Serotonin passes through myoendothelial gap junctions to promote pulmonary arterial smooth muscle cell differentiation

Gairhe, Salina; Bauer, Natalie; Gebb, Sarah A.; McMurtry, Ivan F.

doi:10.1152/ajplung.00183.2012

Cited by 47 publications

(52 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thompson et al, 2006;Iglesias et al, 2008Iglesias et al, , 2009aChekeni et al, 2010;Behringer et al, 2012;Gairhe et al, 2012;Boedtkjer et al, 2013;Zhang et al, 2013 40 Gap27, 37,43 Gap27 Used experimentally to inhibit connexin (Cx37, Cx43) and has been showed to affect pannexin channels. Weingart, 1977;Martin et al, 2004;Turner et al, 2004;Aperia, 2007;Boedtkjer et al, 2013 Heptanol Aliphatic alcohol, gap junction uncoupler/inhibitor 200 mM-3 mM 2/+ ++ Takens- Kwak et al, 1992;Garcia-Dorado et al, 1997;Pelegrin and Surprenant, 2006;Nishida et al, 2008;Li et al, 2010;Li et al, 2012 b +, Partial inhibition; 2/+, conflicting reports; ++, greater than 50% inhibition; 2, no effect; +++, complete inhibition; n/a, no information available a R and S represent the two stereoisomers of mefloquine (Iglesias et al, 2009b) b…”

Section: ++(S)mentioning

confidence: 99%

“…Endothelium-derived hyperpolarizing factor Edwards et al, 1998;Hutcheson et al, 1999;Yamamoto et al, 1999;Beny and Schaad, 2000;Kansui et al, 2004;Mather et al, 2005;Rath et al, 2012;Howitt et al, 2013Vascular conducted responses Kruger et al, 2002Dora et al, 2003b;Simon and McWhorter, 2003;Wolfle et al, 2007;Duling, 2008 Feedback on vasoconstriction Dora et al, 1997;Straub et al, 2011 Smooth muscle cell proliferation Chadjichristos et al, 2006;Liao et al, 2007;Johnstone et al, 2010;Zhong et al, 2012 a Smooth muscle cell differentiation Kwak et al, 2003;Chadjichristos et al, 2008;Shen et al, 2010;Gairhe et al, 2011Gairhe et al, , 2012 Endothelial cell proliferation Larson et al, 1997;Kwak et al, 2001;Yeh et al, 2006;Nakano et al, 2008;Wang et al, 2008 c Endothelial cell dysfunction Xie and Hu, 1994;Makino et al, 2008;Chadjichristos et al, 2010;Wang et al, 2012;Ebong and Depaola, 2013 Endothelial cell migration Pepper and Meda, 1992;Pepper et al, 1989;Kwak et al, 2001 a Evidence that gap junction independent pathways are involved in this regulation . b Evidence that although connexin expression and/or gap junction communication levels correlated to disease they do not appear to be directly linked...…”

Section: Physiologic Function Referencesmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of Cellular Communication by Signaling Microdomains in the Blood Vessel Wall

et al. 2014

View full text Add to dashboard Cite

Section: ++(S)mentioning

confidence: 99%

Section: Physiologic Function Referencesmentioning

confidence: 99%

Regulation of Cellular Communication by Signaling Microdomains in the Blood Vessel Wall

et al. 2014

View full text Add to dashboard Cite

“…Hence, the interendothelial Cx40-containing gap junctions appear to be critically involved in hypoxic vasoconstriction and the pathobiology of PH in this species (97). In isolated rat pulmonary arteries, sustained constriction, Rho kinase activation, and (92,99), which leads to increased vascular smooth muscle remodeling through the activation of similar mothers against decapentaplegic protein (SMAD) signaling (92,99,135) and phosphorylated TGF-associated kinase 1 (TAK1-p)-MAPK signaling pathways (136). Serotonin may also stimulate the production of superoxide anions by nicotinamide adenine dinucleotide phosphate reduced oxidase (NOX) in VSMCs (101,102).…”

Section: Myoendothelial Junction Mechanismsmentioning

confidence: 99%

“…There is increasing evidence that MEJs are also involved in regulating PASMC phenotype (92,99). When rat pulmonary arterial ECs (PAECs) and PASMCs are touch cocultured on a porous Transwell membrane, MEJs are formed because Cx43 has been found on projections extending into the membrane from both cell types and dye transfers from PAECs to PASMCs, but Cx43 is not present when cells were not touch cocultured.…”

Section: Myoendothelial Junction Mechanismsmentioning

confidence: 99%

“…The monoamine can be detected by immunostaining in both PAECs and PASMCs in touch-coculture but not in non-touch-coculture settings. Furthermore, inhibition of gap junctions but not the serotonin transporter prevents serotonin transfer from PAECs to PASMCs (99). Therefore, serotonin, a vasoconstrictor and a potent mitogen for PASMCs (100)(101)(102), is synthesized by PAEC and transferred through MEJs into PASMCs, where it regulates cell differentiation via the TGF-b signaling pathway (99) (Figure 2).…”

Section: Myoendothelial Junction Mechanismsmentioning

confidence: 99%

See 1 more Smart Citation

Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension

Gao

Chen

Raj

2016

Am J Respir Cell Mol Biol

119

View full text Add to dashboard Cite

In the pulmonary vasculature, the endothelial and smooth muscle cells are two key cell types that play a major role in the pathobiology of pulmonary vascular disease and pulmonary hypertension. The normal interactions between these two cell types are important for the homeostasis of the pulmonary circulation, and any aberrant interaction between them may lead to various disease states including pulmonary vascular remodeling and pulmonary hypertension. It is well recognized that the endothelial cell can regulate the function of the underlying smooth muscle cell by releasing various bioactive agents such as nitric oxide and endothelin-1. In addition to such paracrine regulation, other mechanisms exist by which there is cross-talk between these two cell types, including communication via the myoendothelial injunctions and information transfer via extracellular vesicles. Emerging evidence suggests that these nonparacrine mechanisms play an important role in the regulation of pulmonary vascular tone and the determination of cell phenotype and that they are critically involved in the pathobiology of pulmonary hypertension.Keywords: paracrine; myoendothelial injunction; microvesicles; vasoconstriction; vascular remodelingIn the pulmonary vasculature, endothelial cells (ECs) and smooth muscle cells (SMCs) are the key cell types involved in the regulation of vessel diameter in most of the pulmonary vascular tree and thereby they regulate pulmonary arterial pressure and total vascular resistance. ECs, which are strategically located as the innermost layer of the blood vessel and are in contact with the circulating blood, exert a delicate and constant influence on the underlying vascular smooth muscle cells (VSMCs). It is well recognized that the regulation of pulmonary vasoreactivity by the endothelium is predominantly accomplished by paracrine signaling through the release of various vasoactive agents such as nitric oxide (NO), endothelin-1 (ET-1) (1-3), and others (4-8). However, there is increasing evidence that the relationship between the EC and the SMC is not a simple one-way interaction from the endothelium to the SMC; rather, there are complicated interactions between them (9-11). Moreover, the communication patterns are not limited to paracrine signaling; cross-talk through myoendothelial gap junctions (MEJs), extracellular vesicles (EVs), and other mechanisms is critically involved (12)(13)(14)(15)(16)(17)(18)(19)(20). These mechanisms operate in a complicated but co-ordinated manner to maintain the homeostasis of the pulmonary circulation. Under pathological conditions, the interaction between ECs and VSMCs may be chronically altered so that a sustained increase in vasocontractility and abnormal vascular proliferation develops, which leads to high pulmonary artery pressure, vascular remodeling, right ventricular hypertrophy, and the clinical condition, pulmonary hypertension (PH) (1,(21)(22)(23)(24). This article discusses the recent progress in our knowledge of the interactions between ECs and SMCs thr...

show abstract

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

Mathews

Levin

2016

Developmental Neurobiology

121

View full text Add to dashboard Cite

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.

show abstract

Serotonin passes through myoendothelial gap junctions to promote pulmonary arterial smooth muscle cell differentiation

Abstract: Gairhe S, Bauer NN, Gebb SA, McMurtry IF. Serotonin passes through myoendothelial gap junctions to promote pulmonary arterial smooth muscle cell differentiation.

Cited by 47 publications

References 64 publications

Regulation of Cellular Communication by Signaling Microdomains in the Blood Vessel Wall

Regulation of Cellular Communication by Signaling Microdomains in the Blood Vessel Wall

Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension

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

Contact Info

Product

Resources

About