Hypoxic remodelling of Ca2+ stores does not alter human cardiac myofibroblast invasion

Riches, Kirsten; Hettiarachchi, Nishani T.; Porter, Karen E.; Peers, Chris

doi:10.1016/j.bbrc.2010.11.060

Cited by 3 publications

(2 citation statements)

References 29 publications

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“…Previous studies demonstrated myofibroblasts played an important role in remodeling after inflammation or injury (17,30,44). During the processes, including cutaneous wound repair, myocardial infarction, and liver fibrosis, the directed migration of myofibroblasts led to accumulation at the sites of specified tissue (26,27,42). Therefore, defected myofibroblast migration might be associated with the abnormal location of myofibroblasts and contribute to alveolar developmental arrest.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide disrupts the directional persistence of alveolar myofibroblast migration through EGF receptor

Yuan

Tang

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Bronchopulmonary dysplasia (BPD) is characterized by alveolar simplification with decreased alveolar number and increased airspace size. Formation of alveoli involves a process known as secondary septation triggered by myofibroblasts. This study investigated the underlying mechanisms of altered lung morphogenesis in a rat model of BPD induced by intra-amniotic injection of lipopolysaccharide (LPS). Results showed that LPS disrupted alveolar morphology and led to abnormal localization of myofibroblasts in the lung of newborn rats, mostly in primary septa with few in secondary septa. To identify potential mechanisms, in vitro experiments were carried out to observe the migration behavior of myofibroblasts. The migration speed of lung myofibroblasts increased with LPS treatment, whereas the directional persistence decreased. We found that LPS induced activation of EGFR and overexpression of its ligand, TGF-α in myofibroblasts. AG1478, an EGFR inhibitor, abrogated the enhanced locomotivity of myofibroblasts by LPS and also increased the directional persistence of myofibroblast migration. Myofibroblasts showed a high asymmetry of phospho-EGFR localization, which was absent after LPS treatment. Application of rhTGF-α to myofibroblasts decreased the directional persistence. Our findings indicated that asymmetry of phospho-EGFR localization in myofibroblasts was important for cell migration and its directional persistence. We speculate that LPS exposure disrupts the asymmetric localization of phospho-EGFR, leading to decreased stability of cell polarity and final abnormal location of myofibroblasts in vivo, which is critical to secondary septation and may contribute to the arrested alveolar development in BPD.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide disrupts the directional persistence of alveolar myofibroblast migration through EGF receptor

Yuan

Tang

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…These cells express α-smooth muscle actin (α-SMA) and are referred to as α-SMA-containing stress fibers [ 62 ]. The cells are joined by gap junctions that express Cx43 [ 63 ], enabling Ca 2+ signaling that causes the release of Ca 2+ from the endoplasmic reticulum in response to ATP, histamine, 5-hydroxytryptamine (5-HT) [ 64 ] (Lundqvist et al, unpublished), or bradykinin [ 65 ]. These cells produce extracellular matrix, exhibit high Na + /K + -ATPase activity levels in the extracellular matrix [ 66 ], and also produce and release a substantial number of cytokines and growth factors into their environment, thereby regulating cell function in an autocrine and paracrine manner [ 62 ].…”

Section: Coupled Cell Network In Different Body Organsmentioning

confidence: 99%

Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation

Hanssoń

Skiöldebrand

2015

J Inflamm

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Several organs in the body comprise cells coupled into networks. These cells have in common that they are excitable but do not express action potentials. Furthermore, they are equipped with Ca2+ signaling systems, which can be intercellular and/or extracellular. The transport of small molecules between the cells occurs through gap junctions comprising connexin 43. Examples of cells coupled into networks include astrocytes, keratinocytes, chondrocytes, synovial fibroblasts, osteoblasts, connective tissue cells, cardiac and corneal fibroblasts, myofibroblasts, hepatocytes, and different types of glandular cells. These cells are targets for inflammation, which can be initiated after injury or in disease. If the inflammation reaches the CNS, it develops into neuroinflammation and can be of importance in the development of systemic chronic inflammation, which can manifest as pain and result in changes in the expression and structure of cellular components. Biochemical parameters of importance for cellular functions are described in this review.

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Differential regulation of collagen secretion by kinin receptors in cardiac fibroblast and myofibroblast

Catalán

Smolic

Contreras

et al. 2012

Toxicology and Applied Pharmacology

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Hypoxic remodelling of Ca2+ stores does not alter human cardiac myofibroblast invasion

Cited by 3 publications

References 29 publications

Lipopolysaccharide disrupts the directional persistence of alveolar myofibroblast migration through EGF receptor

Lipopolysaccharide disrupts the directional persistence of alveolar myofibroblast migration through EGF receptor

Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation

Differential regulation of collagen secretion by kinin receptors in cardiac fibroblast and myofibroblast

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