No-reflow disrupts the expression and distribution of Connexin 43 in a swine model
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No reflow phenomenon
Immunofluorescence
Gap junctions are intercellular connections that enable direct communication between neighboring cells. They are important in tissue homeostasis, cell growth, and differentiation. They are composed of connexin proteins, of which the most common and most studied is connexin 43. The role of connexin 43 in the development and progression of tumors is contradictory. The aim of this paper is to summarize the current state of knowledge on the expression of connexin 43 in various primary and secondary tumors, in order to explain its role in the development and progression of malignant tumors. Previous studies have examined the expression of connexin 43 in various primary and secondary tumors, as well as its association with prognosis. The expression of connexin 43 has been shown to be associated with various aspects of tumor behavior. However, it has been shown that the expression of connexin 43 differs between different types and localizations of tumors, as well as between different stages in tumor progression, which indicates the complex role of connexin 43 in tumor evolution. Since gap junctions play a role in carcinogenesis, invasion, and metastasis of malignant cells, further studies should clarify whether connexin 43 can be used as a diagnostic biomarker.
Tumor progression
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Abstract Focal disorganization of gap junctional distribution and down‐regulation of the major gap junctional protein connexin 43 are typical features of myocardial remodelling in the failing human heart. Increasing evidence indicates that connexin 43 interacts with zonula‐occludens‐1 (ZO‐1), and it has recently been shown that ZO‐1 promotes the formation and growth of gap junctional plaques. In the present study, distribution patterns of ZO‐1 and connexin 43 were studied in normal and in heart failure patients using double‐label immunohistochemistry and confocal microscopy. ZO‐1 was found to be co‐localized with connexin 43 at intercalated disks. Importantly, in patients with heart failure due to dilated or ischaemic cardimyopathy, areas of diminished connexin 43 expression were characterized by a markedly reduced ZO‐1 staining. Based on these data it is concluded that in patients with heart failure, down‐regulation of ZO‐1 matches the diminished expression levels of connexin 43, suggesting that ZO‐1 plays an important role in gap junction formation and gap junction plaque stability.
Intercalated disc
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Connexon
Connexin 32
Polyclonal antibodies
Carbenoxolone
Neuroglia
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The connexin gene family is the most prevalent gene that contributes to hearing loss. Connexins 26 and 30, encoded by GJB2 and GJB6, respectively, are the most abundantly expressed connexins in the inner ear. Connexin 43, which is encoded by GJA1, appears to be widely expressed in various organs, including the heart, skin, the brain, and the inner ear. The mutations that arise in GJB2, GJB6, and GJA1 can all result in comprehensive or non-comprehensive genetic deafness in newborns. As it is predicted that connexins include at least 20 isoforms in humans, the biosynthesis, structural composition, and degradation of connexins must be precisely regulated so that the gap junctions can properly operate. Certain mutations result in connexins possessing a faulty subcellular localization, failing to transport to the cell membrane and preventing gap junction formation, ultimately leading to connexin dysfunction and hearing loss. In this review, we provide a discussion of the transport models for connexin 43, connexins 30 and 26, mutations affecting trafficking pathways of these connexins, the existing controversies in the trafficking pathways of connexins, and the molecules involved in connexin trafficking and their functions. This review can contribute to a new way of understanding the etiological principles of connexin mutations and finding therapeutic strategies for hereditary deafness.
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Objective To investigate the effect and status of connexin 43 on myocardial protection in ischemic preconditioning.Methods 48 Sprague-Dawley rats were randomly divided into four groups: S,IR,IP,5-HD+IP.The myocardial infarct size and arrhythmia score were measured.The expression of connexin 43 was detected by RT-PCR.Results Compared with group IP,arrhythmia score and IS/AAR was higher and the expression of connexin 43 was notablely lower in group IR and group 5-HD+IP(P0.01).Ischemic preconditioning might reduced arrhythmogenesis and myocardial infarct size,meanwhile enhanced the expression of connexin 43.5-hydroxydecanoate acid might interdicted the myocardial protection of IP(P0.01).Conclusion Ischemic preconditioning might play an important role in myocardial protection by activating mitochondrial ATP sensitive potassium channel and preserving connexin 43 posphorylation.
Ischemic Preconditioning
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Specific serum antibody levels in Leishmania infantum-infected dogs treated with a combination of glucantime and allopurinol were estimated by indirect immunofluorescence and Western blotting. The sensitivity of Western blot was greater than that obtained with immunofluorescence titration. In general, both diagnostic methods concurred with the post-treatment clinical status of the animals. Clinical improvement of successfully treated dogs was related to lower immunofluorescence titers and simpler and/or less reactive immunodetection patterns in Western blotting. The recognition, by infected dogs, of certain low molecular weight antigens, particularly one of approximately 26 kDa, was restricted to pretreatment samples and a single animal in relapse thus apparently constituting an active infection marker.
Immunofluorescence
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Connexins are the building blocks of gap junctions. Mutations in connexin are the most common cause of non-syndromic hereditary deafness. The authors looked at the results of connexin mutations in children identified with varying types (unilateral and bilateral) and degrees of their hearing losses since 2002 in Bolton. Our case mix consisted of children identified through the Newborn Hearing Screening Programme, which was introduced in our area in 2003, and older children with hearing loss already in the system. Connexin 26 was tested in all children identified with permanent childhood hearing impairment, but more recently connexin 30 is also being tested. The authors present the variability of mutations in connexin in relation to their phenotype.
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Abstract Gap junctions or hemichannels are expressed on all cells in our body, and have a highly significant role in homeostasis and in disease states. There are 21 connexins found in humans and they have distinct characteristics that compensate for each other. The anatomical expression pattern also differs between each connexin; some of them are expressed together and some are not. Genetically mutated connexin genes induce inheritable diseases, but acquired disorders can also be caused by primary or secondary connexin dysfunctions. In the central nervous system, glial cells are the main connexin‐expressing cells. They utilize connexin gap junctions to assemble glial networks. The present review not only describes the basic structures and functions of connexins, it also examines the relationships between connexins and their role in disease pathology.
Homeostasis
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The connexin gene family is the most prevalent gene that contributes to hearing loss. Connexins 26 and 30, encoded by GJB2 and GJB6 respectively, are the most abundant expressed connexins in the inner ear. Connexin 43 which is encoded by GJA1 appears to be widely expressed in various organs, including the heart, skin, brain, and inner ear. The mutations that arise in GJB2, GJB6 and GJA1 can all result in comprehensive or non-comprehensive genetic deafness in newborns. As it is predicted that connexins include at least 20 isoforms in humans, the biosynthesis, structural composition, and degradation of connexins must be precisely regulated so that the gap junctions can operate properly. Certain mutations result in connexins possessing a faulty subcellular localization, failing to transport to the cell membrane and preventing gap junction formation, ultimately leading to connexin dysfunction and hearing loss. In this review, we provide a discussion of the transport models for connexin 43, connexins 30 and 26, mutations affecting trafficking pathways of connexin 26, the existing controversies in trafficking pathways of connexins, and the molecules involved in connexin trafficking and their functions. This review can contribute to a new way of understanding the etiological principles of connexin mutations and finding therapeutic strategies for hereditary deafness.
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