DigitalUM :: Browsing by Subject "Connexin"

Browsing by Subject "Connexin"

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Open Access
An attempt to isolate genes responsible for spontaneous and experimental metastasis in the mouse model
(Murcia : F. Hernández, 2002) Ito, A.; Watabe, K.; Koma, Y.; Kitamura, Y.
Cancer develops and progresses as genetic alterations occur subsequently. Onset process of cancer has become well understood in some types of cancer, such as colorectal cancers. In this process, responsible alterations were identified in numbers of oncogenes such as k-ras, and tumor suppressor genes such as p53, as Vogelstein proposed earlier in the multistage carcinogenesis theory. In contrast, our understanding remains short to draw such an adequate diagram for the process during which cancer becomes more malignant, i.e., metastatic. To examine the molecular basis for this progression step, mouse metastasis models have been established where tumor cell lines are inoculated into mice and metastasize to specific organs. The model using B16 melanoma cells is one of the most developed. BL6 subline, one of the most metastatic, was obtained from F10 subline simply through six rounds of in vitro selection. Nonetheless, BL6 cells metastasize lungs much more heavily than F10 cells when injected subcutaneously. The difference in gene expression between the two sublines is considered rather small but relevant for spontaneous metastasis. We began our research by elaborating a method for the construction of subtracted cDNA libraries, and made it applicable to BL6 and F10 cells. As a result, we were able to isolate a couple of genes that were expressed differently between the two sublines. As might be expected, each of the genes appeared to play a role more or less in distinct aspects of spontaneous metastasis of B16 melanoma cells. Moreover, similar roles were expected for the genes in the process by which human melanoma cells metastasize.
Open Access
Emerging role of gap junctions in epilepsy
(Murcia : F. Hernández, 2005) Nemani, V.M.; Binder, D.K.
This review highlights the contribution of gap junctions to the pathophysiology of epilepsy. The tissue expression and spatiotemporal regulation of connexins is discussed, and the phenotypes of specific connexin knockouts are considered. Electrophysiologic studies have implicated gap junctions in the generation of very fast oscillations preceding seizures. Gap junction inhibitors have shown powerful anticonvulsant effects, to date primarily in in vitro studies. Specific inhibition of gap junctions in vivo along with more detailed human tissue studies are needed to understand more fully the role of gap junctions in epileptogenesis.
Open Access
Gap junction channel: new roles in disease
(Murcia : F. Hernández, 1997) Donaldson, P.; Ecker, R.; Green, C.; Kistler, J.
The irnportance of intercellular communication to complex cellular processes such as development, differentiation, growth, propagation of electrical impulses and diffusional feeding has long been appreciated. The realization that intercellular communication is mediated by gap junction channels, which are in turn comprised of a diverse family of proteins called the connexins, has provided new tools and avenues for studying the role of intercellular communication in these important cellular processes. The identification of different connexin isoforms has not only enabled the development of specific reagents to study connexin expression patterns, but has also allowed the functional properties of the different connexin isoforms and how they interact with each other, to be explored. Increasingly, the knowledge gained from studying connexin diversity is being used to investigate the role played by gap junction channels in a number of diseases. In this article we highlight selected cases where gap junction channels have been shown or are believed to be directly involved in the disease process.
Open Access
Gap junctions and expression of Cx36 Cx43 and Cx45 in the posterodorsal medial amygdala of adult rats
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Zancan, Mariana; Malysz, Tais; Moura, Dinara J.; Morás, Ana Moira; Steffens, Luiza; Rasia-Filho, Alberto
The posterodorsal medial amygdala (MePD) has a synaptic organization that dynamically modulates reproduction and other social behaviors in rats. Discrete gap junctions between glial cells were previously reported in the MePD neuropil. Connexins (Cx) are components of gap junctions and indicative of cellular electrical coupling. Here, we report the ultrastructural occurrence of gap junctions between neurons in the MePD and demonstrate the expression and immunofluorescent labeling of Cx36, Cx43 and Cx45 in this subcortical area of adult male rats. Few neuronal gap junctions were found in the MePD and, when identified, occurred between dendrites. On the other hand, there is a diffuse presence and distribution of punctate labelling for the tested Cxs. Puncta were visualized isolated or forming clusters in the same focal plane of cell bodies or along the MePD neuropil. The Cx36 puncta were found in neurons, Cx43 in astrocytes and Cx45 in both neurons and astrocytes. Our data indicate the presence of few gap junctions and different Cxs composition in the MePD. Because Cxs can assemble, form hemichannel units and/or serve as transcriptional regulator, it is likely that additional modulation of intercellular communication can occur besides the chemical transmission in the MePD of adult rats.
Open Access
Involvement of gap junctional communication and connexin expression in trophoblast differentiation of the human placenta
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2001) Cronier, L.; Bastide, B.; Defamie, N.; Niger, C.; Pointis, G.; Gasc, J. M.; Malassine, A.
Gap junctional intercellular communication (GJIC) permits coordinated cellular activities during development and d ifferentiation processes, and its dysfunction or mutation of connexin genes have been implicated in pathologies. In the human placenta, two distinct differentiation pathways of cytotrophoblastic cell coexist leading to a double model: fusion phenotype (villous trophoblast) a nd proliferative/ invasive phenotype (extravillous trophob last). This review focuses on current knowledge on the connexin expression and the implication of GJIC in trophoblastic differentiation. Experimental evidence obtained in human placenta demonstrates the involvement of connexin 43-gap junctions in the trophoblastic fusion process and of a connexin switch during the spatially and temporally controlled proliferation/invasion process.
Open Access
Localization of connexins in neurons and glia cells of the Helix aspersa suboesophageal brain ganglia by immunocytochemistry
(Murcia : F. Hernández, 2007) Azanza, M.J.; Pes, N.; Pérez-Bruzón, R.N.; Aisa, J.; Raso, M.; Junquera, C.; Lahoz, M.; Maestú, C.; Martínez Ciriano, M.C.; Pérez-Castejon, C.; Vera-Gil, A.; Del Moral, A.
The aim of the present study was to examine the distribution of cells expressing connexin 26 (Cx26) in the suboesophageal visceral, left and right parietal and left and right pleural ganglia of the snail Helix aspersa by immunocytochemistry. Altogether we have found approximately 452 immunoreactive neurons which represent the 4.7% of the total neurons counted. The stained large neurons (measured diameter 55-140 μm) occurred mostly on the peripheral surface of the ganglia while the small immunostained cells (5-25 μm diameter) were observed in groups near the neuropil. The number of large neurons giving positive Cx26-like immunostaining was small in comparison with that for medium (30-50 μm diameter) and small sized cells. The expression of Cx26 was also observed in the processes of glia cells localized among neurons somata and in the neuropil showing that the antiserum recognized epitopes in both protoplasmic and fibrous glia cells of Helix aspersa. The neuropils of all ganglia showed fibers densely immunostained. While we have observed a good specificity for Cx26-antiserum in neurons, a lack of reaction for Cx43 antiserum was observed in neurons and glia cells. The reaction for enolase antiserum in neurons was light and non-specific and a lack of reaction in glia cells and processes for GFAP antiserum was observed. Although the percentage of positive neurons for Cx26 antiserum was low is suggested that in normal physiological conditions or under stimulation the results can be considered of interest in the interpretation of Helix aspersa elemental two neuron networks synchronizing activity, observed under applied extremely low frequency magnetic fields.
Open Access
Role of stress-related glucocorticoid changes in astrocyte-oligodendrocyte interactions that regulate myelin production and maintenance
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Miguel Hidalgo, José Javier
Repeated activation of stress responses and elevated corticosteroids result in alterations of neuronal physiology and metabolism, and lead to disturbances of normal connectivity between neurons in various brain regions. In addition, stress responses are also associated with anomalies in the function of glial cells, particularly astrocytes and oligodendrocytes, which in turn may further contribute to the mechanisms of neuronal dysfunction. The actions of corticosteroids on astrocytes are very likely mediated by the presence of intracellular and cell membrane-bound CORT receptors. Although apparently less abundant than in astrocytes, activation of CORT receptors in oligodendrocytes also leads to structural changes that are reflected in myelin maintenance and plasticity. The close interactions between astrocytes and oligodendrocytes through extracellular matrix molecules, soluble factors and astrocyte-oligodendrocyte gap junctions very likely mediate part of the disturbances in myelin structure, leading to plastic myelin adaptations or pathological myelin disruptions that may significantly influence brain connectivity. Likewise, the intimate association of the tips of some astrocytes processes with a majority of nodes of Ranvier in the white matter suggest that stress and overexposure to corticosteroids may lead to remodeling of node of Ranvier and their specific extracellular milieu
Open Access
Suicide gene therapy with Herpes simplex virus thymidine kinase and ganciclovir is enhanced with connexins to improve gap junctions and bystander effects
(Murcia : F. Hernández, 2003) Nicholas, T.W.; Read, S.B.; Burrows, F.J.; Kruse, C.A.
Connexins are proteins that form gap junctions between cells in various mammalian tissues. Because of their role in intercellular communication, connexins are important in the bystander cell death seen in Herpes simplex virus-thymidine kinase (HSV-TK) gene therapy for brain tumors. A selective review of connexin transduction/transfection studies with particular emphasis to central nervous system tumor cells is presented. In addition, specific references to studies with cell types that demonstrate low gap junction intercellular communication are presented. Data are included with the HT-29 colorectal tumor cell line to support the concept that enhancing gap junction protein expression in otherwise low gap junction communicating HT-29 cells increases bystander cell death and reduces tumor burden beyond what might be expected from HSV-TK and ganciclovir (GCV) treatment alone. Maximum in vitro bystander cell death was always produced when GCV treated co-cultures of TKtransduced and non-TK-transduced HT-29 cell lines were also transduced with connexin-43. When connexin was present in only one group of cells in the co-culture, there was more bystander cell death observed with connexin transduced into the non- TK-transduced cells, rather than the TK-transduced cells. The data presented reinforces conclusions made from earlier findings from cell line mixing experiments in which the non- TKtransduced cell population determined the level of bystander cell death (Burrows et al., 2002).
Open Access
The role of gap junctional intercellular communication (GJIC) disorders in experimental and human carcinogenesis
(Murcia : F. Hernández, 1997) Krutovskikh, V.; Yamasaki, H.
There is a growing body of evidence supporting the etiologic implication of gap junctional intercellular communication disorders in carcinogenesis. Substantial progress has recently be.en made both in molecular biology of gap junction and in the field of cancer research. They provide new insights and conceptions of gap junctional disorders in tumor pathology. Modern understanding of the structure, function and regulation of gap junctions, as well as putative mechanisms of its disorders in human and experimental carcinogenesis are discussed in this review with particular emphasis on fast-moving aspects of this problem.

Browsing by Subject "Connexin"

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