Cell membrane receptors for cardiac glycosides in the heart

1977 ◽  
Vol 72 (4) ◽  
pp. 315-325 ◽  
Author(s):  
E. Erdmann
Keyword(s):  
Cell Membrane ◽  
Cardiac Glycosides ◽  
Membrane Receptors

scholarly journals Reprogramming of Mesothelial-Mesenchymal Transition in Chronic Peritoneal Diseases by Estrogen Receptor Modulation and TGF-β1 Inhibition

2020 ◽  
Vol 21 (11) ◽  
pp. 4158
Author(s):  
Robert B. Wilson ◽  
Rami Archid ◽  
Marc A. Reymond
Keyword(s):  
Estrogen Receptor ◽  
Cell Membrane ◽  
Peritoneal Metastasis ◽  
Tyrosine Kinases ◽  
Membrane Receptors ◽  
Host Cells ◽  
Potential Candidate ◽  
Mesenchymal Transition ◽  
Receptor Modulation ◽  
Tgf Β1

In chronic peritoneal diseases, mesothelial-mesenchymal transition is determined by cues from the extracellular environment rather than just the cellular genome. The transformation of peritoneal mesothelial cells and other host cells into myofibroblasts is mediated by cell membrane receptors, Transforming Growth Factor β1 (TGF-β1), Src and Hypoxia-inducible factor (HIF). This article provides a narrative review of the reprogramming of mesothelial mesenchymal transition in chronic peritoneal diseases, drawing on the similarities in pathophysiology between encapsulating peritoneal sclerosis and peritoneal metastasis, with a particular focus on TGF-β1 signaling and estrogen receptor modulators. Estrogen receptors act at the cell membrane/cytosol as tyrosine kinases that can phosphorylate Src, in a similar way to other receptor tyrosine kinases; or can activate the estrogen response element via nuclear translocation. Tamoxifen can modulate estrogen membrane receptors, and has been shown to be a potent inhibitor of mesothelial-mesenchymal transition (MMT), peritoneal mesothelial cell migration, stromal fibrosis, and neoangiogenesis in the treatment of encapsulating peritoneal sclerosis, with a known side effect and safety profile. The ability of tamoxifen to inhibit the transduction pathways of TGF-β1 and HIF and achieve a quiescent peritoneal stroma makes it a potential candidate for use in cancer treatments. This is relevant to tumors that spread to the peritoneum, particularly those with mesenchymal phenotypes, such as colorectal CMS4 and MSS/EMT gastric cancers, and pancreatic cancer with its desmoplastic stroma. Morphological changes observed during mesothelial mesenchymal transition can be treated with estrogen receptor modulation and TGF-β1 inhibition, which may enable the regression of encapsulating peritoneal sclerosis and peritoneal metastasis.

Cytosolic Calcium Oscillations in Smooth Muscle Cells

Physiology ◽  
2000 ◽  
Vol 15 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Jean-Pierre Savineau ◽  
Roger Marthan
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Smooth Muscle Cells ◽  
Inositol Trisphosphate ◽  
Muscle Cells ◽  
Cytosolic Calcium ◽  
Calcium Oscillations ◽  
Membrane Receptors ◽  
Cell Membrane Potential

In a variety of smooth muscle cells, agonists activating membrane receptors induce oscillations in the cytoplasmic Ca2+ concentration via an inositol trisphosphate-activated mechanism. Ca2+ oscillations participate in the control of cell membrane potential and the tone of smooth muscle. There is evidence that alterations in Ca2+ oscillations modulate smooth muscle responsiveness.

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