Immunolocalization of Transforming Growth Factor-α, Epidermal Growth Factor (EGF), and EGF-Receptor in Normal and Injured Developing Human Lung

Strandjord, Thomas P.; Clark, John D.; Guralnick, Daniel E; Madtes, David K.

doi:10.1203/00006450-199512000-00005

Cited by 80 publications

(62 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…TGF␣ is expressed in bronchioles and saccular epithelia in late gestational lungs (Strandjord et al, 1993(Strandjord et al, , 1994(Strandjord et al, , 1995Ruocco et al, 1996). It was reported that the expression is decreased by 50% during the transition from the canalicular (E19 -E20) to the saccular (E21) stage in late-term fetal rat lung (Kubiak et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

HB‐EGF decelerates cell proliferation synergistically with TGFα in perinatal distal lung development

Minami

Iwamoto

Mekada

2007

Developmental Dynamics

View full text Add to dashboard Cite

Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a member of the EGF family of growth factors that is suggested to be involved in distal lung development. In HB-EGF null (HB del/del ) newborns, a histopathologic analysis revealed abnormally thick saccular walls occurring from embryonic day 18.5 that reduced the terminal saccular space area. HB-EGF gene deletion resulted in a significant increase in cell proliferation, indicating that HB-EGF suppresses distal lung cell proliferation. Furthermore, an analysis of saccular morphology and proliferation in HB-EGF and transforming growth factor-␣ (TGF␣) double-mutant newborns revealed that HB-EGF and TGF␣ function synergistically in this suppression. Finally, crosses between HB del/del mice and waved 2 mice, a hypomorphic EGF receptor (EGFR) mutant strain, suggest that HB-EGF and EGFR cooperate in this process. Thus, HB-EGF has a novel suppressive function that contributes to decelerating distal lung cell proliferation synergistically with TGF␣ through EGFR in perinatal distal lung development. Developmental Dynamics 237:247-258, 2008.

show abstract

Section: Discussionmentioning

confidence: 99%

HB‐EGF decelerates cell proliferation synergistically with TGFα in perinatal distal lung development

Minami

Iwamoto

Mekada

2007

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…In addition, overactivation of the AKT/mTOR pathway has been reported in bronchial epithelium with conditional deletion of phosphatase and tensin homolog (PTEN), which brings about papillary epithelial hyperplasia analogous to that observed in Mig-6 -/-lungs (Dave et al, 2007;Yanagi et al, 2007). An increase in EGFR ligands, such as EGF, HbEGF and AREG in Mig-6 -/-lungs, has also been observed in human fetal and neonatal lungs with BPD and in injured lungs, suggesting that the autocrine/paracrine regulation of EGF signaling might contribute to the pathogenesis of Mig-6 -/-lungs (Singh and Harris, 2005;Stahlman et al, 1989;Strandjord et al, 1995).…”

Section: Research Articlementioning

confidence: 99%

Mig-6is required for appropriate lung development and to ensure normal adult lung homeostasis

et al. 2009

View full text Add to dashboard Cite

), the lungs were normal. Knockdown of MIG-6 in H441 human bronchiolar epithelial cells increased phospho-EGFR and phospho-AKT levels as well as cell proliferation, whereas knockdown of MIG-6 in human lung microvascular endothelial (HMVEC-L) cells promoted their apoptosis. These results demonstrate that Mig-6 is required for prenatal and perinatal lung development, in part through the regulation of EGF signaling, as well as for maintaining proper pulmonary vascularization.

show abstract

“…The hematopoietic cytokine granulocyte macrophage colony stimulating factor (GM-CSF) is up-regulated by inflammation (12) and plays an important role in surfactant homeostasis (13). TGF-␣ disrupts lung morphogenesis in mice (14) and has been implicated in the pathogenesis of BPD (15). Finally, TGF-␤1 is a cytokine essential for normal lung development (16), although its overexpression decreases alveolarization in animal models (17).…”

Section: B Ronchopulmonary Dysplasia (Bpd) Is a Chronic Lung Dis-mentioning

confidence: 99%

Early Alterations of Growth Factor Patterns in Bronchoalveolar Lavage Fluid From Preterm Infants Developing Bronchopulmonary Dysplasia

Been

Debeer²,

Iwaarden

et al. 2010

Pediatr Res

View full text Add to dashboard Cite

Chronic lung disease of prematurity (bronchopulmonary dysplasia; BPD) is characterized by an arrest in lung development. We hypothesized that early alterations in pulmonary expression of growth factors important for normal lung development would precede development of BPD. Bronchoalveolar lavage fluid (BALF) was obtained from ventilated preterm infants (n ϭ 62) on postnatal d 0, 1, 3, and 7 and analyzed for total phospholipids (PL), VEGF, PDGF-BB, TGF-␣ and -␤1, granulocyte macrophage colony stimulating factor (GM-CSF), and keratinocyte growth factor (KGF). Levels (Ln transformed) were compared between infants developing BPD and BPD-free survivors, adjusted for potential confounders.

show abstract

Immunolocalization of Transforming Growth Factor-α, Epidermal Growth Factor (EGF), and EGF-Receptor in Normal and Injured Developing Human Lung

Cited by 80 publications

References 23 publications

HB‐EGF decelerates cell proliferation synergistically with TGFα in perinatal distal lung development

HB‐EGF decelerates cell proliferation synergistically with TGFα in perinatal distal lung development

Mig-6is required for appropriate lung development and to ensure normal adult lung homeostasis

Early Alterations of Growth Factor Patterns in Bronchoalveolar Lavage Fluid From Preterm Infants Developing Bronchopulmonary Dysplasia

Contact Info

Product

Resources

About