Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3

Liao, Chih Kai; Wang, Seu Mei; Chen, Yuh‐Lien; Wang, Hwai Shi; Wu, Jyh‐Lin

doi:10.1016/j.biocel.2010.01.016

Cited by 55 publications

(37 citation statements)

References 38 publications

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“…Integrin b1 signaling in the presence of laminin also triggered an increase in gap junction formation between FS cells in our previous report (Horiguchi et al 2011). There are some reports that caveolin 3 upregulated the expression of connexin 43 in gap junction channel protein (Chung et al 2009, Liao et al 2010. This leads us to speculate that caveolin 3 plays a role in gap junction formation between FS cells.…”

Section: Discussionmentioning

confidence: 73%

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Horiguchi¹,

Fujiwara²,

Ilmiawati³

et al. 2011

Journal of Endocrinology

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Folliculostellate (FS) cells in the anterior pituitary gland are believed to have multifunctional properties. Using transgenic rats that express green fluorescent protein (GFP) specifically in FS cells in the anterior pituitary gland (S100b-GFP rats), we recently revealed that FS cells in primary culture exhibited marked proliferation in the presence of laminin, an extracellular matrix (ECM) component of the basement membrane. In a process referred to as matricrine action, FS cells receive ECM as a signal through their receptors, which results in morphological and functional changes. In this study, we investigated matricrine signaling in FS cells and observed that the proliferation of FS cells is mediated by integrin b1, which is involved in various signaling pathways for cell migration and proliferation in response to ECM. Then, we analyzed downstream events of the integrin b1 signaling pathway in the proliferation of FS cells and identified caveolin 3 as a potential candidate molecule. Caveolin 3 is a membrane protein that binds cholesterol and a number of signaling molecules that interact with integrin b1. Using specific small interfering RNA of caveolin 3, the proliferation of FS cells was inhibited. Furthermore, caveolin 3 drove activation of the mitogen-activated protein kinase (MAPK) signaling cascades, which resulted in upregulation of cyclin D1 in FS cells. These findings suggest that matricrine signaling in the proliferation of FS cells was transduced by a caveolin 3-mediated integrin b1 signaling pathway and subsequent activation of the MAPK pathway.

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Section: Discussionmentioning

confidence: 73%

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Horiguchi¹,

Fujiwara²,

Ilmiawati³

et al. 2011

Journal of Endocrinology

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“…Hemichannel activity, however, seems to be consistently upregulated by LPS [45,[57][58][59][60]. A number of mechanisms have been proposed to underlie LPS-induced modifications in GJIC, including nitric oxide signaling [43,54,56] and activation of kinase pathways [55,61]. In fact, some of these pathways may be at the basis of the differential outcome observed for LPS on gap junctions and connexin hemichannels.…”

Section: Escherichia Colimentioning

confidence: 99%

“…Thus, both downregulated [33][34][35][36][37][38][39] and upregulated [35,37,[40][41][42][43][44][45][46][47][48] connexin protein quantities have been observed upon exposure of cells to LPS from E. coli in in vitro and in vivo settings, whether or not in combination with IFN-c. In some cases [38,41,43,44,47,48], but not all [34,38], LPS also targeted connexin mRNA production. The deterioration of Cx32 protein in rat liver after LPS administration, for instance, was found to result from its corresponding mRNA degradation, which in turn was a consequence of shortening of the poly(A)tail [49,50].…”

Section: Escherichia Colimentioning

confidence: 99%

Modulation of connexin signaling by bacterial pathogens and their toxins

Ceelen

Haesebrouck

Vanhaecke

et al. 2011

Cell. Mol. Life Sci.

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Inherent to their pivotal tasks in the maintenance of cellular homeostasis, gap junctions, connexin hemichannels, and pannexin hemichannels are frequently involved in the dysregulation of this critical balance. The present paper specifically focuses on their roles in bacterial infection and disease. In particular, the reported biological outcome of clinically important bacteria including Escherichia coli, Shigella flexneri, Yersinia enterocolitica, Helicobacter pylori, Bordetella pertussis, Aggregatibacter actinomycetemcomitans, Pseudomonas aeruginosa, Citrobacter rodentium, Clostridium species, Streptococcus pneumoniae, and Staphylococcus aureus and their toxic products on connexin- and pannexin-related signaling in host cells is reviewed. Particular attention is paid to the underlying molecular mechanisms of these effects as well as to the actual biological relevance of these findings.

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“…In addition to physiological maintenance, growing evidence suggests that the astrocyte gap junctions (GJs) play an important role in various central nervous system (CNS) pathological conditions, such as AD, HD, and ischemia (Nakase and Naus 2004;Kielian 2008). Changes to gap junctional intercellular communication (GJIC) in astrocytes and excessive inflammation may trigger brain damage and neurodegenerative diseases (Liao et al 2010). However, very little is known about the role of astrocyte GJs in Parkinson's disease (PD).…”

Section: Introductionmentioning

confidence: 99%

Reversal of Rotenone-Induced Dysfunction of Astrocytic Connexin43 by Opening Mitochondrial ATP-Sensitive Potassium Channels

et al. 2010

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Growing evidence suggests that the astrocytic gap junctions (GJs), mainly formed by connexin 43 (Cx43), play an important role in physiological maintenance and various central nervous system (CNS) pathological conditions. However, little is known about the role of Cx43 in Parkinson's disease (PD). In this article, we report that rotenone, a classic neurotoxin for PD, could inhibit expression of astrocytic Cx43 and gap junction permeability. ATP-sensitive potassium (K(ATP)) channel openers, iptakalim (IPT) and diazoxide (DZ), exerted protective effect on rotenone-induced dysfunction of Cx43 and astrocyte apoptosis, which was reversed by selective mitochondrial K(ATP) (mitoK(ATP)) channel blocker 5-hydroxydecanoate (5-HD). Taken together, our findings reveal that rotenone-induced dysfunction of astrocytic Cx43 may be involved in the pathology of PD. Moreover, opening mitoK(ATP) channels in astrocytes can reverse rotenone-induced dysfunction of astrocytic Cx43 and therefore protect against toxicity of rotenone on astrocytes.

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Lipopolysaccharide-induced inhibition of connexin43 gap junction communication in astrocytes is mediated by downregulation of caveolin-3

Cited by 55 publications

References 38 publications

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Modulation of connexin signaling by bacterial pathogens and their toxins

Reversal of Rotenone-Induced Dysfunction of Astrocytic Connexin43 by Opening Mitochondrial ATP-Sensitive Potassium Channels

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