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The response of endothelial cells to endogenous bioelectric fields
Published in Ze Zhang, Mahmoud Rouabhia, Simon E. Moulton, Conductive Polymers, 2018
Endothelial cells are the primary producers of NO, a well-documented vasodilator. NO is synthesized by endothelial nitric oxide synthase (eNOS), from the substrate L-arginine. eNOS has been shown to associate with the plasma membrane of endothelial cells. There, it interacts with a number of receptor families, modulating the production of NO via calcium- and phosphorylation-dependent pathways. After the stimulation of a G protein–coupled receptor (e.g., bradykinin or acetylcholine), inositol trisphosphate (IP3) is generated and binds to the IP3 receptor on the endoplasmic reticulum. The intracellular calcium level increases, due to the emptying of the endoplasmic reticulum and the concomitant flux of extracellular calcium into the cell. This elevated intracellular calcium then binds calmodulin ([Ca2+]i–calmodulin), activating an electron transport chain that facilitates the above eNOS reaction, which converts L-arginine into NO and L-citrullene (Becker et al. 2006).
Preparation of pure lower-order myo-Inositol phosphates on laboratory scale for physiological and enzymatic studies
Published in Preparative Biochemistry & Biotechnology, 2021
Enzymatic phytate dephosphorylation was applied to have access to individual lower-order myo-inositol phosphates. To increase the yield of a specific myo-inositol phosphate isomer in the reaction mixture, enzymatic dephosphorylation could be controlled for example by adjusting incubation time, phytate concentration or the phytase level. In the present study, only incubation time was used to control the amount of myo-inositol pentakis-, -tetrakis-, -trisphosphates in the reaction mixture (Fig. 2). With Natuphos, the highest myo-inositol pentakisphosphate concentration in the reaction mixture was obtained after 10 min of enzymatic phytate dephosphorylation. An incubation time between 20 and 60 min resulted in the presence of predominantly myo-inositol tetrakisphosphate in the reaction mixture, reaching a peak at an incubation time of 40 min. At an incubation time of 80 and 100 min, myo-inositol trisphosphate was identified as the major phytate dephosphorylation product. A very similar course of phytate dephosphorylation was also obtained with Natuphos E (data not shown).
Targeting gap junctional intercellular communication by hepatocarcinogenic compounds
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Kaat Leroy, Alanah Pieters, Andrés Tabernilla, Axelle Cooreman, Raf Van Campenhout, Bruno Cogliati, Mathieu Vinken
Gap junctions are a group of cell-to-cell contacts composed of 2 hemichannels of adjacent cells, which in turn are built up by 6 connexin (Cx) proteins (Figure 1) (Cooreman et al. 2019). Thus far, more than 21 human connexin family members were identified, all that are expressed in a cell type-specific manner (Cooreman et al. 2019; Tachikawa et al. 2020). In liver, hepatocytes abundantly produce Cx32 and to a lesser extent Cx26, whereas non-parenchymal hepatic cell populations, including Kupffer cells, endothelial cells and stellate cells, mainly express Cx43 (Berthoud et al. 1992; Fischer et al. 2005; Greenwel et al. 1993; Saez 1997). Cx32 is uniformly produced by hepatocytes, while Cx26 is preferentially expressed in the periportal acinar area (Rosenberg, Spray, and Reid 1992). All connexin proteins are named after their respective molecular weight and share the same topology consisting of 4 transmembrane regions, 2 extracellular loops, 1 cytoplasmic loop and an intracellular C-terminus and N-terminus. Approximately 3% of the membrane surface of hepatocytes is covered with gap junctions, which are organized in plaques. A gap junction typically measures 180Å in length and 15Å in diameter, enabling passive diffusion of small and hydrophilic molecules, such as glutamate, glucose, inositol trisphosphate, glutathione, adenosine trisphosphate and cyclic adenosine monophosphate (cAMP), as well as ions, including calcium, potassium and sodium (Vinken et al. 2008b). Thus, gap junctions control all facets of the cellular life cycle ranging from cell growth to cell death (Vinken et al. 2006).
Intra-carotid body inter-cellular communication
Published in Journal of the Royal Society of New Zealand, 2023
Liam P. Argent, Aabharika Bose, Julian F. R. Paton
For example: type I cells release ACh when stimulated (Zhang et al. 2000) and the activation of type I cell α4 and α7 nAChRs depolarises type I cells (Wyatt and Peers 1993; Meza et al. 2012). Further, the activation of either nAChRs or mAChRs expressed by type I cells elevates type I cell [Ca2+]i (Dasso et al. 1997). In the case of mAChRs, the [Ca2+]i response was found to be biphasic, with a rapid initial phase that was dependent on internal Ca2+ stores and a slower secondary phase that was dependent on external Ca2+ (Dasso et al. 1997). [Ca2+]i is increased above baseline in both phases (Dasso et al. 1997). These observations are consistent with the mAChRs in question being Gq coupled (i.e. either M1, M3 or M5 mAChRs) as the first and second phases are well explained by inositol trisphosphate receptor-mediated Ca2+ release from the ER and the inhibition of background K+ leak TASK channels via diacylglycerol respectively (Ortiz and Varas 2010). Indeed, it does appears that M1 mAChRs have a functional, excitatory role in the carotid body (Bairam et al. 1985, 2006; Wang and Fitzgerald 2002) and are expressed by glomus cells (Shirahata et al. 2004) (M2 mAChRs are seemingly also expressed by glomus cells (Shirahata et al. 2004 but are presumably functionally dominated either by M1 mAChRs alone or M1 mAChRs working in concert with M3 and / or M5 mAChRs). The combination of stimulation-induced release of ACh from type I cells together with ACh providing excitatory input to those same cells strongly suggests an ACh-specific positive feedback loop via ACh autoreceptors. This mechanism would be expected to spread an excited state amongst localised type I cells, thus effectively creating a syncytial system.