Connexin43-containing gap junctions potentiate extracellular Ca2+-induced odontoblastic differentiation of human dental pulp stem cells via Erk1/2

Li, Shiting; He, Hai‐Tao; Zhang, Gang; Wang, Fei; Zhang, Ping; Tan, Yinghui

doi:10.1016/j.yexcr.2015.09.008

Cited by 24 publications

(30 citation statements)

References 48 publications

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“…On the other hand, increasing Cx43 expression by the treatment of all-trans retinoic acid resulted in more differentiation and maturation of lens epithelial cells20. Furthermore, Cx43 overexpression potentiated and induced dentin sialophosphoprotein expression and enhanced odontoblastic differentiation of dental pulp stem cells21.…”

mentioning

confidence: 99%

Connexin 32-mediated cell-cell communication is essential for hepatic differentiation from human embryonic stem cells

Qin¹,

Chang²,

Wang³

et al. 2016

Sci Rep

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Gap junction-mediated cell-cell interactions are highly conserved and play essential roles in cell survival, proliferation, differentiation and patterning. We report that Connexin 32 (Cx32)-mediated gap junctional intercellular communication (GJIC) is necessary for human embryonic stem cell-derived hepatocytes (hESC-Heps) during step-wise hepatic lineage restriction and maturation. Vitamin K2, previously shown to promote Cx32 expression in mature hepatocytes, up-regulated Cx32 expression and GJIC activation during hepatic differentiation and maturation, resulting in significant increases of hepatic markers expression and hepatocyte functions. In contrast, negative Cx32 regulator 2-aminoethoxydiphenyl borate blocked hESC-to-hepatocyte maturation and muted hepatocyte functions through disruption of GJIC activities. Dynamic gap junction organization and internalization are phosphorylation-dependent and the p38 mitogen-activated protein kinases pathway (MAPK) can negatively regulate Cxs through phosphorylation-dependent degradation of Cxs. We found that p38 MAPK inhibitor SB203580 improved maturation of hESC-Heps correlating with up-regulation of Cx32; by contrast, the p38 MAPK activator, anisomycin, blocked hESC-Heps maturation correlating with down-regulation of Cx32. These results suggested that Cx32 is essential for cell-cell interactions that facilitate driving hESCs through hepatic-lineage maturation. Regulators of both Cx32 and other members of its pathways maybe used as a promising approach on regulating hepatic lineage restriction of pluripotent stem cells and optimizing their functional maturation.

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mentioning

confidence: 99%

Connexin 32-mediated cell-cell communication is essential for hepatic differentiation from human embryonic stem cells

Qin¹,

Chang²,

Wang³

et al. 2016

Sci Rep

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“…Recent data have shown that GJ-mediated signaling is a powerful regulator of these properties, especially in stem cells (Oviedo and Levin, 2007;Wong et al, 2008). GJs are involved in regulating multipotency (Dyce et al, 2014), differentiation (Bani-Yaghoub et al, 1999;Zhang et al, 2002;Araya et al, 2003;Gu et al, 2003b;Hirschi et al, 2003;Araya et al, 2005;Li et al, 2015), self-renewal (Hitomi et al, 2015), proliferation (Paraguassu-Braga et al, 2003;Pearson et al, 2005;Starich et al, 2014), and motility (Huang et al, 1998a;Xu et al, 2001;Zahler et al, 2003;Marins et al, 2009;Kotini and Mayor, 2015). Neural stem cells exhibit a unique signature based on GJC and ion transporters, and GJC based on Cx43 and Cx45 is essential for their survival and proliferation (Cai et al, 2004).…”

Section: Gjc and Stem Cellsmentioning

confidence: 99%

Gap junctional signaling in pattern regulation: Physiological network connectivity instructs growth and form

Mathews

Levin

2016

Developmental Neurobiology

121

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Gap junctions (GJs) are aqueous channels that allow cells to communicate via physiological signals directly. The role of gap junctional connectivity in determining single-cell functions has long been recognized. However, GJs have another important role: the regulation of large-scale anatomical pattern. GJs are not only versatile computational elements that allow cells to control which small molecule signals they receive and emit, but also establish connectivity patterns within large groups of cells. By dynamically regulating the topology of bioelectric networks in vivo, GJs underlie the ability of many tissues to implement complex morphogenesis. Here, a review of recent data on patterning roles of GJs in growth of the zebrafish fin, the establishment of left-right patterning, the developmental dysregulation known as cancer, and the control of large-scale head-tail polarity, and head shape in planarian regeneration has been reported. A perspective in which GJs are not only molecular features functioning in single cells, but also enable global neural-like dynamics in non-neural somatic tissues has been proposed. This view suggests a rich program of future work which capitalizes on the rapid advances in the biophysics of GJs to exploit GJ-mediated global dynamics for applications in birth defects, regenerative medicine, and morphogenetic bioengineering. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 643-673, 2017.

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“…The Cx family is divided into 13 different members according to molecular weight. Previous research uncovered crucial roles of Cxs in stem cell proliferation and differentiation, for instance, modulation of Cx43 involved in differentiation of osteoblast [ 9 ], odontoblast [ 10 ], and lens epithelial cells [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Connexin 32 and connexin 43 are involved in lineage restriction of hepatic progenitor cells to hepatocytes

Pei¹,

Zhai²,

Li³

et al. 2017

Stem Cell Res Ther

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BackgroundBi-potential hepatic progenitor cells can give rise to both hepatocytes and cholangiocytes, which is the last phase and critical juncture in terms of sequentially hepatic lineage restriction from any kind of stem cells. If their differentiation can be controlled, it might access to functional hepatocytes to develop pharmaceutical and biotechnology industries as well as cell therapies for end-stage liver diseases.MethodsIn this study, we investigated the influence of Cx32 and Cx43 on hepatocyte differentiation of WB-F344 cells by in vitro gain and loss of function analyses. An inhibitor of Cx32 was also used to make further clarification. To reveal p38 MAPK pathway is closely related to Cxs, rats with 70% partial hepatectomy were injected intraperitoneally with a p38 inhibitor, SB203580. Besides, the effects of p38 MAPK pathway on differentiation of hepatoblasts isolated from fetal rat livers were evaluated by addition of SB203580 in culture medium.ResultsIn vitro gain and loss of function analyses showed overexpression of Connexin 32 and knockdown of Connexin 43 promoted hepatocytes differentiation from hepatic progenitor cells. In addition, in vitro and ex vivo research revealed inhibition of p38 mitogen-activated protein kinase pathway can improve hepatocytes differentiation correlating with upregulation of Connexin 32 expression and downregulation of Connexin 43 expression.ConclusionsHere we demonstrate that Connexins play crucial roles in facilitating differentiation of hepatic progenitors. Our work further implicates that regulators of Connexins and their related pathways might provide new insights to improve lineage restriction of stem cells to mature hepatocytes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-017-0703-2) contains supplementary material, which is available to authorized users.

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Connexin43-containing gap junctions potentiate extracellular Ca2+-induced odontoblastic differentiation of human dental pulp stem cells via Erk1/2

Cited by 24 publications

References 48 publications

Connexin 32-mediated cell-cell communication is essential for hepatic differentiation from human embryonic stem cells

Connexin 32-mediated cell-cell communication is essential for hepatic differentiation from human embryonic stem cells

Gap junctional signaling in pattern regulation: Physiological network connectivity instructs growth and form

Connexin 32 and connexin 43 are involved in lineage restriction of hepatic progenitor cells to hepatocytes

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