Transforming growth factor ?2, but not ?1 and ?3, is critical for early rat lung branching

Liu, Jason; Tseu, Irene; Wang, Jinxia; Tanswell, Keith; Post, Martin

doi:10.1002/(sici)1097-0177(200004)217:4<343::aid-dvdy2>3.0.co;2-f

Cited by 42 publications

(30 citation statements)

References 66 publications

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“…This pattern is dynamic and changes with the stage of development, and this tendency is also reported in the development of mammary glands and other glandular organs [1,7,15,19,25,27,29]. Moreover, the overlapping patterns of TGF-beta expression in morphogenetically active epithelial structures are reported in structures of murine head and neck, such as whisker follicle, salivary gland and tooth bud [25].…”

Section: Discussionmentioning

confidence: 87%

Developing human minor salivary glands: morphological parallel relation between the expression of TGF-beta isoforms and cytoskeletal markers of glandular maturation

et al. 2007

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Morphogenesis of salivary glands involves complex coordinated events. Synchronisation between cell proliferation, polarisation and differentiation, which are dependent on epithelial-mesenchymal interactions and on the microenvironment, is a requirement. Growth factors mediate many of these orchestrated biological processes and transforming growth factor-beta (TGF-beta) appear to be relevant. Using immunohistochemistry and immunofluorescence, we have mapped the distribution of TGF-beta 1, 2 and 3 and compared it with the expression of maturation markers in human salivary glands obtained from foetuses ranging from weeks 4 to 24 of gestation. TGF-beta 1 first appeared during canalisation stage in the surrounding mesenchyme and, in the more differentiated stages, was expressed in the cytoplasm of acinar cells throughout the adult gland. TGF-beta 2 was detected since the bud stage of the salivary gland. Its expression was observed in ductal cells and increased along gland differentiation, TGF-beta 3 was detected from the canalisation stage of the salivary gland, being weakly expressed on ductal cells, and it was the only factor detected on myoepithelial cells. The data suggest that TGF-beta have a role to play in salivary gland development and differentiation.

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Section: Discussionmentioning

confidence: 87%

Developing human minor salivary glands: morphological parallel relation between the expression of TGF-beta isoforms and cytoskeletal markers of glandular maturation

et al. 2007

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“…At first sight, the finding that TGF-β1 induces tubule formation appears difficult to reconcile with previous in vitro and in vivo studies suggesting a negative regulatory role for TGF-βs in branching morphogenesis. It is noteworthy, however, that while most experimental evidence points to an inhibitory activity of TGF-βs [81-86], studies in embryonic lung have shown that low concentrations of TGF-β2 promote branching morphogenesis, whereas higher concentrations are inhibitory [87]. The prevalent notion that TGF-βs are negative modulators of branching morphogenesis is based on three main sets of experimental data.…”

Section: Discussionmentioning

confidence: 99%

Low concentrations of transforming growth factor-beta-1 induce tubulogenesis in cultured mammary epithelial cells

2007

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Background: Formation of branching tubes is a fundamental step in the development of glandular organs. To identify extracellular cues that orchestrate epithelial tubulogenesis, we employed an in vitro assay in which EpH4-J3B1A mammary epithelial cells form spheroidal cysts when grown in collagen gels under serum-free conditions, but form branching tubules in the presence of fetal calf serum (FCS).

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“…al Lyons et al, 1991;Liu et al, 2000). In the presence of stromal support cells, TGF-β1 has a biphasic effect on osteoclast differentiation from marrow precursors, in that TGF-β1 stimulates differentiation at a low dose while inhibiting differentiation at a higher dose (Shinar and Rodan, 1990;Mundy, 1991;Yamaguchi and Kishi, 1995).…”

mentioning

confidence: 99%

Roles of stromal cell RANKL, OPG, and M‐CSF expression in biphasic TGF‐β regulation of osteoclast differentiation

Karst

Gorny

Galvin

et al. 2004

Journal Cellular Physiology

164

125

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To better understand the complex roles of transforming growth factor-beta (TGF-β) in bone metabolism, we examined the impact of a range of TGF-β concentrations on osteoclast differentiation. In co-cultures of support cells and spleen or marrow osteoclast precursors, low TGF-β concentrations stimulated while high concentrations inhibited differentiation. We investigated the influences of TGF-β on macrophage colony stimulating factor (M-CSF), receptor activator of NF-κB ligand (RANKL), and osteoprotegerin (OPG) expression and found a dose dependent inhibition of M-CSF expression. RANKL expression was elevated at low TGF-β concentrations with a less dramatic increase in OPG. Addition of OPG blocked differentiation at the stimulatory TGF-β dose. Thus, low TGF-β concentrations elevated the RANKL/OPG ratio while high concentrations did not, supporting that, at low TGF-β concentrations, there is sufficient M-CSF and a high RANKL/OPG ratio to stimulate differentiation. At high TGF-β concentrations, the RANKL/OPG ratio and M-CSF expression were both repressed and there was no differentiation. We examined whether TGF-β-mediated repression of osteoclasts differentiation is due to these changes by adding M-CSF and/or RANKL and did not observe any impact on differentiation repression. We studied direct TGF-βimpacts on osteoclast precursors by culturing spleen or marrow cells with M-CSF and RANKL. TGF-β treatment dose-dependently stimulated osteoclast differentiation. These data indicate that low TGF-β levels stimulate osteoclast differentiation by impacting the RANKL/OPG ratio while high TGF-β levels repress osteoclast differentiation by multiple avenues including mechanisms independent of the RANKL/OPG ratio or M-CSF expression regulation.Transforming growth factor-beta (TGF-β) is a ubiquitous multifunctional cytokine that has a spectrum of influences. The variety of reported responses to TGF-β depends, at least in part, on experimental conditions as well as the cell type under study. Within the bone environment, TGF-β is a key regulator of bone metabolism. Although all TGF-β isoforms bind to the same receptor complex, there have been some reports of different cellular responses to the different isoforms (Jennings et al

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Transforming growth factor ?2, but not ?1 and ?3, is critical for early rat lung branching

Cited by 42 publications

References 66 publications

Developing human minor salivary glands: morphological parallel relation between the expression of TGF-beta isoforms and cytoskeletal markers of glandular maturation

Developing human minor salivary glands: morphological parallel relation between the expression of TGF-beta isoforms and cytoskeletal markers of glandular maturation

Low concentrations of transforming growth factor-beta-1 induce tubulogenesis in cultured mammary epithelial cells

Roles of stromal cell RANKL, OPG, and M‐CSF expression in biphasic TGF‐β regulation of osteoclast differentiation

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