Characterization of the Gene and Promoter for RTI40, a Differentiation  Marker of Type I Alveolar Epithelial Cells

Vanderbilt, Jeff N.; Dobbs, Leland G.

doi:10.1165/ajrcmb.19.4.3121

Cited by 36 publications

(22 citation statements)

References 38 publications

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“…Overall, the size and exon-intron organization of the mouse podoplanin gene closely resembles that determined for the rat counterpart (Vanderbilt and Dobbs, 1998) and is given together with the strategy for gene disruption in Figure 6a.…”

Section: ) Micementioning

confidence: 72%

Cardiac malformations and myocardial abnormalities in podoplanin knockout mouse embryos: Correlation with abnormal epicardial development

Mahtab

Wijffels

Akker

et al. 2008

Developmental Dynamics

135

141

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Section: ) Micementioning

confidence: 72%

Cardiac malformations and myocardial abnormalities in podoplanin knockout mouse embryos: Correlation with abnormal epicardial development

Mahtab

Wijffels

Akker

et al. 2008

Developmental Dynamics

135

141

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“…To evaluate effects of TO and sham operation on the distal pulmonary epithelium, we used methods described below to measure RTI 40 and RTII70, proteins specific in the lung to the apical membranes of rat type I and type II pneumonocytes, respectively (13,14,16), and mRNA for RTI40 (48), as well as surfactant proteins (SP)-A and -B, and mRNAs for SP-A, -B, and -C.…”

Section: Methodsmentioning

confidence: 99%

Tracheal occlusion stimulates cell cycle progression and type I cell differentiation in lungs of fetal rats

Yoshizawa

Chapin

Sbragia

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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. Tracheal occlusion stimulates cell cycle progression and type I cell differentiation in lungs of fetal rats. Am J Physiol Lung Cell Mol Physiol 285: L344-L353, 2003. First published April 4, 2003 10.1152/ajplung.00281.2002 has been reported to stimulate lung growth but decreases number and maturation of type II cells, effects that vary with gestational age and duration of TO. We examined effects of a novel method of TO (unipolar microcautery to seal the trachea) produced at 19.5-20 days (d) of gestation in fetal rats; fetuses were delivered at term, 22 d. Controls were sham operated and unoperated littermates. TO increased wet lung weight but not dry lung weight or lung DNA and protein. To evaluate further the effects of TO, we examined the cell cycle regulators, cyclins D1 and A, in fetal lungs. Cyclin D1 increased with TO (P Ͻ 0.005). TO also increased expression of the type I epithelial cell marker RTI40 (mRNA and protein). TO decreased mRNA for surfactant proteins (SP)-A and -C but did not affect protein levels of SP-A and -B and of RTII70, a type II epithelial cell marker. We conclude that TO by microcautery, even of short duration, has diverse pulmonary effects including stimulating increased levels of cyclin D1 with probable cell cycle progression, type I cell differentiation, and possibly inhibiting type II cell function.cyclins; fetal lung development; lung growth; pulmonary epithelial differentiation; pulmonary surfactant LATE IN GESTATION, the fetal lung rapidly changes in appearance from an almost glandular tissue into a lacy, thin-walled organ capable of efficient gas exchange and surfactant production. During this period lung growth, septal thinning, maturation of the surfactant system, and differentiation of alveolar type I and type II cells occur. Normal fetal lung development is crucial for survival in extrauterine life, but factors that control these developmental processes and their interdependence have been incompletely defined.Lung growth and maturation of the surfactant system are the most widely studied aspects of late fetal lung development. Fetal lung growth is dependent on several mechanical factors, including adequate intrathoracic space, sufficient amniotic fluid volume, normal fetal breathing movements, and a positive transpulmonary distending pressure (21,27). In contrast, maturation of the surfactant system is highly dependent on endocrine factors (4, 50). There is relatively little information about factors that are responsible for differentiation of alveolar epithelial type I and type II cells in vivo.Several investigators have shown that occlusion of the trachea in experimental animals increases lung growth but has adverse affects on type II cell number and function (2,10,11,15,40). These changes occur when tracheal occlusion (TO) is produced relatively early in gestation and maintained for a prolonged period. In contrast, when TO is produced later in gestation for a relatively short period, lung growth is stimulated, and adverse affects on the type II cell population are di...

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“…To evaluate the effects of oligohydramnios on the distal pulmonary epithelium, we used methods described below to measure RTI 40 and RTII70, proteins specific in lung to the apical membranes of rat type I and type II pneumonocytes, respectively (13,20), and mRNA for RTI40 (47).…”

Section: Methodsmentioning

confidence: 99%

Effects of oligohydramnios on lung growth and maturation in the fetal rat

Kitterman

Chapin

Vanderbilt

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI 40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA (P Ͻ 0.05) and protein (P Ͻ 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter (P Ͻ 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells. fetal lung development; lung distension; pulmonary epithelial differentiation; pulmonary hypoplasia; pulmonary surfactant IN LATE GESTATION, the fetal lung undergoes marked changes in preparation for the transition to extrauterine life. These changes include growth, enlargement of distal potential air spaces, thinning of the septa, maturation of the surfactant system, and differentiation of distal pulmonary epithelium into mature alveolar type I and type II cells. Several studies have shown that fetal lung growth is controlled primarily by mechanical factors, especially distension of the lung (for reviews, see Refs. 26 and 29) and that maturation of the surfactant system is controlled primarily by endocrine factors (for reviews, see Refs. 3 and 48). In contrast, relatively little is known about factors that regulate differentiation of the alveolar epithelium.In 1977, Alcorn and associates (2) reported that tracheal ligation in fetal sheep, which increased lung distension, caused accelerated lung growth and a qualitative reduction in the number of alveolar type II cells; conversely, chronic drainage of tracheal fluid, which inhibited lung distension, retarded lung growth and increased the number of type II cells. However, they reported neither quantitative data for cell counts nor measurements of indicators of surfactant, which is produced by type II cells. Subsequently, other investigators have studied tracheal ligation in fetal sheep and have confirmed that an increase in lung distension results in a lower number of type II cells (6,11,37) and a higher percentage of type I cells (18). Tracheal ligation also results in lower concentrations in the lung of surfactant protein (SP)-A and saturated phosphatidylcholine (SatPC), the major surface-active lipid in pulmonary surfactant (28), as well as mRNA for SP-A, -B, and -C (32). Conversely, transection of the cervical spinal cord (which abolishes fetal breathing movemen...

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Characterization of the Gene and Promoter for RTI40, a Differentiation Marker of Type I Alveolar Epithelial Cells

Cited by 36 publications

References 38 publications

Cardiac malformations and myocardial abnormalities in podoplanin knockout mouse embryos: Correlation with abnormal epicardial development

Cardiac malformations and myocardial abnormalities in podoplanin knockout mouse embryos: Correlation with abnormal epicardial development

Tracheal occlusion stimulates cell cycle progression and type I cell differentiation in lungs of fetal rats

Effects of oligohydramnios on lung growth and maturation in the fetal rat

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