Insulin modulation of bronchial epithelial cell fibronectin in vitro

Romberger, Debra J.; Pladsen, P.; Claassen, L.; Yoshida, Makoto; Beckmann, Joe D.; Rennard, Stephen I.

doi:10.1152/ajplung.1995.268.2.l230

Cited by 3 publications

(2 citation statements)

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“…In a similar study, Rickard and associates (22) demonstrated that both freshly isolated and cultured bovine bronchial epithelial cells adhered equally well to fibronectin, laminin, and collagen IV. Epithelial cells make fibronectin in response to inflammatory mediators (23,24), and it has been suggested that both fibronec- Figure 5. Closure of monolayer wounds in GPTEC monolayers after treatment with EGF.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Migration and Wound Repair of Guinea-Pig Airway Epithelial Cells in Response to Epidermal Growth Factor

Kim

McKinnis

Nawrocki

et al. 1998

Am J Respir Cell Mol Biol

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Repair of the airway epithelium after injury involves cell proliferation, migration, and spreading into the injury site. The growth factor, epidermal growth factor (EGF), elicits proliferation of many epithelial cell types in vitro and in vivo, including airways epithelium. However, its effects on cell migration and spreading are less clear. We studied the effects of EGF on guinea-pig tracheal epithelial cell (GPTEC) chemotaxis and migration during wound repair. Primary GPTEC were allowed to migrate through a gelatin-coated filter for 6 h in a chemotaxis chamber, after which the number of migrated cells were counted. EGF elicited migration of GPTEC that was substantial and concentration-dependent. Treatment with EGF accelerated closure of small wounds in confluent epithelial monolayers substantially as measured by video microscopy over 24 h. These effects of EGF were concentration-dependent and seen in monolayer wounds of different size. Effects of EGF did not depend on the underlying matrix on which cells were grown; cells grown on laminin, fibronectin, or collagen had similar wound closure velocities in response to EGF. Early effects of EGF on wound closure were not due to cell proliferation at the wound edge. These data demonstrate that EGF elicits both chemotaxis and migration of airway epithelial cells in culture.

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Section: Discussionmentioning

confidence: 99%

Stimulation of Migration and Wound Repair of Guinea-Pig Airway Epithelial Cells in Response to Epidermal Growth Factor

Kim

McKinnis

Nawrocki

et al. 1998

Am J Respir Cell Mol Biol

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“…Insulin Promotes the survival of epithelial cells 11 Participates in epithelium restoration integrity after its damage 12 Stimulates NO release from epithelial cells 13 Relaxes precontracted airways 13 Respiratory system is considered an alternative route for insulin administration for the treatment of type 1 diabetes mellitus 71 Low incidence of asthma in patients with diabetes mellitus 72…”

Section: Endogenous Factorsmentioning

confidence: 99%

Physiological Parameters Affecting the Modulatory Role of Airway Epithelium on Airway Smooth Muscle Responsiveness

Hatziefthimiou

Paschalis-Adam²,

Paraskeva³

2014

Pulm Res Respir Med Open J

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Numerous studies have revealed the significant action of airway epithelium as a nonspecific defence mechanism in airways. In addition, epithelial cells release biologically active agents, which modulate airway tone. Importantly, airway epithelium function is influenced by physiological parameters, including the release of endogenous factors, age, gender, load, and bronchi size. The primary goal of this review is to summarize knowledge concerning the effect of the aforementioned parameters on the modulatory role of airway epithelium on airway smooth muscle responsiveness. These effects may be implicated in the pathophysiology of airway diseases like asthma and Chronic Obstructive Pulmonary Disease (COPD).

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Pressuromodulation at the cell membrane as the basis for small molecule hormone and peptide regulation of cellular and nuclear function

Sarin¹

2015

J Transl Med

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Building on recent knowledge that the specificity of the biological interactions of small molecule hydrophiles and lipophiles across microvascular and epithelial barriers, and with cells, can be predicted on the basis of their conserved biophysical properties, and the knowledge that biological peptides are cell membrane impermeant, it has been further discussed herein that cellular, and thus, nuclear function, are primarily regulated by small molecule hormone and peptide/factor interactions at the cell membrane (CM) receptors. The means of regulating cellular, and thus, nuclear function, are the various forms of CM Pressuromodulation that exist, which include Direct CM Receptor-Mediated Stabilizing Pressuromodulation, sub-classified as Direct CM Receptor-Mediated Stabilizing Shift Pressuromodulation (Single, Dual or Tri) or Direct CM Receptor-Mediated Stabilizing Shift Pressuromodulation (Single, Dual or Tri) cum External Cationomodulation (≥3+ → 1+); which are with respect to acute CM receptor-stabilizing effects of small biomolecule hormones, growth factors or cytokines, and also include Indirect CM- or CM Receptor-Mediated Pressuromodulation, sub-classified as Indirect 1ary CM-Mediated Shift Pressuromodulation (Perturbomodulation), Indirect 2ary CM Receptor-Mediated Shift Pressuromodulation (Tri or Quad Receptor Internal Pseudo-Cationomodulation: SS 1+), Indirect 3ary CM Receptor-Mediated Shift Pressuromodulation (Single or Dual Receptor Endocytic External Cationomodulation: 2+) or Indirect (Pseudo) 3ary CM Receptor-Mediated Shift Pressuromodulation (Receptor Endocytic Hydroxylocarbonyloetheroylomodulation: 0), which are with respect to sub-acute CM receptor-stabilizing effects of small biomolecules, growth factors or cytokines. As a generalization, all forms of CM pressuromodulation decrease CM and nuclear membrane (NM) compliance (whole cell compliance), due to pressuromodulation of the intracellular microtubule network and increases the exocytosis of pre-synthesized vesicular endogolgi peptides and small molecules as well as nuclear-to-rough endoplasmic reticulum membrane proteins to the CM, with the potential to simultaneously increase the NM-associated chromatin DNA transcription of higher molecular weight protein forms, secretory and CM-destined, mitochondrial and nuclear, including the highest molecular weight nuclear proteins, Ki67 (359 kDa) and Separase (230 kDa), with the latter leading to mitogenesis and cell division; while, in the case of growth factors or cytokines with external cationomodulation capability, CM Receptor External Cationomodulation of CM receptors (≥3+ → 1+) results in cationic extracellular interaction (≥3+) with extracellular matrix heparan sulfates (≥3+ → 1+) concomitant with lamellopodesis and cell migration. It can be surmised that the modulation of cellular, and nuclear, function is mostly a reactive process, governed, primarily, by small molecule hormone and peptide interactions at the cell membrane, with CM receptors and the CM itself. These insights taken together, provide...

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Insulin modulation of bronchial epithelial cell fibronectin in vitro

Cited by 3 publications

References 0 publications

Stimulation of Migration and Wound Repair of Guinea-Pig Airway Epithelial Cells in Response to Epidermal Growth Factor

Stimulation of Migration and Wound Repair of Guinea-Pig Airway Epithelial Cells in Response to Epidermal Growth Factor

Physiological Parameters Affecting the Modulatory Role of Airway Epithelium on Airway Smooth Muscle Responsiveness

Pressuromodulation at the cell membrane as the basis for small molecule hormone and peptide regulation of cellular and nuclear function

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