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Ion Channels in Immune Cells
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Devasena Ponnalagu, Shridhar Sanghvi, Shyam S. Bansal, Harpreet Singh
Connexins are ubiquitous, integral membrane proteins present in almost all of the cells of the body. Connexins are known to form cell-cell communication in tissues and between the extracellular environment and cytoplasm by forming gap junctions. In electrically excitable cells like cardiomyocytes, connexins serve as a powerful coordinator for allowing the cell-to-cell passage of ions to facilitate uniform electrical conduction throughout the heart159–161.
Stem Cells and Nanotechnology
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
In a rat model of sensorineural hearing loss (SHNL), BM-MSC were transplanted in the perilymph and found in the cochlear injured area (Kamiya et al., 2007): These cells could express connexin 26 and connexin 30, indicating a reactivation of gap junctions between neighboring cells. The transplanted rat group showed hearing recovery (Kamiya et al., 2007).
Keratitis–Ichthyosis–Deafness Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
With a short half-life of 2–4 h, connexins participate in intracellular connexin−protein interaction, cell−extracellular space exchange, and cell−cell communication through formation of hemichannels and GJC Specifically, six connexin subunits gather together as hemichannel (or gap junction hemichannel, also known as connexon) in the endoplasmic reticulum or Golgi body and then move to cellular membranes, where two hemichannels join through hydrophobic interactions to form GJC, which is an aqueous pore between the cytoplasm of two adjacent cells, facilitating the exchange of ions (K+, Ca2+), signaling molecules (IP3, cAMP, cGMP, ATP) and metabolites (e.g., glucose, sugar, amino acid, glutathione) (Figure 42.1). Via these activities, connexins activate signaling pathways and affect cellular phenotypes. Not surprisingly, total or partial connexin dysfunctions may lead to a variety of genetic disorders such as skin abnormalities, cardiopathies, neurodegenerative and developmental diseases, cataracts, hereditary deafness, and cancer (collectively known as connexinopathies) (Table 42.1) [4–6].
The cardiac toxicity of radiotherapy – a review of characteristics, mechanisms, diagnosis, and prevention
Published in International Journal of Radiation Biology, 2021
In the meantime, other molecular mechanisms such as DNA damage, mitochondrial dysfunction, and microRNA changes have been raised by some researchers. DNA breakage due to radiation directly has been recognized as the initiation of cell apoptosis. Meanwhile, ROS can regulate DNA methylation, histone methylation, and acetylation. And the release of ROS can induce genomic instability (Yakovlev 2013; Yahyapour et al. 2018). Mitochondrial dysfunction and irreversible damage are vital in cell apoptosis after radiation. Excessive ROS leads to endoplasmic reticulum (ER) damage and promotes the release of calcium. ROS and calcium overload are involved in MPT which depolarizes the mitochondrial membrane and decouples oxidative phosphorylation (Sridharan et al. 2014). And mitochondria can produce more ROS as a vicious cycle (Wang et al. 2019). Gene regulators such as microRNA are involved in cardiac hypertrophy by irradiation (Kura et al. 2017). Thus microRNA has potential as a bio-marker and radioprotective agent of cardiovascular injury or inflammation in RIHD (Kenchegowda et al. 2018; Kura et al. 2019). From what has been discussed above, greater efforts are needed to identify the clinical applications of connexin proteins and their channels.
Review of the mechanism underlying mefloquine-induced neurotoxicity
Published in Critical Reviews in Toxicology, 2021
Airton C. Martins, Monica M. B. Paoliello, Anca O. Docea, Abel Santamaria, Alexey A. Tinkov, Anatoly V. Skalny, Michael Aschner
In addition to mefloquine’s effects on change voltage-dependent channels, mefloquine toxicity also has been associated with dysfunction of connexins (Cxs) (Schlagenhauf et al. 2010). Connexins are proteins associated with gap junction intercellular communications in several organs, and are widely distributed in neuronal tissue. Indeed, Cxs play an essential role in controlling neuronal metabolism and homeostasis, and are involved in cognitive processes as well as motor functions. Accordingly, Cxs dysfunction has been associated with several neuropsychiatric diseases and conditions, such as suicide attempts and epilepsy. Connexins are labeled according to numbers corresponding to their molecular weight, such as Cx36, Cx50, Cx43, to name a few (Cruikshank et al. 2004; Bodendiek and Raman 2010; Seemann et al. 2018).
Inhibition of Gap Junction–Mediated Intercellular Communication by Poly(I:C) in Cultured Human Corneal Fibroblasts
Published in Current Eye Research, 2020
Hui Zheng, Ye Liu, Dan Xu, Pingping Liu, Xiuxia Yang, Bing Li, Zimu Cao, Yang Liu, Xiaoshuo Zheng
Connexins play a key role in the regulation of cell growth, death, and function in the immune response, hematopoiesis, and development of progenitor cells.25,26 The expression of Cx43 in the cornea has been found to be altered at both the mRNA and protein levels in association with chemical burns, infection, and Stevens-Johnson syndrome.27 Blocking of gap junction function by the Cx43 mimetic peptide Gap27 was also shown to reduce corneal inflammation.12 Poly(I:C) is a synthetic analog of viral dsRNA, which is present in some RNA viruses as well as an intermediate that forms during viral replication, and as such it activates Toll-like receptor 3 on host cells. Exposure of HCFs to poly(I:C) was previously shown to induce the production of proinflammatory cytokines such as interleukin-6 and chemokines such as interleukin-8 and granulocyte colony-stimulating factor6 as well as to trigger the release of matrix metalloproteinases such as MMP-1 and MMP-3.28 In the present study, poly(I:C) was also found to down-regulate GJIC activity in these cells. All of these effects induced by viral dsRNA likely contribute to the promotion of stromal inflammation during corneal viral infection.