Reproduction
Frank J. Dye in Human Life Before Birth, 2019
In addition to cells communicating over relatively long distances, for example, by nerve impulses and neurotransmitters of the nervous system or by hormones of the endocrine system, cells may communicate over shorter distances. Cell communication over shorter distances occurs by paracrine, juxtacrine, or autocrine signaling. If a cell has receptors for signal molecules it itself produces, this is called autocrine signaling, a relatively rare kind of signaling, but exemplified by the cytotrophoblast cells of the placenta, which make and secrete platelet-derived growth factor (PDGF), the receptors for which are found on the very same cells, this results in the explosive growth of the cytotrophoblast, which is instrumental in the implantation of the embryo into the lining of the uterus, whereby a pregnancy is initiated. If the signaling molecules are embedded in the plasma membranes of the cells producing them, and the receptors for them are embedded in the plasma membranes of neighboring cells, then juxtacrine signaling is occurring. If the cells making and secreting the signaling molecules attach to receptors of nearby cells, then paracrine signaling is occurring.
Tissue injury and repair
C. Simon Herrington in Muir's Textbook of Pathology, 2020
At least three types of extracellular signal can initiate these events. First, there are substances that are secreted by the cells themselves, i.e. a cell produces a growth factor together with the relevant receptor and can, therefore, control its own proliferation. This is referred to as autocrine signalling and occurs in epithelial proliferation in skin wounds and in liver regeneration; it is also a feature of some tumours. The second form is where the molecules stimulating proliferation are produced by cells near the target cell. As we shall see, this occurs in the connective tissue response of repair where, for example, growth factors produced by inflammatory cells can stimulate the proliferation of endothelial and mesenchymal cells. This is referred to as paracrine signalling. Finally, substances produced at a distant site, such as a separate organ, and carried by the blood can also control cell proliferation. This is referred to as endocrine signalling (Figure 3.14).
Finding a Target
Nathan Keighley in Miraculous Medicines and the Chemistry of Drug Design, 2020
There are three forms of signalling mediated by secreted molecules: paracrine, synaptic, and endocrine. Signalling molecules secreted by cells to act as local mediators, which only effect cells in the immediate environment, must not be allowed to diffuse too far, so are rapidly taken up by the neighbouring cells, or destroyed by extracellular enzymes, or immobilised by the extracellular matrix. This is called paracrine signalling. For multicellular organisms to be able to coordinate cell behaviour across the entire organism, some signalling molecules must travel far afield to distant cells. This is achieved in two ways: by networks of nerve cells and by the action of hormones. Synaptic signalling involves routes of neurones along which electrochemical impulses travel to stimulate the release of chemical signals called neurotransmitter, which carry the signal on between neurones across gaps called synaptic junctions and propagate the electrochemical impulse in the adjoining neurone. Endocrine cells release hormones, which are signalling molecules that travel in the bloodstream of an animal (or sap in plants) and thus distribute widely throughout the body, enabling signals to be carried to distant cells. Since this process relies on diffusion, it is much slower than synaptic signalling.
Epicardial transplantation of autologous atrial appendage micrografts: evaluation of safety and feasibility in pigs after coronary artery occlusion
Published in Scandinavian Cardiovascular Journal, 2022
Annu Nummi, Tommi Pätilä, Severi Mulari, Milla Lampinen, Tuomo Nieminen, Mikko I. Mäyränpää, Antti Vento, Ari Harjula, Esko Kankuri
The number of cardiomyocytes in adult heart remains approximately the same during a lifetime [41,42] and the growth in adult mammalian heart occurs in cell size rather than increase in cells. Despite numerous efforts to generate new cardiac muscle cells via stem/progenitor cell technologies, there is no desired outcome. Bin Zhou and colleagues provided evidence that there is no cardiomyocyte producing stem cell population in the adult mammalian heart [43]. Yet there are promising results documented in improvement of LVEF, ventricular remodeling, and reduction of the infarct scar in both preclinical and clinical studies with stem cells [38–45]. With this paradoxical result, further investigations, especially focusing on elucidating the mechanism of action, on cell therapy in heart failure are necessary. The effect and importance of paracrine signaling, different delivery methods, cell sources, and used cell types all need better understanding and more large-scale, randomized trials.
The evolution into personalized therapies in pancreatic ductal adenocarcinoma: challenges and opportunities
Published in Expert Review of Anticancer Therapy, 2018
Anteneh A. Tesfaye, Mandana Kamgar, Asfar Azmi, Philip A. Philip
PSCs, whose exact origin is unknown, play an important role in this network. In the normal pancreas, they make up 4% of all parenchymal cells [37]. These cells are activated by paracrine signaling from the surrounding cancer cells, immune or endothelial cells in the context of benign inflammation or malignancy [38]. Upon activation, these cells undergo transformation into myofibroblast-like cells expressing the cytoskeletal protein alpha smooth muscle actin. In this conformation, the stellate cells increase their proliferation, migration, and ECM protein synthesis [39]. Activated PSCs can induce cancer cell proliferation, while decreasing cancer cell apoptosis. They can also stimulate cancer cell migration, through increased epithelial mesenchymal transition of cancer cells [40]. PSCs have chemotactic effect on CD8+ T cells through secretion of CXCL12 [41] and on myeloid-derived suppressor cells (MDSCs) through the secretion of IL 6 [42]. MDSCs are known to suppress immune response to the tumor, and hence lead to immune evasion by cancer cells. PSCs also produce vascular endothelial growth factor (VEGF) and the hepatocyte growth factor and activate cMET pathway hence promoting angiogenesis [43,44]. It has been proposed that PSCs can also travel to metastatic site and facilitate seeding, survival, and proliferation of the metastatic cancer cells at their new sites [43]. It is important to note that these findings are derived from in vitro studies and in vivo murine models and that there are species as well as donor-dependent variances between murine and human PSCs
Immune vulnerability of ovarian cancer stem-like cells due to low CD47 expression is protected by surrounding bulk tumor cells
Published in OncoImmunology, 2020
Chih-Long Chang, Chao-Chih Wu, Yun-Ting Hsu, Yi-Chiung Hsu
A recent study showed that chemotherapy usually leaves behind an entity of CSC-like cells, which are more invasive and induce disease relapse.8 Conversely, recurrent ovarian cancers are enriched with CSCs, indicating that CSCs might contribute to cancer recurrence.9 Residual CSCs that survive chemotherapy might provide a favorable microenvironment to facilitate the growth of residual cells. This environment provides not only autocrine and paracrine signaling but also has a complex immune network interacting with surrounding cells. Understanding CSC immunoreactivity is important to improve the treatment and prevention of ovarian cancer recurrence.
Related Knowledge Centers
- Autocrine Signaling
- Cell Biology
- Cell Signaling
- Diffusion
- Endocrine System
- Circulatory System
- Cell
- Hormone
- Juxtacrine Signalling
- Receptor