors.</p>

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Books on the topic "Paracrine"

1

Krey, Lewis C., Bela J. Gulyas, and John A. McCracken, eds. Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5751-3.

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Reproductive Endocrinology Study Section Workshop on Autocrine and Paracrine Mechanisms in Reproductive Endocrinology (1988 Shrewsbury, Mass.). Autocrine and paracrine mechanisms in reproductive endocrinology. Plenum Press, 1989.

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3

Marshall, Joanne Louise. Paracrine regulation of renal function in the rat. University of Birmingham, 1998.

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Nikula, Hannu. Endocrine and paracrine modulation of gonadotropin action in the rat testis. Turun Yliopisto, 1990.

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R, Bellvé Anthony, and Vogel Henry J. 1920-, eds. Molecular mechanisms in cellular growth and differentiation. Academic Press, 1991.

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6

J, Dietze Guenther, ed. A symposium, autocrine and paracrine signaling between contracting myocardium and coronary endothelium during ischemia: Effect of insulin resistance. Excerpta Medica, 1997.

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7

Susan, Heyner, and Wiley Lynn M, eds. Early embryo development and paracrine relationships: Proceedings of a UCLA Symposia Colloquium, held at Taos, New Mexico, February 3-8, 1989. Wiley-Liss, 1990.

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1942-, Sowers James R., ed. Endocrinology of the vasculature. Humana Press, 1996.

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9

Walter, Helen Jane. The spatio-temporal modulation of the insulin-like growth factor[s] axis in the lesioned central nervous system: Implications for endocrine, paracrine and autocrine activities. University of Birmingham, 1996.

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10

Lise, Cédard, and Firth Anthony, eds. Placental signals: Autocrine and paracine control of pregnancy. University of Rochester Press, 1992.

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Book chapters on the topic "Paracrine"

1

Boregowda, Siddiraju V., and Donald G. Phinney. "MSCs: Paracrine Effects." In Mesenchymal Stromal Cells. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_9.

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Welle, Stephen. "Endocrine, Paracrine, and Autocrine Regulation." In Human Protein Metabolism. Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8_6.

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Gupta, G. S. "Paracrine Role of Sertoli Cell." In Proteomics of Spermatogenesis. Springer US, 2005. http://dx.doi.org/10.1007/0-387-27655-6_2.

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García, A. G., J. M. Hernández-Guijo, I. Mayorgas, and L. Gandía. "Exocytosis Calcium Channels: Autocrine/Paracrine Modulation." In Slow Synaptic Responses and Modulation. Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66973-9_16.

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Creutzfeldt, Werner. "Evidence for Paracrine Function of Somatostatin." In Somatostatin. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5326-3_19.

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Ratajczak, Mariusz Z., Gabriela Schneider, and Janina Ratajczak. "Paracrine Effects of Fetal Stem Cells." In Fetal Stem Cells in Regenerative Medicine. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3483-6_3.

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Robberecht, W., and C. Denef. "Paracrine Interactions in the Anterior Pituitary." In Neuroendocrine Perspectives. Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3478-4_3.

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Engel, Felix B. "Stem Cell Secretome and Paracrine Activity." In Stem Cell Biology and Regenerative Medicine. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25427-2_8.

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Haigler, Harry T. "Lipocortins and Related Proteins may be Involved in Intracellular Signal Transduction." In Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5751-3_1.

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Barcellos-Hoff, M. H., and M. J. Bissell. "A Role for the Extracellular Matrix in Autocrine and Paracrine Regulation of Tissue-Specific Functions." In Autocrine and Paracrine Mechanisms in Reproductive Endocrinology. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5751-3_10.

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Conference papers on the topic "Paracrine"

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Wingate, Kathryn, Yan Tan, and Wei Tan. "The Effects of Mechanical and Chemical Stimuli on Mesenchymal Stem Cell Vascular Trans-Differentiation and Paracrine Signaling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14742.

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Mesenchymal Stem Cells (MSCs) show great promise for the treatment of cardiovascular diseases by tissue engineering and cell therapy. MSCs are particularly useful for vascular therapies as they are easily obtainable, allogenic, trans-differentiate into specific vascular cells, and assist in regenerating vascular tissue through paracrine signaling. [1] However, the mechanisms which direct MSC trans-differentiation and paracrine signaling are not well defined. [2] Incorrect differentiation of MSC can lead to catastrophic side effects such as the development of a dysfunctional endothelium. [3] To safely utilize these cells for the treatment of vascular diseases it is critical to understand the underlying mechanisms that direct MSC differentiation and paracrine signaling.

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Früh, EH, and I. Rustenbeck. "Direct and paracrine regulation of glucagon secretion." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641811.

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Byrne, RN, TJ van Haaften, G. Rey-Parra, FC Eaton, LI Coltan, and B. Thebaud. "Stem Cell-Derived Paracrine Activity Prevents Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2009.

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Rosen, JM. "Abstract ES1-2: Paracrine signaling and intratumoral heterogeneity." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-es1-2.

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Terzian, Tamara, Nema Sobhani, Rohan Mylavarapu, et al. "Abstract 4503: The paracrine role of p53 in skin." 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.am2018-4503.

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Williams-Villalobo, Abie, Yun Zhang, B. Liu, S. Xiong, G. Chau, and G. Lozano. "The Paracrine Action of Mutant P53 In Breast Cancer." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.562150.

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Sherman, Mara H., Eric Collisson, Michael Downes, and Ronald M. Evans. "Abstract A42: Paracrine regulation of the pancreatic cancer epigenome." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a42.

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Fritton, J. Christopher, Yuki Kawashima, Hui Sun, et al. "Bone Marrow Adipogenesis Is Affected by Insulin-Like Growth Factor-1 Complexes." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206158.

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Fat tissue, which is composed of lipid-filled adipocytes that accumulate during aging, displaces mineralized tissue and reduces the mechanical integrity bone. Bone marrow adipocytes provide stroma for maintenance of mesencymal stem cells (MSC) and reside at sites of bone turnover (i.e., endosteal surfaces where osteoblasts form new bone), potentially influencing cell activity via a paracrine route.

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West, J., J. Johnson, L. Robinson, T. Blackwell, and K. Lane. "Macrophages Modulate the BMP Pathway through Paracrine and Autocrine Mechanisms." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2361.

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Dulyaninova, Natalya G., Adriana Levine, Jonathan M. Backer, and Anne R. Bresnick. "Abstract 3168A: S100A4 mediates paracrine interactions with breast tumor cells." 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.am2018-3168a.

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Reports on the topic "Paracrine"

1

Hayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada435853.

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Hayward, Simon W. Paracrine Regulation of Prostatic Carcinogenesis. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada423319.

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Yu, Min. Autocrine and Paracrine Hh Signaling Regulate Prostate Development. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada567961.

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Rosner, William, and Scott M. Kahn. Autocrine and Paracrine Control of Breast Cancer Growth by Sex Hormone-Binding Globulin. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada437693.

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Dean, James. Identification and Therapeutic Targeting of Paracrine Senescence Factors in the Prostate Tumor Microenvironment. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada484356.

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Dean, James P. Identification and Therapeutic Targeting of Paracrine Senescence Factors in the Prostate Tumor Microenvironment. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada525781.

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Dean, James. Identification and Therapeutic Targeting of Paracrine Senescence Factors in the Prostate Tumor Microenvironment. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada504966.

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Galileo, Deni S. Novel Quantitation of Autocrine/Paracrine Stimulation of Cell Motility in Vitro and Metastasis. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada510235.

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Rosner, William. Autocine and Paracrine Control of Breast Cancer Growth by Sex Hormone-Binding Globulin. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada425713.

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Nelson, Corwin D., Donald C. Beitz, Timothy A. Reinhardt, and John D. Lippolis. Regulation of Immune Responses to Mycobacteria bovis by a Paracrine Mechanism of Vitamin D Signaling in Cattle. Iowa State University, 2011. http://dx.doi.org/10.31274/ans_air-180814-646.

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