Galectin-1 in secondary alveolar septae of neonatal mouse lung

Foster, Jennifer J.; Goss, Kelli L.; George, Caroline; Bangsund, Peter J.; Snyder, Jeanne M.

doi:10.1152/ajplung.00054.2006

Cited by 23 publications

(20 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Regardless, we identified a set of six genes that met these criteria and whose expression peaks at the initiation of alveolar formation. Among these, Lgals1 (galectin-1) has recently been shown to have the expression pattern described by the array data, and to be expressed within secondary alveolar septae uniquely being formed at this stage (39). In addition, spatial and temporal changes in the expression of rbp1 may participate in retinoid-dependent alveolar formation (40)(41)(42)(43)(44)(45)(46).…”

Section: Discussionmentioning

confidence: 92%

Expression Profiles of the Mouse Lung Identify a Molecular Signature of Time-to-Birth

Kho

Bhattacharya

Mecham

et al. 2009

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 92%

Expression Profiles of the Mouse Lung Identify a Molecular Signature of Time-to-Birth

Kho

Bhattacharya

Mecham

et al. 2009

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

“…FOSTER et al [19] generated mRNA expression data from the tips of growing P6 septae isolated by laser-capture microscopy. Interestingly, only three of the 25 genes being most intensively upregulated were also significantly changed in our data (see online supplementary table), namely tenascin-XB and C as well as drebrin 1, whereas tenascin-XB was downregulated in our lung homogenate.…”

Section: Previous Investigations In the Fieldmentioning

confidence: 99%

Comparative gene expression profiling of post-natal and post-pneumonectomy lung growth

Wilhelm²,

Fink³

et al. 2009

Eur Respir J

View full text Add to dashboard Cite

Although increasing numbers of patients suffer from chronic destructive lung diseases, there are no effective therapeutic options apart from transplantation. Understanding the mechanisms of physiological and regenerative alveolar septation is prerequisite for the development of regenerative therapies for the lung. We compared lung gene expression in the phase of induction of post-natal and post-pneumonectomy alveolarisation to identify regulatory genes involved in both processes.We performed genome-wide microarray screenings of newborn and pneumonectomised mouse lungs 1 and 3 days after birth or surgery. Selected candidates were validated by real-time PCR, Western blot and in situ hybridisation.We found 58 genes to be regulated in both models with 40 candidates being changed likewise. Many of these genes participated in growth and differentiation processes. Additionally, immune system, structural molecules, respiratory chain, signal transduction and metabolism were involved. Some candidates were not yet linked to specific functions. The highest regulatory concordance was observed for various isoforms of (pro-)collagen molecules, elastin and the elastin-associated protein fibrillin1 being corporately upregulated.Our findings do not definitively support a common regulating mechanism for induction of postnatal and adult alveolarisation, but some candidates in the intersection of both models are promising for further investigations.

show abstract

“…Alveolar formation in mouse begins with eruption of secondary crests accompanied by coordinated expression of contractile proteins by interstitial cells (Adler et al, 1989;Jostarndt-Fogen et al, 1998;Yamada et al, 2005) and increased production of elastic matrix (Mariani et al, 2002;RothKleiner and Post, 2005;Foster et al, 2006). Many available mouse genetic models showing severe lung defects in the first postnatal week (Bostrom et al, 1996;Weinstein et al, 1998;Neptune et al, 2003) highlight the importance of the specialized constituents of the lung elastic matrix or the numbers and behavior of interstitial myofibroblasts in secondary septation (reviewed in Bourbon et al, 2005).…”

Section: Mutant Micementioning

confidence: 99%

Role for ephrinB2 in postnatal lung alveolar development and elastic matrix integrity

Wilkinson

Schittny

Reinhardt

et al. 2008

Developmental Dynamics

View full text Add to dashboard Cite

Alveoli are formed in the lung by the insertion of secondary tissue folds, termed septa, which are subsequently remodeled to form the mature alveolar wall. Secondary septation requires interplay between three cell types: endothelial cells forming capillaries, contractile interstitial myofibroblasts, and epithelial cells. Here, we report that postnatal lung alveolization critically requires ephrinB2, a ligand for Eph receptor tyrosine kinases expressed by the microvasculature. Mice homozygous for the hypomorphic knockin allele ephrinB2 ⌬V/⌬V , encoding mutant ephrinB2 with a disrupted C-terminal PDZ interaction motif, show severe postnatal lung defects including an almost complete absence of lung alveoli and abnormal and disorganized elastic matrix. Lung alveolar formation is not sensitive to loss of ephrinB2 cytoplasmic tyrosine phosphorylation sites. Postnatal day 1 mutant lungs show extracellular matrix alterations without differences in proportions of major distal cell populations. We conclude that lung alveolar formation relies on endothelial ephrinB2 function. Developmental Dynamics 237:2220 -2234, 2008.

show abstract

Galectin-1 in secondary alveolar septae of neonatal mouse lung

Abstract: in secondary alveolar septae of neonatal mouse lung.

Cited by 23 publications

References 41 publications

Expression Profiles of the Mouse Lung Identify a Molecular Signature of Time-to-Birth

Expression Profiles of the Mouse Lung Identify a Molecular Signature of Time-to-Birth

Comparative gene expression profiling of post-natal and post-pneumonectomy lung growth

Role for ephrinB2 in postnatal lung alveolar development and elastic matrix integrity

Contact Info

Product

Resources

About