Isolation of alveolar type II cells from fetal rat lung by differential adherence in monolayer culture

Batenburg, Joseph J.; Otto-Verberne, C. J. M.; Have-Opbroek, A. A. W. Ten; Klazinga, Wies

doi:10.1016/0005-2760(88)90053-7

Cited by 58 publications

(31 citation statements)

References 35 publications

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“…fAEC II Isolation and Culture-fAEC II were isolated as described (20). The Oklahoma State University Animal use and Care Committee approved all the procedures used in this study.…”

Section: Methodsmentioning

confidence: 99%

Pleiotrophin Regulates Lung Epithelial Cell Proliferation and Differentiation during Fetal Lung Development via β-Catenin and Dlk1

Weng¹,

Gao

Bhaskaran

et al. 2009

Journal of Biological Chemistry

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The role of pleiotrophin in fetal lung development was investigated. We found that pleiotrophin and its receptor, proteintyrosine phosphatase receptor ␤/, were highly expressed in mesenchymal and epithelial cells of the fetal lungs, respectively. Using isolated fetal alveolar epithelial type II cells, we demonstrated that pleiotrophin promoted fetal type II cell proliferation and arrested type II cell trans-differentiation into alveolar epithelial type I cells. Pleiotrophin also increased wound healing of injured type II cell monolayer. Knockdown of pleiotrophin influenced lung branching morphogenesis in a fetal lung organ culture model. Pleiotrophin increased the tyrosine phosphorylation of ␤-catenin, promoted ␤-catenin translocation into the nucleus, and activated T cell factor/lymphoid enhancer factor transcription factors. Dlk1, a membrane ligand that initiates the Notch signaling pathway, was identified as a downstream target of the pleiotrophin/␤-catenin pathway by endogenous dlk1 expression, promoter assay, and chromatin immunoprecipitation. These results provide evidence that pleiotrophin regulates fetal type II cell proliferation and differentiation via integration of multiple signaling pathways including pleiotrophin, ␤-catenin, and Notch pathways.Fetal lung development is a complex biological process. Rat lung originates from the foregut endoderm as a bifurcation at embryonic day 10 (E10) and undergoes several generations of dichotomous branching morphogenesis to form a respiratory tree thereafter (1). The columnar epithelial cells differentiate into Clara cells and epithelial cells. Although surfactant protein C is detected as early as E13, fetal alveolar epithelial type II cells (fAEC II) 3 are not fully differentiated until E18 when glycogen pool-enriched cells become cuboidal and differentiate into cells containing lamellar bodies. fAEC II can further differentiate and give rise to the alveolar epithelial type I cells (AEC I).The regulation of fetal lung development includes coordinated regulation of molecular pathways as well as reciprocal interactions among mesenchymal cells, epithelial cells, and the extracellular matrix (2). Precise signals from mesenchymal cells regulate lung branching morphogenesis and lead to cell fate determination and the subsequent generation of cell type diversity in the lung epithelium. For example, mesenchymal cells secrete fibroblast growth factor 10 (3, 4). Fibroblast growth factor 10 in turn binds to its receptor, which is located on the surface of epithelial cells. The binding transduces a message to downstream signaling to regulate cell proliferation, differentiation, migration, and branching morphogenesis. Similarly, the epithelial cells also secrete signal molecules to interact with the mesenchyme. Sonic hedgehog (Shh) is growth factor expressed in the developing epithelium. Its receptor, Patched-1 (Ptc), is located on mesenchymal cells. The interaction between Shh and Ptc has been shown to be required for lung bud formation (5). Other growth factors such as pl...

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“…fAEC II Isolation and Culture-fAEC II were isolated as described (20). The Oklahoma State University Animal use and Care Committee approved all the procedures used in this study.…”

Section: Methodsmentioning

confidence: 99%

Pleiotrophin Regulates Lung Epithelial Cell Proliferation and Differentiation during Fetal Lung Development via β-Catenin and Dlk1

Weng¹,

Gao

Bhaskaran

et al. 2009

Journal of Biological Chemistry

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“…FLE cells were harvested according to methods previously described by ourselves (16) and others (20) and were grown in primary cultures. In brief, timed gestation 20 d (term = 22 d) fetal Wistar rats had their lungs removed and minced into !-mm3 pieces.…”

Section: Methodsmentioning

confidence: 99%

“…Thompson, Scarborough, Ontario, Canada) 100 mesh filter. The cells were then incubated with 0.1% collagenase and purified using a dif-ferential adhesion and centrifugation technique (16,20). After each incubation step, protease activity was stopped using 5% FCS.…”

Section: Methodsmentioning

confidence: 99%

Arginine Vasopressin and Atrial Natriuretic Peptide Do Not Alter Ion Transport by Cultured Fetal Distal Lung Epithelium

1992

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ABSTRAa. Previous studies have shown that i.v. arginine vasopressin (AVP) decreases but does not stop lung fluid secretion in term fetuses not in labor. Although it has been presumed that the response to AVP results from augmented sodium transport, there is controversy whether AVP actually does affect sodium transport in mammalian lung epithelium. To determine if AVP or aldosterone could alone or together augment sodium transport in the perinatal lung, we studied primary cultures of fetal rat distal lung epithelium in Ussing chambers. The short circuit current of these sodium-transporting cells was not affected by the application of either 30 or 300 mU/mL AVP whether or not they were previously exposed to aldosterone M). Aldosterone also did not affect the baseline bioelectric properties. Short circuit current increased in response to 8-bromo cAMP M) and 3-isobutyl-1-methylxanthine M) to levels 169 f 16 (SEM) and 172 f 7% of respective baseline values. AVP had no effect in cells pretreated with 3-isobutyl-1-methylxanthine. Monolayers also did not respond to atrial natriuretic peptide (lo-" to lo-' M). Monolayers of Na-absorbing A6 renal epithelium did increase short circuit current with either aldosterone or AVP. AVP increased endogenous cAMP levels in A6 but not fetal rat distal lung epithelium cells, suggesting that fetal rat distal lung epithelium lacks V2 receptors. These studies demonstrate that AVP does not increase ion ' transport in cultured fetal distal lung epithelium although these cells possess the necessary second messenger system. (Pediatr Res 31: 318-322,1992) Abbreviations AVP, arginine vasopressin FLE, fetal rat distal lung epithelium Isc, short circuit current IBMX, isobutyl-1-methylxanthine 8 Br, bromoadenosine HBSS, Hanks' balanced salt solution PD, potential difference R, resistance ANP, atrial natriuretic peptide MEM, minimum essential medium At birth, the newborn lung is filled with fluid, which must be cleared before efficient gas exchange can take place. Epithelial have demonstrated that the sodium transport blocker amiloride can block p-agonist-induced fluid absorption in the fetal lamb lung ( 1 ) and delay fluid clearance in newborn guinea piglets (2). Studies using amiloride analogs have also suggested that the ability of amiloride to delay postnatal lung water clearance results from its blockade of epithelial sodium channels (3). To investigate mechanisms that could increase this perinatal lung epithelial sodium transport, we chose to study AVP because it reduces fluid secretion in fetal goats ( 4 ) and lambs ( 5 ) and circulates in the fetus in increased concentrations during normal delivery (6).Numerous studies (e.g. Refs. 7-1 1 ) have demonstrated that AVP can increase sodium transport in some non-lung tissues by increasing the number of active membrane-associated sodium channels (10). It is unknown whether these observations can be extrapolated to different species or to different epithelial membranes. For example, it has been reported that the AVP increases sodium transport i...

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“…Type II cells and fibroblasts were isolated from 19-day fetal rat lungs by differential adherence, as described before [33].…”

Section: 2 Cell Tsolation and Incubationmentioning

confidence: 99%

Pre‐translational regulation by glucocorticoid of fatty acid and phosphatidylcholine synthesis in type II cells from fetal rat lung

Batenburg

Elfring

1992

FEBS Letters

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Enposure to fibroblast-eonditioncd eortisol-eontaining medium increased fatty acid synthas¢ activity and f~tty acid syntltas¢, acetyl-CoA carboxylase and ATP citrate lyase mRNA abundance in fetal type II alveolar epithelial cells. Both fibroblast conditioning and cortisol in the medium were required for maximal effect on the mRNA levels, indieatin~ involvement of mesenehymal-¢pith¢lial interaction in the ¢ortisol effects. The observed effects provide evidence for an earlier hypothesis that increased activity of CTP:phosphocboline cytidylyltransfera~e in lung tissue caused by ghcocorticoid is due to increased fatty acid synthesis. However, evidence suggesting pre-translat ional regulation of this enzyme by glucoeortieoid was also found.

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Isolation of alveolar type II cells from fetal rat lung by differential adherence in monolayer culture

Cited by 58 publications

References 35 publications

Pleiotrophin Regulates Lung Epithelial Cell Proliferation and Differentiation during Fetal Lung Development via β-Catenin and Dlk1

Pleiotrophin Regulates Lung Epithelial Cell Proliferation and Differentiation during Fetal Lung Development via β-Catenin and Dlk1

Arginine Vasopressin and Atrial Natriuretic Peptide Do Not Alter Ion Transport by Cultured Fetal Distal Lung Epithelium

Pre‐translational regulation by glucocorticoid of fatty acid and phosphatidylcholine synthesis in type II cells from fetal rat lung

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