Embryonic mouse lung morphogenesis and type II cytodifferentiation in serumless, chemically defined medium using prolonged in vitro cultures

Jaskoll, Tina; Don-Wheeler, Grace; Johnson, R.B.; Slavkin, Harold C.

doi:10.1016/0045-6039(88)90062-0

Cited by 52 publications

(47 citation statements)

References 21 publications

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“…Organ cultures were performed according to our modification of the method of Jaskoll et al (28). Briefly, E13.5 or E14.5 intestines were dissected from the embryos in cold DPBS (Invitrogen 14040-133), connective tissue was separated, and intestines were placed on transwells (Costar 3428) in BGJb media (Invitrogen 12591-038) supplemented with 1% pen/strep (vol/ vol) (Invitrogen 15140-122) and 0.1 mg/mL ascorbic acid.…”

Section: Methodsmentioning

confidence: 99%

“…To probe the role of Hh signaling in cluster formation and villus emergence, we developed an organ-culture system based on a modification of the Jaskoll et al protocol (28). Intestines were dissected from embryos between E13.5 and E14.5 (before the onset of villus formation), placed on transwell membranes, and cultured over media without serum supplement (Fig.…”

Section: Multiple Rounds Of Cluster Formation Give Rise To Approximatelymentioning

confidence: 99%

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Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Walton

Kolterud

Czerwinski

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

145

230

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In the adult intestine, an organized array of finger-like projections, called villi, provide an enormous epithelial surface area for absorptive function. Villi first emerge at embryonic day (E) 14.5 from a previously flat luminal surface. Here, we analyze the cell biology of villus formation and examine the role of paracrine epithelial Hedgehog (Hh) signals in this process. We find that, before villus emergence, tight clusters of Hh-responsive mesenchymal cells form just beneath the epithelium. Cluster formation is dynamic; clusters first form dorsally and anteriorly and spread circumferentially and posteriorly. Statistical analysis of cluster distribution reveals a patterned array; with time, new clusters form in spaces between existing clusters, promoting approximately four rounds of villus emergence by E18.5. Cells within mesenchymal clusters express Patched1 and Gli1, as well as Pdgfrα, a receptor previously shown to participate in villus development. BrdU-labeling experiments show that clusters form by migration and aggregation of Hh-responsive cells. Inhibition of Hh signaling prevents cluster formation and villus development, but does not prevent emergence of villi in areas where clusters have already formed. Conversely, increasing Hh signaling increases the size of villus clusters and results in exceptionally wide villi. We conclude that Hh signals dictate the initial aspects of the formation of each villus by controlling mesenchymal cluster aggregation and regulating cluster size.epithelial-mesenchymal cross-talk | field pattern | villus morphogenesis

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Section: Methodsmentioning

confidence: 99%

Section: Multiple Rounds Of Cluster Formation Give Rise To Approximatelymentioning

confidence: 99%

Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Walton

Kolterud

Czerwinski

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

145

230

View full text Add to dashboard Cite

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“…Embryonic BIO.A mouse lung primordia have previously been shown to undergo extensive epithelial branching and histodifferentiation in serumless, chemically defined medium (Jaskoll et al, 1988;Slavkin et al, 1989). When E11.5 or E l 2 lung primordia were cultured for up to 7 days in hormone-free, chemically defined medium, morphogenesis (epithelial proliferation and branching) occurred (Figs.…”

Section: Effect Of Tnf-c~ Supplementation On Embryonic Lung Morphogenmentioning

confidence: 99%

“…Given that the addition of exogenous CORT to cultured embryonic BIO.A mouse lung primordia has been shown to stimulate pulmonary maturation, type I1 cell histodifferentiation, and SP-A synthesis (Jaskoll et al, 1988), that CORT regulates TNF-a expression Kutteh et al, 1991;Martinet et al, 19921, and that CORT receptor-mediated stimulation of histodifferentiation may involve the modulation of a growth stimulus (Schule et al, 1990), we hypothesized Representative lung primordium cultured in control medium for 7 days. In the early and mid-pseudoglandular stages (A and B), TNF-R is randomly distributed throughout the mesenchyme (m) and in the basement membrane region (arrows), as well as on the apical (arrowheads) and basal surfaces of the pulmonary epithelia.…”

Section: Relationship Between Tnf-a Immunoreactive Proteins and Cortmentioning

confidence: 99%

“…As a first approach to this question, we utilized a previously described (Jaskoll et al, 1988) serumless, chemically defined lung organ culture model to investigate the effect of TNF-a supplementation on embryonic mouse lung primordia. In these in vitro experiments, TNF-a has a marked dose-dependent stimulatory effect on branching morphogenesis and SP-A expression.…”

Section: Relationship Between Tnf-a Immunoreactive Proteins and Cortmentioning

confidence: 99%

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Tumor necrosis factor‐α and embryonic mouse lung morphogenesis

Jaskoll

Boyer

Melnick

1994

Developmental Dynamics

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The ontogeny of the embryonic and fetal lung involves complex interactions between epithelial and mesenchymal primordia which require a specific program of gene regulation and signal transduction. Past studies in our laboratory using congenic mouse strains indicate that one or more genes which map to the H-2 region of chromosome 17 regulate the rate of lung morphogenesis, defined in this context as differentiative heterochrony among strains. Since hormones and growth factors are the messengers of morphogenesis, it was logical to propose that tumor necrosis factor-a (TNF-a), a well-characterized cytokine whose gene maps to the D-region of the H-2 complex, is a putative mediator of lung morphogenesis. We investigated this proposition using immunochemical methods and a serumless, chemically defined in vitro model system. Our results demonstrate that: (1) TNF-a has a specific spatiotemporal localization, in vivo and in vitro; (2) TNF-a receptor, in vivo and in vitro, is localized throughout the embryonic lung; (3) TNF-a supplementation in vitro of embryonic lung primordia has a marked dose-dependent, stimulatory effect on branching morphogenesis and surfactant-associated protein (SP-A) expression; (4) multiple immunoreactive proteins, including 17,26, and 68 kDa species, are expressed during development in vivo, and a subset of these are expressed in vitro; and (5) both time-and glucocorticoid-dependent changes occur in the in vivo expression pattern of TNF-a immunoreactive proteins after 4 and 7 days in vitro, including the up-regulation of a novel 40 kDa protein. Given that glucocorticoids (CORT) regulate TNF-a expression and TNF-a's ability to stimulate pulmonary morphodifferentiation and histodifferentiation, we conclude that TNF-a is an autocrine/paracrine pulmonary cytokine, probably a component of the lung morphogenesis pathway regulated by CORT. o 1994 WiIey-Liss, Inc.

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Glucocorticoids, tumor necrosis factor-α, and epidermal growth factor regulation of pulmonary morphogenesis: a multivariate in vitro analysis of their related actions

1996

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Embryonic mouse lung morphogenesis and type II cytodifferentiation in serumless, chemically defined medium using prolonged in vitro cultures

Cited by 52 publications

References 21 publications

Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Tumor necrosis factor‐α and embryonic mouse lung morphogenesis

Glucocorticoids, tumor necrosis factor-α, and epidermal growth factor regulation of pulmonary morphogenesis: a multivariate in vitro analysis of their related actions

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