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Journal articles on the topic 'Paracrine signalling'

Author: Grafiati

Published: 3 June 2025

Last updated: 19 July 2025

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1

Michael Lavigne, G., Hayley Russell, Barbara Sherry, and Ruian Ke. "Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host." Proceedings of the Royal Society B: Biological Sciences 288, no. 1945 (2021): 20203002. http://dx.doi.org/10.1098/rspb.2020.3002.

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The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.

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2

Faccenda, Danilo, and Michelangelo Campanella. "Mitochondria Regulate Inflammatory Paracrine Signalling in Neurodegeneration." Journal of Neuroimmune Pharmacology 15, no. 4 (2020): 565–66. http://dx.doi.org/10.1007/s11481-020-09952-5.

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3

Lin, Yongshun, and Fen Wang. "FGF signalling in prostate development, tissue homoeostasis and tumorigenesis." Bioscience Reports 30, no. 5 (2010): 285–91. http://dx.doi.org/10.1042/bsr20100020.

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The FGFs (fibroblast growth factors) regulate a broad spectrum of biological activities by activating transmembrane FGFR (FGF receptor) tyrosine kinases and their coupled intracellular signalling pathways. In the prostate, the mesenchymal–epithelial interactions mediated by androgen signalling and paracrine factors are essential for gland organogenesis, homoeostasis and tumorigenesis. FGFs mediate these mesenchymal–epithelial interactions in the prostate by paracrinal crosstalk through a diverse set of ligands and receptors. Gain- and loss-of-function studies in mouse models have demonstrated the requirement for the FGF signalling axis in prostate development and homoeostasis. The aberrant induction of this axis in either compartment of the prostate results in developmental disorders, disrupts the homoeostatic balance and leads to prostate carcinogenesis. FGFs are also implicated in mediating androgen signalling in the prostate between mesenchymal and epithelial compartments. Therefore studying FGF signalling in the prostate will help us to better understand the underlying molecular mechanisms by which the gland develops, maintains homoeostasis and undergoes carcinogenesis; as well as yield clues on how androgens mediate these processes and how advanced-tumour prostate cells escape strict androgen regulations.

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4

Yauch, Robert L., Stephen E. Gould, Suzie J. Scales, et al. "A paracrine requirement for hedgehog signalling in cancer." Nature 455, no. 7211 (2008): 406–10. http://dx.doi.org/10.1038/nature07275.

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5

Momiji, Hiroshi, Kirsty L. Hassall, Karen Featherstone, et al. "Disentangling juxtacrine from paracrine signalling in dynamic tissue." PLOS Computational Biology 15, no. 6 (2019): e1007030. http://dx.doi.org/10.1371/journal.pcbi.1007030.

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6

Schumacher, Neele, Stefan Rose-John, and Dirk Schmidt-Arras. "ADAM-Mediated Signalling Pathways in Gastrointestinal Cancer Formation." International Journal of Molecular Sciences 21, no. 14 (2020): 5133. http://dx.doi.org/10.3390/ijms21145133.

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Tumour growth is not solely driven by tumour cell-intrinsic mechanisms, but also depends on paracrine signals provided by the tumour micro-environment. These signals comprise cytokines and growth factors that are synthesized as trans-membrane proteins and need to be liberated by limited proteolysis also termed ectodomain shedding. Members of the family of A disintegrin and metalloproteases (ADAM) are major mediators of ectodomain shedding and therefore initiators of paracrine signal transduction. In this review, we summarize the current knowledge on how ADAM proteases on tumour cells but also on cells of the tumour micro-environment contribute to the formation of gastrointestinal tumours, and discuss how these processes can be exploited pharmacologically.

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7

Gonzalez-Meljem, Jose Mario, and Juan Pedro Martinez-Barbera. "Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis." Cellular and Molecular Life Sciences 78, no. 10 (2021): 4521–44. http://dx.doi.org/10.1007/s00018-021-03798-7.

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AbstractCellular senescence is a process that can prevent tumour development in a cell autonomous manner by imposing a stable cell cycle arrest after oncogene activation. Paradoxically, senescence can also promote tumour growth cell non-autonomously by creating a permissive tumour microenvironment that fuels tumour initiation, progression to malignancy and metastasis. In a pituitary tumour known as adamantinomatous craniopharyngioma (ACP), cells that carry oncogenic β-catenin mutations and overactivate the WNT signalling pathway form cell clusters that become senescent and activate a senescence-associated secretory phenotype (SASP). Research in mouse models of ACP has provided insights into the function of the senescent cell clusters and revealed a critical role for SASP-mediated activities in paracrine tumour initiation. In this review, we first discuss this research on ACP and subsequently explore the theme of paracrine tumourigenesis in other tumour models available in the literature. Evidence is accumulating supporting the notion that paracrine signalling brought about by senescent cells may underlie tumourigenesis across different tumours and cancer models.

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8

Zoni, Eugenio, Gabri van der Pluijm, Peter C. Gray та Marianna Kruithof-de Julio. "Epithelial Plasticity in Cancer: Unmasking a MicroRNA Network for TGF-β-, Notch-, and Wnt-Mediated EMT". Journal of Oncology 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/198967.

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Epithelial-to-mesenchymal transition (EMT) is a reversible process by which cancer cells can switch from a sessile epithelial phenotype to an invasive mesenchymal state. EMT enables tumor cells to become invasive, intravasate, survive in the circulation, extravasate, and colonize distant sites. Paracrine heterotypic stroma-derived signals as well as paracrine homotypic or autocrine signals can mediate oncogenic EMT and contribute to the acquisition of stem/progenitor cell properties, expansion of cancer stem cells, development of therapy resistance, and often lethal metastatic disease. EMT is regulated by a variety of stimuli that trigger specific intracellular signalling pathways. Altered microRNA (miR) expression and perturbed signalling pathways have been associated with epithelial plasticity, including oncogenic EMT. In this review we analyse and describe the interaction between experimentally validated miRs and their target genes in TGF-β, Notch, and Wnt signalling pathways. Interestingly, in this process, we identified a “signature” of 30 experimentally validated miRs and a cluster of validated target genes that seem to mediate the cross talk between TGF-β, Notch, and Wnt signalling networks during EMT and reinforce their connection to the regulation of epithelial plasticity in health and disease.

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9

Moreira, Lucia M., Abhijit Takawale, Mohit Hulsurkar, et al. "Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia." Nature 587, no. 7834 (2020): 460–65. http://dx.doi.org/10.1038/s41586-020-2890-8.

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10

Hooper, Joan E. "Distinct pathways for autocrine and paracrine Wingless signalling inDrosophila embryos." Nature 372, no. 6505 (1994): 461–64. http://dx.doi.org/10.1038/372461a0.

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11

Goudet, Ghylène. "Fertilisation in the horse and paracrine signalling in the oviduct." Reproduction, Fertility and Development 23, no. 8 (2011): 941. http://dx.doi.org/10.1071/rd10285.

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The mammalian oviduct plays a crucial role in the preparation of gametes for fertilisation (transport and final maturation) and fertilisation itself. An increasing number of studies offers a comprehensive overview of the functions of the oviduct and its secretions, but this topic has had limited investigation in the horse. Limited data are available on the final oocyte maturation in the equine oviduct. However, in vitro and in vivo systems have been established to analyse the influence of equine oviduct epithelial cells (OEC) during maturation on the potential of oocytes for fertilisation and development. Most studies focus on the role of the oviduct in equine sperm function, such as spermatozoa transport, attachment to oviduct epithelium, viability, motility and capacitation. Moreover, some possible candidate molecules for sperm–oviducal interactions have been identified in the horse. Finally, the low efficiency of conventional in vitro fertilisation and the in vivo fertilisation of equine oocytes transferred into the oviduct of an inseminated mare predicted an influence of oviduct in equine fertilisation. Actually, in vivo and in vitro experiments demonstrated a role of the oviduct in equine fertilisation. Moreover, recent studies showed a beneficial effect of homologous and heterologous OEC on equine in vitro fertilisation, and some candidate molecules have been studied.

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12

Neuzil, Jiri, Emma Swettenham, Xiu-Fang Wang, Lan-Feng Dong та Michael Stapelberg. "α-Tocopheryl succinate inhibits angiogenesis by disrupting paracrine FGF2 signalling". FEBS Letters 581, № 24 (2007): 4611–15. http://dx.doi.org/10.1016/j.febslet.2007.08.051.

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13

Schumacher, Matthias, and Michael Gelinsky. "Strontium modified calcium phosphate cements – approaches towards targeted stimulation of bone turnover." Journal of Materials Chemistry B 3, no. 23 (2015): 4626–40. http://dx.doi.org/10.1039/c5tb00654f.

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Strontium modified calcium phosphate cements can target local bone turnover by stimulating osteoblast proliferation and differentiation (1) as well as bone mineralisation (2), reducing osteoclastogenesis (3) and resorption activity, increase osteoclast apoptosis (4) and affect osteoblast/osteoclast paracrine signalling (5).

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14

Salter, D. M., S. J. Millward‐Sadler, G. Nuki, and M. O. Wright. "Differential responses of chondrocytes from normal and osteoarthritic human articular cartilage to mechanical stimulation." Biorheology: The Official Journal of the International Society of Biorheology 39, no. 1-2 (2002): 97–108. http://dx.doi.org/10.1177/0006355x2002039001002012.

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Mechanical stimulation is critically important for the maintenance of normal articular cartilage integrity. Molecular events regulating responses of chondrocytes to mechanical forces are beginning to be defined. Chondrocytes from normal human knee joint articular cartilage show increased levels of aggrecan mRNA following 0.33 Hz mechanical stimulation whilst at the same time relative levels of MMP3 mRNA are decreased. This anabolic response, associated with membrane hyperpolarisation, is activated via an integrin‐dependent interleukin (IL)‐4 autocrine/paracrine loop. Work in our laboratory suggests that this chondroprotective response may be aberrant in osteoarthritis (OA). Chondrocytes from OA cartilage show no changes in aggrecan or MMP3 mRNA following 0.33 Hz mechanical stimulation. α5β1 integrin is the mechanoreceptor in both normal and OA chondrocytes but downstream signalling pathways differ. OA chondrocytes show membrane depolarisation following 0.33 Hz mechanical stimulation consequent to activation of an IL1β autocrine/paracrine loop. IL4 signalling in OA chondrocytes is preferentially through the type I (IL4α/cγ) receptor rather than via the type II (IL4α/IL13R) receptor. Altered mechanotransduction and signalling in OA may contribute to changes in chondrocyte behaviour leading to increased cartilage breakdown and disease progression.

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15

Gilchrist, Robert B., and Lesley J. Ritter. "Differences in the participation of TGFB superfamily signalling pathways mediating porcine and murine cumulus cell expansion." REPRODUCTION 142, no. 5 (2011): 647–57. http://dx.doi.org/10.1530/rep-11-0196.

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It is widely held that mammalian cumulus cell (CC) expansion requires oocyte-paracrine signalling, however in three of the four species studied to date, CC expansion occurs in the absence of the oocyte. This study was conducted to examine the paracrine and SMAD/MAPK intracellular signalling mechanism mediating porcine CC expansion, and to compare these to the mouse. Cumulus–oocyte complexes (COCs) and oocyte-free complexes (OOXs) from pigs and eCG-primed mice were treated in vitro with FSH and a broad range of TGFB superfamily antagonists. Expansion of porcine COCs and OOXs was unaffected by neutralisation of growth differentiation factor 9, TGFB, activin A, activin B and a broad spectrum bone morphogenetic protein antagonist. A SMAD-responsive luciferase reporter assay confirmed that porcine oocytes secreted factors that activate SMAD3 and SMAD1/5/8 in granulosa cells, but murine oocytes activated SMAD3 only. Treatment of COCs with a SMAD2/3 phosphorylation inhibitor (SB431542) partially inhibited porcine CC expansion and expression of TNFAIP6, but ablated murine CC expansion. SB431542 was equally effective at attenuating porcine CC expansion in the presence or absence of the oocyte. By contrast, a SMAD1/5/8 phosphorylation inhibitor (dorsomorphin) had no effect on porcine or murine CC function. Inhibition of ERK1/2 and p38 MAPK signalling pathways prevented porcine COC expansion and expression of most matrix genes examined. The activation of CC SMAD signalling by oocytes, and the requirement of SMAD2/3 signalling for expansion, is notably contrasted in pigs and mice. Nonetheless, porcine CC SMAD2/3 signalling is likely to be needed for optimal matrix formation, possibly by facilitating essential MAPK signals.

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16

Moyes, Amie J., and Adrian J. Hobbs. "C-Type Natriuretic Peptide: A Multifaceted Paracrine Regulator in the Heart and Vasculature." International Journal of Molecular Sciences 20, no. 9 (2019): 2281. http://dx.doi.org/10.3390/ijms20092281.

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C-type natriuretic peptide (CNP) is an autocrine and paracrine mediator released by endothelial cells, cardiomyocytes and fibroblasts that regulates vital physiological functions in the cardiovascular system. These roles are conveyed via two cognate receptors, natriuretic peptide receptor B (NPR-B) and natriuretic peptide receptor C (NPR-C), which activate different signalling pathways that mediate complementary yet distinct cellular responses. Traditionally, CNP has been deemed the endothelial component of the natriuretic peptide system, while its sibling peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are considered the endocrine guardians of cardiac function and blood volume. However, accumulating evidence indicates that CNP not only modulates vascular tone and blood pressure, but also governs a wide range of cardiovascular effects including the control of inflammation, angiogenesis, smooth muscle and endothelial cell proliferation, atherosclerosis, cardiomyocyte contractility, hypertrophy, fibrosis, and cardiac electrophysiology. This review will focus on the novel physiological functions ascribed to CNP, the receptors/signalling mechanisms involved in mediating its cardioprotective effects, and the development of therapeutics targeting CNP signalling pathways in different disease pathologies.

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17

Htet, Myo, Jane E. Nally, Patricia E. Martin, and Yvonne Dempsie. "New Insights into Pulmonary Hypertension: A Role for Connexin-Mediated Signalling." International Journal of Molecular Sciences 23, no. 1 (2021): 379. http://dx.doi.org/10.3390/ijms23010379.

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Pulmonary hypertension is a serious clinical condition characterised by increased pulmonary arterial pressure. This can lead to right ventricular failure which can be fatal. Connexins are gap junction-forming membrane proteins which serve to exchange small molecules of less than 1 kD between cells. Connexins can also form hemi-channels connecting the intracellular and extracellular environments. Hemi-channels can mediate adenosine triphosphate release and are involved in autocrine and paracrine signalling. Recently, our group and others have identified evidence that connexin-mediated signalling may be involved in the pathogenesis of pulmonary hypertension. In this review, we discuss the evidence that dysregulated connexin-mediated signalling is associated with pulmonary hypertension.

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18

Robinson, Hugh P. C., and Leanne Li. "Autocrine, paracrine and necrotic NMDA receptor signalling in mouse pancreatic neuroendocrine tumour cells." Open Biology 7, no. 12 (2017): 170221. http://dx.doi.org/10.1098/rsob.170221.

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N -Methyl- d -aspartate receptor (NMDAR) activation is implicated in the malignant progression of many cancer types, as previously shown by the growth-inhibitory effects of NMDAR antagonists. NMDAR-mediated calcium influx and its downstream signalling depend critically, however, on the dynamics of membrane potential and ambient glutamate concentration, which are poorly characterized in cancer cells. Here, we have used low-noise whole-cell patch-clamp recording to investigate the electrophysiology of glutamate signalling in pancreatic neuroendocrine tumour (PanNET) cells derived from a genetically-engineered mouse model (GEMM) of PanNET, in which NMDAR signalling is known to promote cancer progression. Activating NMDARs caused excitation and intracellular calcium elevation, and intracellular perfusion with physiological levels of glutamate led to VGLUT-dependent autocrine NMDAR activation. Necrotic cells, which are often present in rapidly-growing tumours, were shown to release endogenous cytoplasmic glutamate, and necrosis induced by mechanical rupture of the plasma membrane produced intense NMDAR activation in nearby cells. Computational modelling, based on these results, predicts that NMDARs in cancer cells can be strongly activated in the tumour microenvironment by both autocrine glutamate release and necrosis.

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19

Fang, Hsiao Yu, Alfonso Martinez-Arias, and Joaquín de Navascués. "Autocrine and paracrine Wingless signalling in the Drosophila midgut by both continuous gradient and asynchronous bursts of wingless expression." F1000Research 5 (March 10, 2016): 317. http://dx.doi.org/10.12688/f1000research.8170.1.

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Wingless (Wg)/ Wnt signalling is a major regulator of homeostasis in both the mammalian and Drosophila intestine. In Drosophila the organisation and function of Wingless signalling in the adult intestine remain poorly understood. Here we characterise the pattern of expression of wg, the stabilisation of its effector Armadillo in the adult Drosophila midgut, and correlate them with the response of the cells to Wg signalling activation. We show that in normal homeostasis there is a gradient of Wingless signalling in the intestinal stem cell (ISC) and the undifferentiated progenitor cell (enteroblast, EB) populations along the posterior midgut, with a high point at the midgut-hindgut boundary (pylorus). This gradient results from a combination of two sources of Wingless: a distant source outside the epithelium (the pylorus) and a local one from the ISCs and EBs themselves. Altogether, our studies show that Wingless expression and signalling in the epithelium is not continuous, but operates through bursts that occur randomly in space and time.

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20

Winder, Michael, Gunnar Tobin, Daša Zupančič, and Rok Romih. "Signalling Molecules in the Urothelium." BioMed Research International 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/297295.

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The urothelium was long considered to be a silent barrier protecting the body from the toxic effects of urine. However, today a number of dynamic abilities of the urothelium are well recognized, including its ability to act as a sensor of the intravesical environment. During recent years several pathways of these urothelial abilities have been proposed and a major part of these pathways includes release of signalling molecules. It is now evident that the urothelium represents only one part of the sensory web. Urinary bladder signalling is finely tuned machinery of signalling molecules, acting in autocrine and paracrine manner, and their receptors are specifically distributed among different types of cells in the urinary bladder. In the present review the current knowledge of the formation, release, and signalling effects of urothelial acetylcholine, ATP, adenosine, and nitric oxide in health and disease is discussed.

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21

Chen-Kiang, Selina, Scott Ely, Maurizio Di Liberto, et al. "Aberrant Autocrine and Paracrine CD40L Signaling Promotes Primary Myeloma Cell Survival and Attenuates Bortezomib-Induced Apoptosis." Blood 106, no. 11 (2005): 1564. http://dx.doi.org/10.1182/blood.v106.11.1564.1564.

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Abstract In multiple myeloma (MM), impaired apoptosis is critical for clonal expansion of malignant MM cells in the bone marrow (BM), although the precise underlying mechanism has not been defined. During physiologic plasma cell differentiation, clonal expansion of antigen-activated B cells in the germinal center requires CD40 signalling, which mediates CD40L signals from activated T cells to promote B cell activation and survival. Terminal differentiation of plasma cells from activated B cells is then accompanied by a progressive reduction of CD40 expression, suggesting that the life span of normal plasma cells may be limited by the loss of CD40L signalling. Here we show that CD40L and CD40 are both aberrantly expressed in primary BM MM cells, but not in normal BM plasma cells, their likely normal counterparts. CD40L is also copiously expressed in multiple cell types in myeloma and normal bone marrows, indicating that autocrine and paracrine CD40L signalling may prolong the survival of MM cells in the bone marrow microenvironment. Supporting this hypothesis, disruption of CD40L signalling by an antagonizing CD40L antibody markedly accelerates apoptosis of BM MM cells ex vivo. In the majority of MM cases (N=50), CD40 is expressed at either greater than 90% of BM MM cells or lower than 30% of BM MM cells in vivo, but rarely in between. However, there is no apparent correlation between the frequency of CD40 expression in BM MM cells in vivo and immunoglobulin isotype or treatment history, including bortezomib therapy. Ex vivo, the level of CD40 expression in BM MM cells is enhanced in response to bortezomib, which rapidly activates CD40 transcription. Moreover, killing of primary BM MM cells by bortezomib ex vivo is attenuated by CD40L signalling, at least in part through sustaining NF-?B activation that is required for MM cell survival. Together, our findings suggest that autocrine and paracrine CD40L signalling is critical for the survival of MM cells in the bone marrow and may contribute to the development of drug resistance.

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22

Lin, Guonan, Na Xu, and Rongwen Xi. "Paracrine Wingless signalling controls self-renewal of Drosophila intestinal stem cells." Nature 455, no. 7216 (2008): 1119–23. http://dx.doi.org/10.1038/nature07329.

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23

Rass, Atarah, Carla Eksteen, and Anna-Mart Engelbrecht. "Paracrine signalling in breast cancer: Insights into the tumour endothelial phenotype." Acta Histochemica 126, no. 5-7 (2024): 152191. http://dx.doi.org/10.1016/j.acthis.2024.152191.

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24

Gilchrist, R. B. "Molecular basis of oocyte-paracrine signalling that promotes granulosa cell proliferation." Journal of Cell Science 119, no. 18 (2006): 3811–21. http://dx.doi.org/10.1242/jcs.03105.

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25

Moreau, M., B. Rivière, J. Ramos, E. Assenat, and U. Hibner. "O029 : HCV triggers Wnt paracrine signalling that modulates metabolic liver zonation." Journal of Hepatology 62 (April 2015): S204. http://dx.doi.org/10.1016/s0168-8278(15)30037-4.

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26

Brownlee, C. "Role of the extracellular matrix in cell–cell signalling: paracrine paradigms." Current Opinion in Plant Biology 5, no. 5 (2002): 396–401. http://dx.doi.org/10.1016/s1369-5266(02)00286-8.

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27

Hervera, Arnau, Celio X. Santos, Francesco De Virgiliis, Ajay M. Shah, and Simone Di Giovanni. "Paracrine Mechanisms of Redox Signalling for Postmitotic Cell and Tissue Regeneration." Trends in Cell Biology 29, no. 6 (2019): 514–30. http://dx.doi.org/10.1016/j.tcb.2019.01.006.

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28

Zunich, Samantha M., Taneka Douglas, Maria Valdovinos, et al. "Paracrine sonic hedgehog signalling by prostate cancer cells induces osteoblast differentiation." Molecular Cancer 8, no. 1 (2009): 12. http://dx.doi.org/10.1186/1476-4598-8-12.

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29

Yu, Jiaquan, Erwin Berthier, Alexandria Craig, et al. "Reconfigurable open microfluidics for studying the spatiotemporal dynamics of paracrine signalling." Nature Biomedical Engineering 3, no. 10 (2019): 830–41. http://dx.doi.org/10.1038/s41551-019-0421-4.

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Thomas, Stacy K., Jesse Lee, and Gregory L. Beatty. "Paracrine and cell autonomous signalling in pancreatic cancer progression and metastasis." EBioMedicine 53 (March 2020): 102662. http://dx.doi.org/10.1016/j.ebiom.2020.102662.

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D'ANDREA, Paola, Alessandra CALABRESE, and Micaela GRANDOLFO. "Intercellular calcium signalling between chondrocytes and synovial cells in co-culture." Biochemical Journal 329, no. 3 (1998): 681–87. http://dx.doi.org/10.1042/bj3290681.

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Intercellular communication allows the co-ordination of cell metabolism between tissues as well as sensitivity to extracellular stimuli. Paracrine stimulation and cell-to-cell coupling through gap junctions induce the formation of complex cellular networks that favour the intercellular exchange of nutrients and second messengers. Heterologous intercellular communication was studied in co-cultures of articular chondrocytes and HIG-82 synovial cells by measuring mechanically induced cytosolic changes in Ca2+ ion levels by digital fluorescence video imaging. In confluent co-cultures, mechanical stimulation induced intercellular Ca2+ waves that propagated to both cell types with similar kinetics. Intercellular wave spreading was inhibited by 18α-glycyrrhetinic acid and by treatments inhibiting the activation of purinoreceptors, suggesting that intercellular signalling between these two cell types occurs both through gap junctions and ATP-mediated paracrine stimulation. In rheumatoid arthritis the formation of the synovial pannus induces structural changes at the chondrosynovial junction, where chondrocyte and synovial cells come into close apposition: these results provide the first evidence for direct intercellular communication between these two cell types.

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Ludwig, Mike, and Javier Stern. "Multiple signalling modalities mediated by dendritic exocytosis of oxytocin and vasopressin." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1672 (2015): 20140182. http://dx.doi.org/10.1098/rstb.2014.0182.

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The mammalian hypothalamic magnocellular neurons of the supraoptic and paraventricular nuclei are among the best understood of all peptidergic neurons. Through their anatomical features, vasopressin- and oxytocin-containing neurons have revealed many important aspects of dendritic functions. Here, we review our understanding of the mechanisms of somato-dendritic peptide release, and the effects of autocrine, paracrine and hormone-like signalling on neuronal networks and behaviour.

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Wiszniak, Sophie, and Quenten Schwarz. "Exploring the Intracrine Functions of VEGF-A." Biomolecules 11, no. 1 (2021): 128. http://dx.doi.org/10.3390/biom11010128.

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Vascular endothelial growth factor A (VEGF-A or VEGF) is a highly conserved secreted signalling protein best known for its roles in vascular development and angiogenesis. Many non-endothelial roles for VEGF are now established, with the discovery that VEGF and its receptors VEGFR1 and VEGFR2 are expressed in many non-vascular cell-types, as well as various cancers. In addition to secreted VEGF binding to its receptors in the extracellular space at the cell membrane (i.e., in a paracrine or autocrine mode), intracellularly localised VEGF is emerging as an important signalling molecule regulating cell growth, survival, and metabolism. This intracellular mode of signalling has been termed “intracrine”, and refers to the direct action of a signalling molecule within the cell without being secreted. In this review, we describe examples of intracrine VEGF signalling in regulating cell growth, differentiation and survival, both in normal cell homeostasis and development, as well as in cancer. We further discuss emerging evidence for the molecular mechanisms underpinning VEGF intracrine function, as well as the implications this intracellular mode of VEGF signalling may have for use and design of anti-VEGF cancer therapeutics.

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Wit, Jan M., Wilma Oostdijk, Monique Losekoot, Hermine A. van Duyvenvoorde, Claudia A. L. Ruivenkamp, and Sarina G. Kant. "MECHANISMS IN ENDOCRINOLOGY: Novel genetic causes of short stature." European Journal of Endocrinology 174, no. 4 (2016): R145—R173. http://dx.doi.org/10.1530/eje-15-0937.

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The fast technological development, particularly single nucleotide polymorphism array, array-comparative genomic hybridization, and whole exome sequencing, has led to the discovery of many novel genetic causes of growth failure. In this review we discuss a selection of these, according to a diagnostic classification centred on the epiphyseal growth plate. We successively discuss disorders in hormone signalling, paracrine factors, matrix molecules, intracellular pathways, and fundamental cellular processes, followed by chromosomal aberrations including copy number variants (CNVs) and imprinting disorders associated with short stature. Many novel causes of GH deficiency (GHD) as part of combined pituitary hormone deficiency have been uncovered. The most frequent genetic causes of isolated GHD areGH1andGHRHRdefects, but several novel causes have recently been found, such asGHSR,RNPC3, andIFT172mutations. Besides well-defined causes of GH insensitivity (GHR,STAT5B,IGFALS,IGF1defects), disorders of NFκB signalling,STAT3andIGF2have recently been discovered. HeterozygousIGF1Rdefects are a relatively frequent cause of prenatal and postnatal growth retardation.TRHAmutations cause a syndromic form of short stature with elevated T3/T4ratio. Disorders of signalling of various paracrine factors (FGFs, BMPs, WNTs, PTHrP/IHH, and CNP/NPR2) or genetic defects affecting cartilage extracellular matrix usually cause disproportionate short stature. HeterozygousNPR2orSHOXdefects may be found in ∼3% of short children, and also rasopathies (e.g., Noonan syndrome) can be found in children without clear syndromic appearance. Numerous other syndromes associated with short stature are caused by genetic defects in fundamental cellular processes, chromosomal abnormalities, CNVs, and imprinting disorders.

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Breznik, Barbara, Helena Motaln, and Tamara Lah Turnšek. "Proteases and cytokines as mediators of interactions between cancer and stromal cells in tumours." Biological Chemistry 398, no. 7 (2017): 709–19. http://dx.doi.org/10.1515/hsz-2016-0283.

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Abstract Proteolytic enzymes are highly relevant in different processes of cancer progression. Their interplay with other signalling molecules such as cytokines represents important regulation of multicellular cross-talk. In this review, we discuss protease regulation mechanisms of cytokine signalling in various types of cancer. Additionally, we highlight the reverse whereby cytokines have an impact on protease expression in an autocrine and paracrine manner, representing complex feedback mechanisms among multiple members of these two protein families. The relevance of the protease-cytokine axis is illustrated in glioblastoma, where interactions between normal mesenchymal stem cells and cancer cells play an important role in this very malignant form of brain cancer.

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Taylor–King, Jake P., Etienne Baratchart, Andrew Dhawan, et al. "Simulated ablation for detection of cells impacting paracrine signalling in histology analysis." Mathematical Medicine and Biology: A Journal of the IMA 36, no. 1 (2018): 93–112. http://dx.doi.org/10.1093/imammb/dqx022.

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Hollins, R., A. I. Freeman, P. J. Cripps, A. D. Radford, and P. J. M. Noble. "PWE-007 Paracrine prostaglandin-E signalling modulates canine gastric epithelial cell migration." Gut 61, Suppl 2 (2012): A299.1—A299. http://dx.doi.org/10.1136/gutjnl-2012-302514d.7.

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Ward, M., X. Shen, and S. Kaur. "Stretch-Activated Paracrine/Autocrine Signalling in the Heart: A Role for Prostaglandins?" Heart, Lung and Circulation 25 (August 2016): S82. http://dx.doi.org/10.1016/j.hlc.2016.06.191.

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Chaudhry, S. I., S. Hooper, E. Nye, P. Williamson, K. Harrington та E. Sahai. "Autocrine IL-1β-TRAF6 signalling promotes squamous cell carcinoma invasion through paracrine TNFα signalling to carcinoma-associated fibroblasts". Oncogene 32, № 6 (2012): 747–58. http://dx.doi.org/10.1038/onc.2012.91.

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Mäkelä, Juho-Antti, Vuokko Saario, Sonia Bourguiba-Hachemi, et al. "Hedgehog signalling promotes germ cell survival in the rat testis." REPRODUCTION 142, no. 5 (2011): 711–21. http://dx.doi.org/10.1530/rep-11-0110.

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Hedgehog (Hh) signalling has a crucial role in testis development. Sertoli cell-derived desert hedgehog (DHH) guides the formation of testis cords and differentiation of foetal-type Leydig cells. Dhh mutant mice are infertile due to a block in germ cell differentiation, hypogonadism and hypoandrogenism. Hh signalling pathway components are also expressed in postnatal testis. In the rat testis the transcription factor of the Hh pathway, glioma-associated oncogene homologue (GLI1), is expressed by a wide variety of germ cells. This suggests that Hh signalling is involved in spermatogenesis at many different levels. Our data show that canonical Hh signalling is turned off in early condensing spermatids that strongly express the negative regulator of the pathway, suppressor of fused (SUFU). Most of the Hh pathway specific mRNAs display the highest values in stages II–VI of the rat seminiferous epithelial cycle. The key endocrine regulator of germ cell differentiation, FSH, down-regulates Dhh mRNA levels in vitro. Hh signalling inhibition in vitro leads to massive apoptosis of germ cells. In prepubertal rat testis imatinib mesylate-induced inhibition of tyrosine kinases impinges on Dhh transcript levels and Hh signalling. Our data indicate that Hh signalling is part of the paracrine signalling network in the rat testis. It promotes the survival of germ cells and is suppressed by FSH.

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Díaz del Moral, Sandra, Maha Benaouicha, Ramón Muñoz-Chápuli, and Rita Carmona. "The Insulin-like Growth Factor Signalling Pathway in Cardiac Development and Regeneration." International Journal of Molecular Sciences 23, no. 1 (2021): 234. http://dx.doi.org/10.3390/ijms23010234.

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Insulin and Insulin-like growth factors (IGFs) perform key roles during embryonic development, regulating processes of cell proliferation and survival. The IGF signalling pathway comprises two IGFs (IGF1, IGF2), two IGF receptors (IGFR1, IGFR2), and six IGF binding proteins (IGFBPs) that regulate IGF transport and availability. The IGF signalling pathway is essential for cardiac development. IGF2 is the primary mitogen inducing ventricular cardiomyocyte proliferation and morphogenesis of the compact myocardial wall. Conditional deletion of the Igf1r and the insulin receptor (Insr) genes in the myocardium results in decreased cardiomyocyte proliferation and ventricular wall hypoplasia. The significance of the IGF signalling pathway during embryonic development has led to consider it as a candidate for adult cardiac repair and regeneration. In fact, paracrine IGF2 plays a key role in the transient regenerative ability of the newborn mouse heart. We aimed to review the current knowledge about the role played by the IGF signalling pathway during cardiac development and also the clinical potential of recapitulating this developmental axis in regeneration of the adult heart.

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Eftekhari, Rahil, Stacy G. de Lima, Yu Liu, et al. "Microenvironment proteinases, proteinase-activated receptor regulation, cancer and inflammation." Biological Chemistry 399, no. 9 (2018): 1023–39. http://dx.doi.org/10.1515/hsz-2018-0001.

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AbstractWe propose that in the microenvironment of inflammatory tissues, including tumours, extracellular proteinases can modulate cell signalling in part by regulating proteinase-activated receptors (PARs). We have been exploring this mechanism in a variety of inflammation and tumour-related settings that include tumour-derived cultured cells from prostate and bladder cancer, as well as immune inflammatory cells that are involved in the pathology of inflammatory diseases including multiple sclerosis. Our work showed that proteinase signalling via the PARs affects prostate and bladder cancer-derived tumour cell behaviour and can regulate calcium signalling in human T-cell and macrophage-related inflammatory cells as well as in murine splenocytes. Further, we found that the tumour-derived prostate cancer cells and immune-related cells (Jurkat, THP1, mouse splenocytes) can produce PAR-regulating proteinases (including kallikreins: kallikrein-related peptidases), that can control tissue function by both a paracrine and autocrine mechanism. We suggest that this PAR-driven signalling process involving secreted microenvironment proteinases can play a key role in cancer and inflammatory diseases including multiple sclerosis.

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Zachary, I. "VEGF signalling: integration and multi-tasking in endothelial cell biology." Biochemical Society Transactions 31, no. 6 (2003): 1171–77. http://dx.doi.org/10.1042/bst0311171.

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The central role of VEGF (vascular endothelial growth factor A) in angiogenesis is dependent upon its ability to co-ordinately regulate multiple endothelial functions. The multifunctionality of VEGF at the cellular level results from its ability to initiate a diverse, complex and integrated network of signalling pathways via its major receptor, kinase-insert-domain-containing receptor (KDR). Activation of phospholipase C-γ, protein kinase C, Ca2+, ERK (extracellular-signal-regulated protein kinase), Akt, Src, focal adhesion kinase and calcineurin pathways has been implicated in mediating multiple VEGF functions, including survival, proliferation, migration, vascular permeability, tubulogenesis, NO and prostanoid synthesis, and gene expression. NO and prostanoids in turn play paracrine and autocrine roles in linking post-receptor signalling to biological functions. Integration between biologically important signalling cascades occurs at several points. Akt and ERK, for example, are key junction points linking together signal transduction involved in survival and NO generation, and proliferation and prostanoid biosynthesis. Together, the multiplicity, functional versatility and integration of VEGF signalling provide a useful framework for understanding the mechanisms underlying the endothelial biological response to this key factor.

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Yang, Y. H. C., M. Szabat, C. Bragagnini, et al. "Paracrine signalling loops in adult human and mouse pancreatic islets: netrins modulate beta cell apoptosis signalling via dependence receptors." Diabetologia 54, no. 4 (2011): 828–42. http://dx.doi.org/10.1007/s00125-010-2012-5.

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Smythe, Gayle, and Jason White. "Therapeutic Strategies that Target Epigenetic, Paracrine and Signalling Control of Skeletal Muscle Regeneration." Recent Patents on Regenerative Medicinee 3, no. 1 (2012): 17–33. http://dx.doi.org/10.2174/2210296511303010017.

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Smythe, Gayle, and Jason White. "Therapeutic Strategies that Target Epigenetic, Paracrine and Signalling Control of Skeletal Muscle Regeneration." Recent Patents on Regenerative Medicine 3, no. 1 (2012): 17–33. http://dx.doi.org/10.2174/22102965130103.

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Paragh, Gyorgy. "Epidermal melanoma prognostic factors: a link to paracrine transforming growth factor‐β signalling". British Journal of Dermatology 186, № 4 (2022): 606–7. http://dx.doi.org/10.1111/bjd.20981.

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Skals, M., and H. A. Praetorius. "Mechanisms of cytolysin-induced cell damage - a role for auto- and paracrine signalling." Acta Physiologica 209, no. 2 (2013): 95–113. http://dx.doi.org/10.1111/apha.12156.

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Köhn-Luque, Alvaro, Walter de Back, Jörn Starruß, et al. "Early Embryonic Vascular Patterning by Matrix-Mediated Paracrine Signalling: A Mathematical Model Study." PLoS ONE 6, no. 9 (2011): e24175. http://dx.doi.org/10.1371/journal.pone.0024175.

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Gilchrist, R. B., L. J. Ritter, S. Myllymaa, et al. "247.Molecular basis of oocyte - paracrine signalling that promotes mouse granulosa cell proliferation." Reproduction, Fertility and Development 16, no. 9 (2004): 247. http://dx.doi.org/10.1071/srb04abs247.

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Oocytes regulate follicle growth and development by secreting paracrine growth factors that act on granulosa cells (GC). We have recently determined that growth differentiation factor-9 (GDF-9) accounts for ~50% of the total mitogenic activity of oocytes, the remaining portion is as yet uncharacterised. This study was conducted to identify the receptor/signalling system utilised by oocytes to promote GC proliferation. We used an established oocyte-secreted mitogen bioassay, where denuded oocytes are co-cultured with primed-mouse mural GC. In this system, oocytes, GDF-9, TGF-b1 and activin-A all promoted GC DNA synthesis in a dose-dependent manner, but bone-morphogenetic protein-6 (BMP-6) and BMP-7 did not. The type-II receptor for GDF-9 is BMPRII and using real-time RT-PCR, cumulus cells (CC) and mural GC were found to express equivalent levels of BMPRII mRNA. We tested the capacity of the receptor ectodomain (ECD) to neutralise oocyte-stimulated mural GC proliferation. The BMPRII ECD antagonised both oocyte and GDF-9 bioactivity in a dose-dependent manner, completely abolishing activity of both mitogens at 1 ug/mL. The BMPRII ECD did not antagonise TGF-β and partially antagonised activin-A bioactivity, demonstrating its specificity. The TGFβR-II ECD, activin R-II ECD and activin R-IIB ECD all failed to neutralise oocyte- or GDF-9-stimulated GC DNA synthesis, whereas they did antagonise the activity of their respective ligands. The BMPRII ECD also completely antagonised oocyte-stimulated CC DNA synthesis. Using this oocyte-factor bioassay with mural GC transfected with Smad luciferase reporter constructs, we found that oocytes, GDF-9 and TGF-β (but not BMP-6) activated the Smad2/3 pathway. Consistent with this, oocytes and GDF-9 led to phosphorylation of GC Smad2 molecules as detected by Western blot. Conversely the Smad1/5/8 pathway was activated by BMP-6, but not by GDF-9, TGF-β nor surprisingly by oocytes. This study provides evidence that BMPRII is a key receptor for transmitting the paracrine actions of oocytes in GC. However, oocyte-secreted factors do not activate the BMP intracellular signalling pathway but rather the TGF-β/activin intracellular pathway.

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