scholarly journals JNK suppresses pulmonary fibroblast elastogenesis during alveolar development

2014 ◽  
Vol 15 (1) ◽  
pp. 34 ◽  
Author(s):  
Sheng Liu ◽  
Harikrishnan Parameswaran ◽  
Sarah M Young ◽  
Brian M Varisco
Keyword(s):  
Alveolar Development ◽  
Pulmonary Fibroblast

scholarly journals Postnatal alveolar development of the rabbit

2002 ◽  
Vol 93 (2) ◽  
pp. 629-635 ◽  
Author(s):  
Jana Kovar ◽  
Peter D. Sly ◽  
Karen E. Willet
Keyword(s):  
Wall Thickness ◽  
Alveolar Wall ◽  
Alveolar Volume ◽  
Surface Fraction ◽  
Alveolar Development ◽  
The Right ◽  
Timing Of Onset ◽  
Alveolar Formation ◽  
Tissue Fraction

Previous studies of alveolarization have used rats or lambs; however, neither closely reflects human alveolar development. We characterized alveolar development in rabbits ( n = 3–7 /group) at 28 days gestation (dg) to 9 mo to determine whether they followed the human pattern more closely. The right lung was made up of 30% alveolar and 50% duct space at 28 dg to 3 days and of 50 and 30%, respectively, at 14 days to 9 mo. Tissue fraction and alveolar wall thickness decreased by 40% 28 dg to birth. At birth, ∼4.5% of the number of alveoli seen at 9 mo were present, with alveolar number increasing progressively well into adulthood. The rate of alveolar formation was high around birth, decreasing progressively with age. Alveolar volume increased more than twofold (28 dg to birth) and continued to increase postnatally to 16 wk. Surface fraction decreased by 17% (28 dg to 3 days), after which it remained uniform. Our findings suggest that the timing of onset of alveolarization in humans and rabbits is similar and that rabbits may be used to model postnatal influences on alveolar development.

PULMONARY FIBROBLAST FUNCTION IN AN ACUTE LUNG INJURY MODEL

1994 ◽  
Vol 37 (1) ◽  
pp. 156
Author(s):  
Andrew Mikulaschek ◽  
Stantey Z Trooskin ◽  
Allen Nonn ◽  
Jason Winfield
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Injury Model ◽  
Lung Injury Model ◽  
Pulmonary Fibroblast

scholarly journals Decreased IGF Type 1 Receptor Signaling in Mammary Epithelium during Pregnancy Leads to Reduced Proliferation, Alveolar Differentiation, and Expression of Insulin Receptor Substrate (IRS)-1 and IRS-2

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3233-3245 ◽  
Author(s):  
Zhaoyu Sun ◽  
Sain Shushanov ◽  
Derek LeRoith ◽  
Teresa L. Wood
Keyword(s):  
Insulin Receptor ◽  
Mammary Epithelium ◽  
Whey Acidic Protein ◽  
Dominant Negative ◽  
Acidic Protein ◽  
Normal Mammary Gland ◽  
Insulin Receptor Substrate ◽  
Alveolar Development ◽  
Pregnancy And Lactation

The IGFs and the IGF type 1 receptor (IGF-1R) are essential mediators of normal mammary gland development in mice. IGF-I and the IGF-1R have demonstrated functions in formation and proliferation of terminal end buds and in ductal outgrowth and branching during puberty. To study the functions of IGF-1R during pregnancy and lactation, we established transgenic mouse lines expressing a human dominant-negative kinase dead IGF-1R (dnhIGF-1R) under the control of the whey acidic protein promoter. We provide evidence that the IGF-1R pathway is necessary for normal epithelial proliferation and alveolar formation during pregnancy. Furthermore, we demonstrate that the whey acidic protein-dnhIGF-1R transgene causes a delay in alveolar differentiation including lipid droplet formation, lumen expansion, and β-casein protein expression. Analysis of IGF-1R signaling pathways showed a decrease in P-IGF-1R and P-Akt resulting from expression of the dnhIGF-1R. We further demonstrate that disruption of the IGF-1R decreases mammary epithelial cell expression of the signaling intermediates insulin receptor substrate (IRS)-1 and IRS-2. No alterations were observed in downstream signaling targets of prolactin and progesterone, suggesting that activation of the IGF-1R may directly regulate expression of IRS-1/2 during alveolar development and differentiation. These data show that IGF-1R signaling is necessary for normal alveolar proliferation and differentiation, in part, through induction of signaling intermediates that mediate alveolar development.

scholarly journals Loss of CD73-mediated extracellular adenosine production exacerbates inflammation and abnormal alveolar development in newborn mice exposed to prolonged hyperoxia

2017 ◽  
Vol 82 (6) ◽  
pp. 1039-1047 ◽  
Author(s):  
Huiling Li ◽  
Harry Karmouty-Quintana ◽  
Ning-Yuan Chen ◽  
Tingting Mills ◽  
Jose Molina ◽  
...  
Keyword(s):  
Newborn Mice ◽  
Extracellular Adenosine ◽  
Alveolar Development

scholarly journals PDGFRα signaling is required for alveolar development in the mouse lung

2017 ◽  
Vol 145 ◽  
pp. S147 ◽  
Author(s):  
Johanna Andrae ◽  
Christer Betsholtz ◽  
Leonor Gouveia
Keyword(s):  
Mouse Lung ◽  
Alveolar Development

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

2012 ◽  
Vol 302 (6) ◽  
pp. L569-L579 ◽  
Author(s):  
Huiping Li ◽  
Xiaobing Yuan ◽  
Jun Tang ◽  
Yongjun Zhang
Keyword(s):  
Egf Receptor ◽  
Migration Behavior ◽  
Lung Morphogenesis ◽  
Alveolar Development ◽  
Underlying Mechanisms ◽  
High Asymmetry ◽  
Treatment Application ◽  
Lps Treatment

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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