Contribution of Connexin Hemichannels to the Decreases in Cell Viability Induced by Linoleic Acid in the Human Lens Epithelial Cells (HLE-B3)

Figueroa, Vania; Jara, Oscar; Oliva, Carolina A.; Ezquer, Marcelo; Ezquer, Fernando; Retamal, Mauricio A.; Martı́nez, Agustı́n D.; Altenberg, Guillermo A.; Vargas, Aníbal A.

doi:10.3389/fphys.2019.01574

Cited by 11 publications

(8 citation statements)

References 65 publications

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“…Connexin hemichannels are involved in initiation of apoptosis, since treatment of lens cells with linoleic acid opens connexin hemichannels. This leads to elevations in intracellular calcium ion concentrations [ 49 ]. Such overload of calcium ions can contribute to cell death via signalling cascades leading to phagocytosis, endoplasmic reticulum stress, mitochondrial permeabilization and nuclear changes.…”

Section: Role Of Connexin Hemichannels In Inflammation and Cell Dementioning

confidence: 99%

“…Such overload of calcium ions can contribute to cell death via signalling cascades leading to phagocytosis, endoplasmic reticulum stress, mitochondrial permeabilization and nuclear changes. Influx of calcium ions also affects connexin hemichannels and associated transfer of vital molecules [ 49 , 50 ]. Another role of connexin hemichannels in cell death includes communication of messages towards surrounding cells in a paracrine manner [ 51 , 52 ].…”

Section: Role Of Connexin Hemichannels In Inflammation and Cell Dementioning

confidence: 99%

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Mechanisms Underlying Connexin Hemichannel Activation in Disease

Campenhout

Gomes

Groof

et al. 2021

IJMS

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Gap junctions and connexin hemichannels mediate intercellular and extracellular communication, respectively. While gap junctions are seen as the “good guys” by controlling homeostasis, connexin hemichannels are considered as the “bad guys”, as their activation is associated with the onset and dissemination of disease. Open connexin hemichannels indeed mediate the transport of messengers between the cytosol and extracellular environment and, by doing so, fuel inflammation and cell death in a plethora of diseases. The present mini-review discusses the mechanisms involved in the activation of connexin hemichannels during pathology.

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Section: Role Of Connexin Hemichannels In Inflammation and Cell Dementioning

confidence: 99%

Section: Role Of Connexin Hemichannels In Inflammation and Cell Dementioning

confidence: 99%

Mechanisms Underlying Connexin Hemichannel Activation in Disease

Campenhout

Gomes

Groof

et al. 2021

IJMS

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“…Previous studies have shown the biphasic, protective, and detrimental roles of Cx43 channels in modulating oxidative stress-induced cellular damage in several different tissues [ 78 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 ]. Whether connexin channels exert a protective or destructive effect in response to oxidative stress is dependent on the insults and cell and tissue types.…”

Section: Connexin Channels In Response To Oxidative Stressmentioning

confidence: 99%

“…By using a Cx43E2 antibody, a specific Cx43 HC inhibitor [ 127 ], our group recently revealed that Cx43 HCs protect lens epithelial cells against oxidative stress (unpublished data). In contrast to the cell-protective effect, it has been reported that Cx43 HCs in lens epithelial cells play a detrimental role in linoleic acid-induced cell death [ 110 ]. This effect of HCs was validated by TATGap19, a specific Cx43 hemichannel inhibitor, but this study did not rule out the involvement of GJIC.…”

Section: Connexin Channels In Response To Oxidative Stressmentioning

confidence: 99%

Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis

Quan

Tong

et al. 2021

Antioxidants

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The lens is continuously exposed to oxidative stress insults, such as ultraviolet radiation and other oxidative factors, during the aging process. The lens possesses powerful oxidative stress defense systems to maintain its redox homeostasis, one of which employs connexin channels. Connexins are a family of proteins that form: (1) Hemichannels that mediate the communication between the intracellular and extracellular environments, and (2) gap junction channels that mediate cell-cell communication between adjacent cells. The avascular lens transports nutrition and metabolites through an extensive network of connexin channels, which allows the passage of small molecules, including antioxidants and oxidized wastes. Oxidative stress-induced post-translational modifications of connexins, in turn, regulates gap junction and hemichannel permeability. Recent evidence suggests that dysfunction of connexins gap junction channels and hemichannels may induce cataract formation through impaired redox homeostasis. Here, we review the recent advances in the knowledge of connexin channels in lens redox homeostasis and their response to cataract-related oxidative stress by discussing two major aspects: (1) The role of lens connexins and channels in oxidative stress and cataractogenesis, and (2) the impact and underlying mechanism of oxidative stress in regulating connexin channels.

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“…Connexins are a family of structurally related transmembrane proteins in humans with approximately 20 members. Every single connexin protein consists of four transmembrane domains (T1-T4), two extracellular loops (EL1, EL2) with a cytoplasmic loop (IL), and cytoplasmic N-terminal and C-terminal components (Figueroa et al, 2019;Mese et al, 2007;Sánchez et al, 2019). Three connexins presented in the lens are α1 (Cx43), α3 (Cx46), and α8 (Cx50), which are encoded by three genes: Gja1, Gja3, and Gja8, respectively (Yue et al, 2021;Ping et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Mutations of CX46/CX50 and Cataract Development

Shi

Yang

2022

Front. Mol. Biosci.

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Cataract is a common disease in the aging population. Gap junction has been considered a central component in maintaining homeostasis for preventing cataract formation. Gap junction channels consist of connexin proteins with more than 20 members. Three genes including GJA1, GJA3, and GJA8, that encode protein Cx43 (connexin43), Cx46 (connexin46), and Cx50 (connexin50), respectively, have been identified in human and rodent lens. Cx46 together with Cx50 have been detected in lens fiber cells with high expression, whereas Cx43 is mainly expressed in lens epithelial cells. Disrupted expression of the two connexin proteins Cx46 and Cx50 is directly related to the development of severe cataract in human and mice. In this review article, we describe the main role of Cx46 and Cx50 connexin proteins in the lens and the relationship between mutations of Cx46 or Cx50 and hereditary cataracts. Furthermore, the latest progress in the fundamental research of lens connexin and the mechanism of cataract formation caused by lens connexin dysfunction are summarized. Overall, targeting connexin could be a novel approach for the treatment of cataract.

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Contribution of Connexin Hemichannels to the Decreases in Cell Viability Induced by Linoleic Acid in the Human Lens Epithelial Cells (HLE-B3)

Cited by 11 publications

References 65 publications

Mechanisms Underlying Connexin Hemichannel Activation in Disease

Mechanisms Underlying Connexin Hemichannel Activation in Disease

Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis

Mutations of CX46/CX50 and Cataract Development

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