Mechanical strain-induced proliferation and signaling in pulmonary epithelial H441 cells

Chess, Patricia R.; Toia, Liana; Finkelstein, Jacob N.

doi:10.1152/ajplung.2000.279.1.l43

Cited by 66 publications

(53 citation statements)

References 44 publications

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“…This is supported by the fact that mechanical stretch has been shown to activate ERK and JNK in cardiac myocytes [25], mesangial cells [26], melanocytes [27], pulmonary endothelial cells [28] and L929 cells [29]. Activation of ERK-1/2 (p42/p44) was reported within 10 min of 20% elongation of H441 pulmonary epithelial cells [30]. In A549 cells, it was shown that 15% strain activated JNK (stress-activated protein kinase) within 30 min and p38 kinase at later time points (2 h), whereas ERK-1/2 was not activated [31].…”

Section: Discussionmentioning

confidence: 89%

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Uhlig

Haitsma²,

Goldmann³

et al. 2002

Eur Respir J

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Mechanical ventilation of patients can be a life-saving treatment, but also imposes additional stress on the lung. Mitogen-activated protein kinases (MAPK) represent a family of protein kinases that become phosphorylated and activated by many different forms of stress.Using Western blot analysis, the present study analysed the effects of high distending pressure ventilation on the activation of the MAPK extracellular signal-related kinases (ERK)-1/2, c-Jun amino-terminal kinases (JNK) and p38 kinase, and on the MAPKactivated transcription factors c-Jun, ETS-like protein (Elk)-1 and activating transcription factor (ATF)-2.In adult rats, ventilation with high pressure (45/10 peak inspiratory pressure/positive end-expiratory pressure in cmH 2 O) for 30 or 60 min did not affect arterial oxygenation, but resulted in enhanced phosphorylation of ERK-1/2, JNK, c-Jun, Elk-1 and ATF-2 compared to normally ventilated (13/3) rats. The activation of ERK-1/2 and JNK was located to cells resembling alveolar type II cells. In addition, high pressure ventilation enhanced phosphorylation of the inhibitor of nuclear factor (NF)-kB and nuclear translocation of the transcription factor NF-kB. In isolated perfused mouse lungs, the MAPK/ERK kinase inhibitor U0126 prevented ventilation-induced activation of ERK-1/2 and Elk-1, but had no effect on ventilation-induced cytokine release.The present authors conclude that mechanical ventilation triggers specific signalling pathways, such as the mitogen-activated protein kinase and the nuclear factor-kB pathways, which may contribute to pulmonary inflammation and proliferation. Eur Respir J 2002; 20: 946-956.

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Section: Discussionmentioning

confidence: 89%

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Uhlig

Haitsma²,

Goldmann³

et al. 2002

Eur Respir J

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“…Several cells respond to mechanical forces by activating MAPK pathways, but little is known about how mechanical stimuli are converted into biochemical signals in AEC (18). Mechanical stress has been shown to stimulate ERK1/2 in endothelial cells (11,29), cardiac myocytes (41), vascular smooth muscle cells (VSMC) (39), and in H441 cells (3). Another component of the MAPK family, the stressactivated protein kinase/c-Jun NH 2 -terminal kinase (SAPK/JNK), is activated by cyclic stretch in A549 cells (21), and stretching these cells induces an interleukin-8 release (33).…”

mentioning

confidence: 99%

Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial cells

Correa-Meyer

Pesce

Guerrero

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

112

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Mechanical stimuli are transduced into intracellular signals in lung alveolar epithelial cells (AEC). We studied whether mitogen-activated protein kinase (MAPK) pathways are activated during cyclic stretch of AEC. Cyclic stretch induced a rapid (within 5 min) increase in extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in AEC. The inhibition of Na ϩ , L-type Ca 2ϩ and stretch-activated ion channels with amiloride, nifedipine, and gadolinium did not prevent the stretch-induced ERK1/2 activation. The inhibition of Grb2-SOS interaction with an SH3 binding sequence peptide, Ras with a farnesyl transferase inhibitor, and Raf-1 with forskolin did not affect the stretch-induced ERK1/2 phosphorylation. Moreover, cyclic stretch did not increase Ras activity, suggesting that stretch-induced ERK1/2 activation is independent of the classical receptor tyrosine kinase-MAPK pathway. Pertussis toxin and two specific epidermal growth factor receptor (EGFR) inhibitors (AG-1478 and PD-153035) prevented the stretch-induced ERK1/2 activation. Accordingly, in primary AEC, cyclic stretch activates ERK1/2 via G proteins and EGFR, in Na ϩ and Ca 2ϩ influxes and Grb2-SOS-, Ras-, and Raf-1-independent pathways. mechanotransduction; mechanical stress; mitogen-activated protein kinase; lung injury; epidermal growth factor receptor MECHANICAL VENTILATION with high lung volumes and pressures causes ventilator-induced lung injury characterized by increased permeability pulmonary edema and inflammation (26,35). During mechanical ventilation with high tidal volumes, alveolar epithelial cells (AEC) can be stretched. These cells are responsible for the normal function of the alveolar capillary barrier, alveolar fluid absorption, and the synthesis of pulmonary surfactant. It is known that AEC respond to mechanical stretch in different ways. A single stretch of AEC caused cytosolic Ca 2ϩ to increase, followed by a stimulation of surfactant secretion at a single cell (37) and at the whole organ level (1).Stretching AEC increased Na

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“…In addition, ERK phosphorylation mediated by different ECM-cell interactions in fetal lung development may not be limited to type II cell differentiation. In fact, strain-induced ERK activation influences cell proliferation in pulmonary epithelial H441 cells (6) and osmotic stress and apoptosis in adult type II cells (11). These studies suggest that strain-induced ERK activation, via ECM-cell interactions, may participate in a variety of cellular processes that are important for fetal lung development, in addition to differentiation.…”

Section: Discussionmentioning

confidence: 90%

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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Mechanical strain-induced proliferation and signaling in pulmonary epithelial H441 cells

Cited by 66 publications

References 44 publications

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial 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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Mechanical strain-induced proliferation and signaling in pulmonary epithelial H441 cells

Cited by 66 publications

References 44 publications

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Ventilation-induced activation of the mitogen-activated protein kinase pathway

Cyclic stretch activates ERK1/2 via G proteins and EGFR in alveolar epithelial 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