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Journal articles on the topic 'Paracrine'

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Published: 4 June 2021
Last updated: 16 June 2025

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1

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

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2

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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3

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

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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Bulletti, Carlo, Dominique De Ziegler, Alessia Albonetti, and Carlo Flamigni. "Paracrine regulation of menstruation." Journal of Reproductive Immunology 39, no. 1-2 (1998): 89–104. http://dx.doi.org/10.1016/s0165-0378(98)00015-1.

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12

Rajaram, Renuga Devi, and Cathrin Brisken. "Paracrine signaling by progesterone." Molecular and Cellular Endocrinology 357, no. 1-2 (2012): 80–90. http://dx.doi.org/10.1016/j.mce.2011.09.018.

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13

Pescovitz, Ora Hirsch, Carolyn H. Srivastava, Paul R. Breyer, and Beverly A. Monts. "Paracrine control of spermatogenesis." Trends in Endocrinology & Metabolism 5, no. 3 (1994): 126–31. http://dx.doi.org/10.1016/1043-2760(94)90094-9.

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14

Weinbauer, G. F., and J. Wessels. "‘Paracrine’ control of spermatogenesis." Andrologia 31, no. 5 (2009): 249–62. http://dx.doi.org/10.1111/j.1439-0272.1999.tb01421.x.

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15

Simón, Carlos, Julio Cesar Martı́n, and Antonio Pellicer. "Paracrine regulators of implantation." Best Practice & Research Clinical Obstetrics & Gynaecology 14, no. 5 (2000): 815–26. http://dx.doi.org/10.1053/beog.2000.0121.

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16

Winters, Stephen, and Joseph Moore. "Paracrine Control of Gonadotrophs." Seminars in Reproductive Medicine 25, no. 5 (2007): 379–87. http://dx.doi.org/10.1055/s-2007-984744.

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17

Yao, Hang, Xiaohui Yuan, Zhonglian Wu, et al. "Fabrication and Performance Evaluation of Gelatin/Sodium Alginate Hydrogel-Based Macrophage and MSC Cell-Encapsulated Paracrine System with Potential Application in Wound Healing." International Journal of Molecular Sciences 24, no. 2 (2023): 1240. http://dx.doi.org/10.3390/ijms24021240.

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A gelatin/sodium alginate-based hydrogel microsphere has been fabricated after reaction condition optimization. Macrophages (RAW246.7) and adipose mesenchymal stem cells (ADSC) have been subsequently encapsulated in the microsphere in order to construct a 3D paracrine system for wound healing treatment. The synthesized microsphere displayed neglectable cytotoxicity toward both encapsulated cells until 10 days of incubation, indicating promising biocompatibility of the microsphere. A qRT-PCR and ELISA experiment revealed positive regulation of cytokines (Arg-1, IL-6, IL-8, IL-10, bFGF, HGF, VEGF, TLR-1, and CXCL13) expression regarding macrophage phenotype transformation and anti-inflammatory performance both inside the microsphere and in the microenvironment of established in vitro inflammatory model. Additionally, positive tendency of cytokine expression benefit wound healing was more pronounced in a fabricated 3D paracrine system than that of a 2D paracrine system. Furthermore, the 3D paracrine system exhibited more efficiently in the wound healing rate compared to the 2D paracrine system in an in vitro model. These results suggested the current paracrine system could be potentially used as a robust wound healing dressing.
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18

Dove, Dwayne E., MacRae F. Linton, and Sergio Fazio. "ApoE-mediated cholesterol efflux from macrophages: separation of autocrine and paracrine effects." American Journal of Physiology-Cell Physiology 288, no. 3 (2005): C586—C592. http://dx.doi.org/10.1152/ajpcell.00210.2004.

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Macrophages in the vessel wall secrete high levels of apolipoprotein E (apoE). Cholesterol efflux from macrophages to apoE has been shown to decrease foam cell formation and prevent atherosclerosis. An apoE molecule can mediate cholesterol efflux from the macrophage that originally secreted it (autocrine effect) or from surrounding macrophages (paracrine effect). Traditional methodologies have not been able to separate these serial effects. The novel methodology presented here was developed to separate autocrine and paracrine effects by using a simple mathematical model to interpret the effects of dilution on apoE-mediated cholesterol efflux. Our results show that, at very dilute concentrations, the paracrine effect of apoE is not evident and the autocrine effect becomes the dominant mediator of efflux. However, at saturating concentrations, paracrine apoE causes 80–90% of the apoE-mediated cholesterol efflux, whereas autocrine apoE is responsible for the remaining 10–20%. These results suggest that the relative importance of autocrine and paracrine apoE depends on the size of the local distribution volume, a factor not considered in previous in vitro studies of apoE function. Furthermore, autocrine effects of apoE could be critical in the prevention of foam cell formation in vivo. This novel methodology may be applicable to other types of mixed autocrine/paracrine systems, such as signal transduction systems.
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19

Lopez, D., H. Vlamakis, R. Losick, and R. Kolter. "Paracrine signaling in a bacterium." Genes & Development 23, no. 14 (2009): 1631–38. http://dx.doi.org/10.1101/gad.1813709.

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20

Jia, L. G., B. J. Canny, and D. A. Leong. "Paracrine communication regulates adrenocorticotropin secretion." Endocrinology 130, no. 1 (1992): 534–39. http://dx.doi.org/10.1210/endo.130.1.1309348.

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21

Theunissen, Jan-Willem, and Frederic J. de Sauvage. "Paracrine Hedgehog Signaling in Cancer." Cancer Research 69, no. 15 (2009): 6007–10. http://dx.doi.org/10.1158/0008-5472.can-09-0756.

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22

Weryha, Georges, and Jacques Leclère. "Paracrine Regulation of Bone Remodeling." Hormone Research 43, no. 1-3 (1995): 69–75. http://dx.doi.org/10.1159/000184240.

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23

Minici, Francesca, Federica Tiberi, Anna Tropea, et al. "Paracrine regulation of endometriotic tissue." Gynecological Endocrinology 23, no. 10 (2007): 574–80. http://dx.doi.org/10.1080/09513590701581721.

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24

AKI, Yasuharu, Youichi ABE, and Toshiaki TAMAKI. "Paracrine regulation of renal hemodynamics." Folia Pharmacologica Japonica 112, no. 5 (1998): 287–97. http://dx.doi.org/10.1254/fpj.112.287.

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25

Hillier, S. G. "Paracrine support of ovarian stimulation." Molecular Human Reproduction 15, no. 12 (2009): 843–50. http://dx.doi.org/10.1093/molehr/gap086.

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26

Navar, L. G. "Paracrine mechanisms regulating renal hemodynamics." Pathophysiology 5 (June 1998): 57. http://dx.doi.org/10.1016/s0928-4680(98)80501-4.

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27

Underwood, Louis E., A. Joseph D'ercole, David R. Clemmons, and Judson J. Van Wyk. "3 Paracrine functions of somatomedins." Clinics in Endocrinology and Metabolism 15, no. 1 (1986): 59–77. http://dx.doi.org/10.1016/s0300-595x(86)80042-1.

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28

Lejeune, Hervé, and José Maria Saez. "Régulation paracrine des fonctions leydigiennes." Andrologie 3, no. 1 (1993): 16–21. http://dx.doi.org/10.1007/bf03034604.

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29

Sucharov, Carmen C. "Paracrine Factors in Uremic Cardiomyopathy." JACC: Basic to Translational Science 5, no. 2 (2020): 167–68. http://dx.doi.org/10.1016/j.jacbts.2020.01.005.

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30

Fitz, Greg. "Paracrine regulation of intestinal secretion." Gastroenterology 107, no. 4 (1994): 1206–8. http://dx.doi.org/10.1016/0016-5085(94)90254-2.

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31

Alderton, Gemma K. "Stromal metabolism has paracrine effects." Nature Reviews Cancer 14, no. 8 (2014): 515. http://dx.doi.org/10.1038/nrc3794.

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32

Christensen, Mette G., and Helle A. Praetorius. "Sorting out the paracrine kidney." American Journal of Physiology-Renal Physiology 308, no. 10 (2015): F1074—F1075. http://dx.doi.org/10.1152/ajprenal.00050.2015.

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33

Huising, Mark O. "Paracrine regulation of insulin secretion." Diabetologia 63, no. 10 (2020): 2057–63. http://dx.doi.org/10.1007/s00125-020-05213-5.

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34

Saez, J. M., M. H. Perrard-Sapori, P. G. Chatelain, E. Tabone, and M. A. Rivarola. "Paracrine regulation of testicular function." Journal of Steroid Biochemistry 27, no. 1-3 (1987): 317–29. http://dx.doi.org/10.1016/0022-4731(87)90323-2.

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35

Dahl, Nancy A. "Paracrine control of photomembrane removal." Neurochemical Research 17, no. 1 (1992): 67–73. http://dx.doi.org/10.1007/bf00966866.

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36

Dor, Jehoshua, Ehud Kokia, and David Bider. "Paracrine mechanism of ovarian regulation." European Journal of Obstetrics & Gynecology and Reproductive Biology 65, no. 1 (1996): 25–28. http://dx.doi.org/10.1016/0028-2243(95)02298-7.

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37

Frolkis, Inna, Jacob Gurevitch, Yael Yuhas, et al. "Interaction between paracrine tumor necrosis factor-alpha and paracrine angiotensin II during myocardial ischemia." Journal of the American College of Cardiology 37, no. 1 (2001): 316–22. http://dx.doi.org/10.1016/s0735-1097(00)01055-x.

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38

Zhou, Qing, Dipali Patel, Timothy Kwa, et al. "Liver injury-on-a-chip: microfluidic co-cultures with integrated biosensors for monitoring liver cell signaling during injury." Lab on a Chip 15, no. 23 (2015): 4467–78. http://dx.doi.org/10.1039/c5lc00874c.

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39

Noble, Peter J. M., Geraint Wilde, Michael R. H. White, Steven R. Pennington, Graham J. Dockray, and Andrea Varro. "Stimulation of gastrin-CCKB receptor promotes migration of gastric AGS cells via multiple paracrine pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 1 (2003): G75—G84. http://dx.doi.org/10.1152/ajpgi.00300.2002.

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Responses to G protein-coupled receptor stimulation may be mediated by paracrine factors. We have developed a coculture system to study paracrine regulation of migration of gastric epithelial (AGS) cells after stimulation of gastrin-CCKBreceptors. In cells expressing this receptor, G-17 stimulated migration by activation of protein kinase C. However, G-17 also stimulated the migration of cells expressing green fluorescent protein, but not the receptor, when they were cocultured with receptor-expressing cells consistent with activation of paracrine signals. The use of various pharmacological inhibitors indicated that gastrin stimulated migration via activation of the EGF receptor (EGR-R), the erbB-2 receptor tyrosine kinase, and the MAP kinase pathway. However, gastrin also released fibroblast growth factor (FGF)-1, and migration was inhibited by the FGF receptor tyrosine kinase inhibitor SU-5402. Flow cytometry indicated that in both cell types, gastrin increased MAP kinase via activation of EGF-R but not FGF-R1 or erbB-2. We conclude that gastrin-CCKB receptors stimulate epithelial cell migration partly via paracrine mechanisms; transactivation of EGF-R is only one component of the paracrine pathway.
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40

Sun, Hualing, Richard E. Pratt, Conrad P. Hodgkinson, and Victor J. Dzau. "Sequential paracrine mechanisms are necessary for the therapeutic benefits of stem cell therapy." American Journal of Physiology-Cell Physiology 319, no. 6 (2020): C1141—C1150. http://dx.doi.org/10.1152/ajpcell.00516.2019.

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Stem cell injections are an attractive therapeutic tool. It has been demonstrated that injected stem cells promote tissue repair and regeneration via paracrine mechanisms. However, the effects of injected stem cells continue for far longer than they are present. We hypothesized that the effects of injected stem cells are prolonged because of a sequential paracrine relay mechanism. Conditioned media was collected from mesenchymal stem cells (MSCs) after 24 h. This media was then added to RAW264.7. Media was collected from the macrophages after 24 h and was then added to endothelial cells (ECs). This conditioned macrophage media, but not control media, promoted wound healing and induced EC differentiation. Similar results were observed with primary macrophages. To identify the active paracrine factors released by macrophages in response to stimulation by MSC conditioned media we used an antibody array, identifying increased expression of the angiogenesis-related proteins stromal cell-derived factor 1 (SDF1) and plasminogen activator inhibitor-1 (PAI-1). Knockdown of either protein inhibited the ability of conditioned media derived from MSC paracrine factor-stimulated macrophages to induce EC differentiation both in vitro and in vivo. Conditioned media derived from postnatal day 7 (P7) mouse macrophages induced EC differentiation. Moreover, SDF1 and PAI-1 levels were >120 higher in P7 macrophages compared with adult macrophages, suggesting that MSC paracrine factors promote adult macrophages to adopt a juvenile phenotype. These results indicate that MSC paracrine factors induce macrophages to secrete SDF1 and PAI-1, in-turn inducing endothelial cells to differentiate. Identification of a sequential paracrine mechanism opens new therapeutic avenues for stem cell therapy.
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41

Costa, Ambra, Davide Ceresa, Antonella De Palma, et al. "Comprehensive Profiling of Secretome Formulations from Fetal- and Perinatal Human Amniotic Fluid Stem Cells." International Journal of Molecular Sciences 22, no. 7 (2021): 3713. http://dx.doi.org/10.3390/ijms22073713.

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We previously reported that c-KIT+ human amniotic-fluid derived stem cells obtained from leftover samples of routine II trimester prenatal diagnosis (fetal hAFS) are endowed with regenerative paracrine potential driving pro-survival, anti-fibrotic and proliferative effects. hAFS may also be isolated from III trimester clinical waste samples during scheduled C-sections (perinatal hAFS), thus offering a more easily accessible alternative when compared to fetal hAFS. Nonetheless, little is known about the paracrine profile of perinatal hAFS. Here we provide a detailed characterization of the hAFS total secretome (i.e., the entirety of soluble paracrine factors released by cells in the conditioned medium, hAFS-CM) and the extracellular vesicles (hAFS-EVs) within it, from II trimester fetal- versus III trimester perinatal cells. Fetal- and perinatal hAFS were characterized and subject to hypoxic preconditioning to enhance their paracrine potential. hAFS-CM and hAFS-EV formulations were analyzed for protein and chemokine/cytokine content, and the EV cargo was further investigated by RNA sequencing. The phenotype of fetal- and perinatal hAFS, along with their corresponding secretome formulations, overlapped; yet, fetal hAFS showed immature oxidative phosphorylation activity when compared to perinatal ones. The profiling of their paracrine cargo revealed some differences according to gestational stage and hypoxic preconditioning. Both cell sources provided formulations enriched with neurotrophic, immunomodulatory, anti-fibrotic and endothelial stimulating factors, and the immature fetal hAFS secretome was defined by a more pronounced pro-vasculogenic, regenerative, pro-resolving and anti-aging profile. Small RNA profiling showed microRNA enrichment in both fetal- and perinatal hAFS-EV cargo, with a stably- expressed pro-resolving core as a reference molecular signature. Here we confirm that hAFS represents an appealing source of regenerative paracrine factors; the selection of either fetal or perinatal hAFS secretome formulations for future paracrine therapy should be evaluated considering the specific clinical scenario.
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42

Sunami, Yoshiaki, Johanna Häußler, Anais Zourelidis, and Jörg Kleeff. "Cancer-Associated Fibroblasts and Tumor Cells in Pancreatic Cancer Microenvironment and Metastasis: Paracrine Regulators, Reciprocation and Exosomes." Cancers 14, no. 3 (2022): 744. http://dx.doi.org/10.3390/cancers14030744.

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Pancreatic cancer is currently the fourth leading cause of cancer deaths in the United States, and the overall 5 year survival rate is still only around 10%. Pancreatic cancer exhibits a remarkable resistance to established therapeutic options such as chemotherapy and radiotherapy, in part due to the dense stromal tumor microenvironment, where cancer-associated fibroblasts are the major stromal cell type. Cancer-associated fibroblasts further play a key role in cancer progression, invasion, and metastasis. Cancer-associated fibroblasts communicate with tumor cells, not only through paracrine as well as paracrine-reciprocal signaling regulators but also by way of exosomes. In the current manuscript, we discuss intercellular mediators between cancer-associated fibroblasts and pancreatic cancer cells in a paracrine as well as paracrine-reciprocal manner. Further recent findings on exosomes in pancreatic cancer and metastasis are summarized.
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43

Titov, V. N. "A modern phylogenetic theory of pathology, pathogenesis of essential arterial hypertension and universal algorhythm of damage to the target organs." Systemic Hypertension 10, no. 2 (2013): 75–82. http://dx.doi.org/10.26442/sg28977.

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Separate regulation of 2 arterial beds – phylogenetically early muscle arterioles (millions of local peristaltic pumps) and phylogenetically late proximal region, heart and elastic arteries – is the basis for the phenomenon that their non-coordination formed at different stages of phylogenesis manifests itself in functional disorders in paracrine cell communities. There is a small number of means to produce any effect on the paracrine cell community function at the level of the organism. Metabolic disorders in these communities can be normalized via the biological reaction of arterial pressure (AP). Pathogenesis of essential arterial hypertension is based on in vivo disorders of the biological functions of homeostasis, exotrophy, endoecology and adaptation. In essential hypertension, primary disorders form at the paracrine cell community level in the distal area of arterial bed, but not in the target organs. Only later, after compensatory activation of the biological reaction of AP and formation of discrepancy between regulations at the organism and paracrine cells communities, the process secondarily involves the target organs: kidneys, lungs and brains which have autonomous hemodynamics systems. The heart is the fourth target organ in essential hypertension. The pathogenesis of essential hypertension is based on phylogenetic discrepancy between metabolism regulation at the levels of the entire body and paracrine cell communities.
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44

DeFelice, Gina, Abdul-Razak Masoud, Paige Deville, et al. "509 Cytokine Profile Following Lipopolysaccharide Stimulation of Adipose-Derived Stem Cells from Burn Patients." Journal of Burn Care & Research 46, Supplement_1 (2025): S109. https://doi.org/10.1093/jbcr/iraf019.138.

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Abstract Introduction Adipose tissue and adipose-derived stem cells (ADSCs) have been demonstrated to have an important role in the mediation of inflammatory response to injury and illness. The secretion of paracrine factors by stem cells, which can have pro- or anti-inflammatory effects, may have wider implications on wound healing. Lipopolysaccharide (LPS) is an important component of the outer membrane of gram-negative bacteria that triggers a strong immune response. The objective of this study was to compare the paracrine factors secreted from damaged adipose tissue from burn patients with and without LPS administration. Methods Fat samples were collected from 28 burn adult patients with TBSA from 10-95% who presented to an ABA Verified Burn Center. Fluorescence-activated single cell sorting (FACS) confirmed the presence of ADSCs. Lipopolysaccharide (LPS) was administered to 12 matched burn samples to mimic an initial inflammatory response, and supernatant was collected from cell culture for analysis. The secretion of 10 paracrine factors were measured by ELISA. A Mann-Whitney u test was performed. Results Levels of all 10 paracrine factors analyzed were greater in samples of ADSCs from burn patients with LPS administration. There was a significant difference in the levels of four specific paracrine factors: IL-6, IL-1-beta, IL-8, and IL-10 (p < 0.05). Conclusions Our findings demonstrate increased secretion of four specific paracrine factors from ADSCs in burn patients following LPS administration. These factors are both pro- and anti-inflammatory and have been previously found to attenuate autoinflammatory syndromes. Future directions will be focused on investigating the effects of increased IL-6, IL-1-beta, IL-8, and IL-10 on wound healing in burn patients with concomitant infections. Applicability of Research to Practice The identification of specific paracrine factors increased in burn patients, especially in those with concomitant infections, will help further understand the mechanisms of wound healing and clinical interventions to improve wound healing and mitigate infections in burn patients. Funding for the Study N/A
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45

Yoon, Sun-Young, and Michael Detmar. "Sostdc1 Secreted from Cutaneous Lymphatic Vessels Acts as a Paracrine Factor for Hair Follicle Growth." Current Issues in Molecular Biology 44, no. 5 (2022): 2167–74. http://dx.doi.org/10.3390/cimb44050146.

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In our previous study, we found that lymphatic vessels stimulate hair follicle growth through paracrine effects on dermal papilla cells. However, the paracrine factors secreted from cutaneous lymphatic vessels that can activate dermal papilla cells are still unknown. In this study, we investigated whether lymphatic endothelial cells might secrete paracrine factors that activate dermal papilla cells in vitro. We found that Sostdc1 was more expressed in lymphatic endothelial cells compared with blood vascular endothelial cells. In addition, Sostdc1 expression levels were significantly increased during the anagen phase in the back skin of C57BL/6J mice, as compared to the telogen phase. We also observed that incubation of dermal papilla cells with 200 ng/mL Sostdc1 for 72 h induced the expression levels of Lef-1, a downstream target of Wnt signaling. Taken together, our results reveal that Sostdc1, a BMP antagonist, secreted from cutaneous lymphatic vessels, may act as a paracrine factor for hair follicle growth.
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46

Smith, Alison A., and Charles F. Bellows. "Efficacy of Paracrine Factors from Mesenchymal Stem Cells for Treating Biofilm-Infected Wounds in a Murine Model." Journal of Wound Management and Research 18, no. 3 (2022): 186–93. http://dx.doi.org/10.22467/jwmr.2022.02040.

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Background: Chronic wounds are a serious medical condition affecting over 6 million people in the United States. Biofilms, which alter the host immune response and establish a microenvironment that prevents wound healing, are intimately associated with the development of chronic wounds. Current treatment options do not specifically target the underlying molecular mechanisms of biofilm pathology. Paracrine factors secreted by mesenchymal stem cells (MSCs) have been demonstrated to play an important role in wound healing. The objective of this study was to examine the effects of the paracrine factors secreted from MSCs on reducing infection and accelerating wound closure in biofilm-infected wounds.Methods: MSCs were cultured by seeding on an extracellular matrix (ECM). The supernatant from MSCs containing paracrine factors were applied to mature <i>Pseudomonas aeruginosa</i> biofilms <i>in vitro</i> and the number of viable bacteria were quantitated. BALB/cJ mice were wounded and infected with <i>P. aeruginosa</i> biofilms and the paracrine factors from reprogrammed MSCs were applied topically. The wound surface area and colony forming units counts of the treatment group were compared to control (culture media) and biofilm (untreated) groups. Results: The paracrine factors from MSCs grown on ECM were found to reduce <i>P. aeruginosa</i> biofilm growth significantly (P<0.01). Wounds in the treatment group had lower bacterial counts and an increased rate of wound closure compared to non-treated mice wounds. Conclusion: The results indicate that paracrine factors from reprogrammed MSCs accelerated wound healing and reduced the bacterial burden in biofilm-infected wounds. Future studies are needed to further characterize this phenomenon.
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47

Navar, L. G., E. W. Inscho, S. A. Majid, J. D. Imig, L. M. Harrison-Bernard, and K. D. Mitchell. "Paracrine regulation of the renal microcirculation." Physiological Reviews 76, no. 2 (1996): 425–536. http://dx.doi.org/10.1152/physrev.1996.76.2.425.

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There has been an explosive growth of interest in the multiple interacting paracrine systems that influence renal microvascular function. This review first discusses the membrane activation mechanisms for renal vascular control. Evidence is provided that there are differential activating mechanisms regulating pre- and postglomerular arteriolar vascular smooth muscle cells. The next section deals with the critical role of the endothelium in the control of renal vascular function and covers the recent findings related to the role of nitric oxide and other endothelial-derived factors. This section is followed by an analysis of the roles of vasoactive paracrine systems that have their origin from adjoining tubular structures. The interplay of signals between the epithelial cells and the vascular network to provide feedback regulation of renal hemodynamics is developed. Because of their well-recognized contributions to the regulation of renal microvascular function, three major paracrine systems are discussed in separate sections. Recent findings related to the role of intrarenally formed angiotensin II and the prominence of the AT1 receptors are described. The possible contribution of purinergic compounds is then discussed. Recognition of the emerging role of extracellular ATP operating via P2 receptors as well as the more recognized functions of the P1 receptors provides fertile ground for further studies. In the next section, the family of vasoactive arachidonic acid metabolites is described. Possibilities for a myriad of interacting functions operating both directly on vascular smooth muscle cells and indirectly via influences on endothelial and epithelial cells are discussed. Particular attention is given to the more recent developments related to hemodynamic actions of the cytochrome P-450 metabolites. The final section discusses unique mechanisms that may be responsible for differential regulation of medullary blood flow by locally formed paracrine agents. Several sections provide perspectives on the complex interactions among the multiple mechanisms responsible for paracrine regulation of the renal microcirculation. This plurality of regulatory interactions highlights the need for experimental strategies that include integrative approaches that allow manifestation of indirect as well as direct influences of these paracrine systems on renal microvascular function.
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48

Janowska-Wieczorek, Anna, Marcin Majka, Janina Ratajczak, and Mariusz Z. Ratajczak. "Autocrine/Paracrine Mechanisms in Human Hematopoiesis." Stem Cells 19, no. 2 (2001): 99–107. http://dx.doi.org/10.1634/stemcells.19-2-99.

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49

Reis, F. M., L. Cobellis, S. Luisi, et al. "Paracrine/autocrine control of female reproduction." Gynecological Endocrinology 14, no. 6 (2000): 464–75. http://dx.doi.org/10.3109/09513590009167720.

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50

HORTON, RICHARD. "Dihydrotestosterone Is a Peripheral Paracrine Hormone." Journal of Andrology 13, no. 1 (1992): 23–27. http://dx.doi.org/10.1002/j.1939-4640.1992.tb01621.x.

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