Effect of retinoic acid on platelet-derived growth factorand lung development in newborn rats

Author(s):  
Chen Hongbing ◽  
Chang Liwen ◽  
Liu Hanchu ◽  
Rong Zhihui ◽  
Zhu Huaping ◽  
...  
2000 ◽  
Vol 48 (4) ◽  
pp. 434-444 ◽  
Author(s):  
Kathleen A Veness-Meehan ◽  
Frank G Bottone ◽  
Alan D Stiles
Keyword(s):  

Development ◽  
2000 ◽  
Vol 127 (14) ◽  
pp. 3057-3067 ◽  
Author(s):  
S. Malpel ◽  
C. Mendelsohn ◽  
W.V. Cardoso

Little is known about how retinoic acid (RA) synthesis, utilization and metabolism are regulated in the embryonic lung and how these activities relate to lung pattern formation. Here we report that early lung bud formation and subsequent branching morphogenesis are characterized by distinct stages of RA signaling. At the onset of lung development RA signaling is ubiquitously activated in primary buds, as shown by expression of the major RA-synthesizing enzyme, RALDH-2 and activation of a RARE-lacZ transgene. Nevertheless, further airway branching appears to require downregulation of RA pathways by decreased synthesis, increased RA degradation in the epithelium via P450RAI-mediated metabolism, and inhibition of RA signaling in the mesenchyme by COUPTF-II expression. These mechanisms controlling local RA signaling may be critical for normal branching, since we show that manipulating RA levels in vitro to maintain RA signaling activated as in the initial stage, leads to an immature lung phenotype characterized by failure to form typical distal buds. We show that this phenotype likely results from RA interfering with the establishment of a distal signaling center, altering levels and distribution of Fgf10 and Bmp4, genes that are essential for distal lung formation. Furthermore, RA upregulates P450RAI expression, suggesting the presence of feedback mechanisms controlling RA availability. Our study illustrates the importance of regional mechanisms that control RA availability and utilization for correct expression of pattern regulators and normal morphogenesis during lung development.


2002 ◽  
Vol 13 (15) ◽  
pp. 1873-1885 ◽  
Author(s):  
Paul Waszak ◽  
Marie-Laure Franco-Montoya ◽  
Marie-Paule Jacob ◽  
Isabelle Deprez ◽  
Micheline Levame ◽  
...  

2017 ◽  
Vol 37 (5) ◽  
pp. 427-434 ◽  
Author(s):  
Amélie Delabaere ◽  
Geoffroy Marceau ◽  
Karen Coste ◽  
Loïc Blanchon ◽  
Pierre-Jean Déchelotte ◽  
...  

Author(s):  
Chang Liwen ◽  
Rong Zhihui ◽  
Zhang Qianshen ◽  
Qian Liling

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
Dawn M. Simon ◽  
Thomas J. Mariani

Understanding lung development has significant importance to public health because of the fact that interruptions in the normal developmental processes can have prominent effects on childhood and adult lung health. It is widely appreciated that the retinoic acid (RA) pathway plays an important role in lung development. Additionally, PPARs are believed to partner with receptors of this pathway and therefore could be considered extensions of retinoic acid function, including during lung development. This review will begin by introducing the relationship between the retinoic acid pathway and PPARs followed by an overview of lung development stages and regulation to conclude with details on PPARs and the retinoic acid pathway as they may relate to lung development.


2016 ◽  
Vol 57 (6) ◽  
pp. 508-514 ◽  
Author(s):  
Liang-Ti Huang ◽  
Hsiu-Chu Chou ◽  
Chun-Mao Lin ◽  
Chung-Ming Chen

2002 ◽  
Vol 283 (5) ◽  
pp. L971-L980 ◽  
Author(s):  
Kathleen A. Veness-Meehan ◽  
Richard A. Pierce ◽  
Billie M. Moats-Staats ◽  
Alan D. Stiles

Exposure of the newborn lung to hyperoxia is associated with impaired alveolar development. In newborn rats exposed to hyperoxia and studied at day 14 of life, retinoic acid (RA) treatment improved survival and increased lung collagen but did not improve alveolar development. To determine whether RA treatment during exposure to hyperoxia results in late improvement in alveolarization, we treated newborn rats with RA and hyperoxia from day 3 to day 14 and then weaned O2 to room air by day 20, and studied the animals on day 42. O2-exposed animals had larger mean lung volumes, larger alveoli, and decreased gas-exchange tissue relative to air-exposed animals, whereas RA-treated O2-exposed animals were not statistically different from air-exposed controls. Relative to control animals, elastin staining at day 14 was decreased in hyperoxia-exposed lung independent of RA treatment, and, at day 42, elastin staining was similar in all treatment groups. At day 14, elastin gene expression was similar in all treatment groups, whereas at day 42 lung previously exposed to hyperoxia showed increased elastin signal independent of RA treatment. These results indicate that RA treatment during hyperoxia exposure promotes septal formation without evidence of effects on elastin gene expression after 4 wk of recovery.


1998 ◽  
Vol 274 (1) ◽  
pp. L1-L7 ◽  
Author(s):  
Mary A. Grummer ◽  
Richard D. Zachman

Lung development and surfactant biosynthesis are affected by retinoic acid (RA) and dexamethasone (Dex). Using a mouse lung epithelial cell line, we are exploring RA-Dex interactions through the study of RA and Dex effects on RA receptor (RAR) and surfactant protein (SP) C mRNA expression. RA increased expression of RAR-β (5.5 times) and SP-C (2 times) mRNA, with maximal effects at 24 h and at 10−6 M. The RA induction was not inhibited by cycloheximide, suggesting RA affects transcription. With added actinomycin D, RA did not affect the disappearance rate of RAR-β mRNA, but SP-C mRNA degradation was slowed, indicating an effect on SP-C mRNA stability. Dex decreased RAR-β and SP-C expression to 75 and 70% of control values, respectively, with greatest effects at 48 h and at 10−7 M. There was no effect of Dex on either RAR-β or SP-C mRNA disappearance with actinomycin D. However, cycloheximide prevented the effect of Dex. Despite Dex, RA increased both RAR-β and SP-C mRNA. This work suggests that RA and Dex affect RAR-β and SP-C genes by different mechanisms.


Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 152 ◽  
Author(s):  
Hugo Fernandes-Silva ◽  
Henrique Araújo-Silva ◽  
Jorge Correia-Pinto ◽  
Rute S Moura

Retinoic acid (RA) is a key molecular player in embryogenesis and adult tissue homeostasis. In embryo development, RA plays a crucial role in the formation of different organ systems, namely, the respiratory system. During lung development, there is a spatiotemporal regulation of RA levels that assures the formation of a fully functional organ. RA signaling influences lung specification, branching morphogenesis, and alveolarization by regulating the expression of particular target genes. Moreover, cooperation with other developmental pathways is essential to shape lung organogenesis. This review focuses on the events regulated by retinoic acid during lung developmental phases and pulmonary vascular development; also, it aims to provide a snapshot of RA interplay with other well-known regulators of lung development.


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