Matrix Protein–Specific Regulation of Cx43 Expression in Cardiac Myocytes Subjected to Mechanical Load

Shanker, Asheesh; Yamada, Kiyomi; Green, Karen G.; Yamada, Kathryn A.; Saffitz, Jeffrey E.

doi:10.1161/01.res.0000158964.42008.a2

Cited by 49 publications

(40 citation statements)

References 41 publications

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“…The reliability of the GJIC assay is supported by a comparison of dye diffusion between the risk and non-risk areas in the same section after coronary occlusion. Several studies have demonstrated causality between Cx43 upregulation and GJIC activation, [11][12][13] and the phosphorylated state of Cx43 also mediates Cx43 distribution to GJs and regulation of GJIC activity. Phosphorylation at serine residues 325, 328 and/or 330 (pS325/328/330-Cx43) promotes distribution of Cx43 to GJs and enhances GJIC, 14 and phosphorylation at serine 365 (pS365-Cx43) has a "gatekeeper" function.…”

Section: Causality Of Cx43 Translocation With Gjic Enhancementmentioning

confidence: 99%

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Shintani-Ishida

Unuma

Yoshida

2009

Circ J

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Section: Causality Of Cx43 Translocation With Gjic Enhancementmentioning

confidence: 99%

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Shintani-Ishida

Unuma

Yoshida

2009

Circ J

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“…Previous studies of other cell types have reported an upregulation of gap junction communication with altered integrin-matrix interactions (Czyz et al, 2005;Lampe et al, 1998;Shanker et al, 2005). CNCs were impaled with microelectrodes and the gap junction permeable fluorescent tracer, carboxyfluorescein, was iontophoretically injected (Fig.…”

Section: Gap Junction Communication Unchanged With Different Fibronecmentioning

confidence: 99%

Connexin 43-mediated modulation of polarized cell movement and the directional migration of cardiac neural crest cells

et al. 2006

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Connexin 43 knockout (Cx43␣1KO) mice have conotruncal heart defects that are associated with a reduction in the abundance of cardiac neural crest cells (CNCs) targeted to the heart. In this study, we show CNCs can respond to changing fibronectin matrix density by adjusting their migratory behavior, with directionality increasing and speed decreasing with increasing fibronectin density. However, compared with wild-type CNCs, Cx43␣1KO CNCs show reduced directionality and speed, while CNCs overexpressing Cx43␣1 from the CMV43 transgenic mice show increased directionality and speed. Altered integrin signaling was indicated by changes in the distribution of vinculin containing focal contacts, and altered temporal response of Cx43␣1KO and CMV43 CNCs to ␤1 integrin function blocking antibody treatment. High resolution motion analysis showed Cx43␣1KO CNCs have increased cell protrusive activity accompanied by the loss of polarized cell movement. They exhibited an unusual polygonal arrangement of actin stress fibers that indicated a profound change in cytoskeletal organization. Semaphorin 3A, a chemorepellent known to inhibit integrin activation, was found to inhibit CNC motility, but in the Cx43␣1KO and CMV43 CNCs, cell processes failed to retract with semaphorin 3A treatment. Immunohistochemical and biochemical analyses suggested close interactions between Cx43␣1, vinculin and other actin-binding proteins. However, dye coupling analysis showed no correlation between gap junction communication level and fibronectin plating density. Overall, these findings indicate Cx43␣1 may have a novel function in mediating crosstalk with cell signaling pathways that regulate polarized cell movement essential for the directional migration of CNCs.

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“…␤ 1 -Integrin is abundantly expressed in type II cells and seems essential for the development of the lung epithelium (2), for cell anchoring to different substrates (9), and as mechanoreceptor in many other cell types (20,29,37,44,48,51,53). In agreement with these studies, cell adhesion experiments demonstrated that ␤ 1 -integrin mediates type II cell attachment to laminin substrates.…”

Section: Discussionmentioning

confidence: 67%

Integrins β₁, α₆, and α₃contribute to mechanical strain-induced differentiation of fetal lung type II epithelial cells via distinct mechanisms

Sanchez‐Esteban¹,

Wang²,

Filardo³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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-Mechanical forces regulate lung maturation in the fetus by promoting type II epithelial differentiation. However, the cell surface receptors that transduce these mechanical cues into cellular responses remain largely unknown. When distal lung type II epithelial cells isolated from embryonic day 19 rat fetuses were cultured on flexible plates coated with laminin, fibronectin, vitronectin, collagen, or elastin and exposed to a level of mechanical strain (5%) similar to that observed in utero, transmembrane signaling responses were induced under all conditions, as measured by ERK activation. However, mechanical stress maximally increased expression of the type II cell differentiation marker surfactant protein C when cells were cultured on laminin substrates. Strain-induced alveolar epithelial differentiation was inhibited by interfering with cell binding to laminin using soluble laminin peptides (IKVIV or YIGSR) or blocking antibodies against integrin ␤1, ␣3, or ␣6. Additional studies were carried out with substrates coated directly with different nonactivating anti-integrin antibodies. Blocking integrin ␤ 1 and ␣6 binding sites inhibited both cell adhesion and differentiation, whereas inhibition of ␣ 3 prevented differentiation without altering cell attachment. These data demonstrate that various integrins contribute to mechanical control of type II lung epithelial cell differentiation on laminin substrates. However, they may act via distinct mechanisms, including some that are independent of their cell anchoring role. laminin; surfactant protein C LUNG GROWTH AND DEVELOPMENT during fetal life are critical for extrauterine survival. Premature infants are often born before sufficient lung maturation has occurred with resultant increased morbidity and mortality. Lung maturation, in part, is controlled mechanically. For example, fetal thoracic movements, which generate ϳ5% changes of the distal lung surface area (14, 15), and cell tractional forces exerted on extracellular matrix (ECM) within tissues have been shown to be critical regulators of fetal lung development (28,35,43).A key component of lung development is the differentiation of type II epithelial cells, the major source of pulmonary surfactant that prevents alveolar collapse during expiration. These cells also participate in fluid homeostasis in the alveolar lumen, host defense, and restoration of normal alveolar epithelium after lung injury (38). Past studies have shown that application of levels of mechanical strain that simulate the cell distortion produced by fetal breathing movements induces fetal type II epithelial cell maturation and that the ERK pathway mediates this response (41, 43). However, the mechanisms by which lung cells sense mechanical forces via mechanoreceptors to activate this intracellular differentiation pathway remain largely unknown.Interactions between pulmonary epithelial cells and ECM proteins such as laminin or fibronectin or different collagen subtypes modulate lung development (34). Laminin is a major glycoprotein component ...

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Matrix Protein–Specific Regulation of Cx43 Expression in Cardiac Myocytes Subjected to Mechanical Load

Cited by 49 publications

References 41 publications

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Connexin 43-mediated modulation of polarized cell movement and the directional migration of cardiac neural crest cells

Integrins β₁, α₆, and α₃contribute to mechanical strain-induced differentiation of fetal lung type II epithelial cells via distinct mechanisms

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Matrix Protein–Specific Regulation of Cx43 Expression in Cardiac Myocytes Subjected to Mechanical Load

Cited by 49 publications

References 41 publications

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Connexin 43-mediated modulation of polarized cell movement and the directional migration of cardiac neural crest cells

Integrins β1, α6, and α3contribute to mechanical strain-induced differentiation of fetal lung type II epithelial cells via distinct mechanisms

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Integrins β₁, α₆, and α₃contribute to mechanical strain-induced differentiation of fetal lung type II epithelial cells via distinct mechanisms