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  • 1
    Keywords: CELLS ; EXPRESSION ; BLOOD ; CELL ; SYSTEM ; GENE ; PROTEIN ; PROTEINS ; METABOLISM ; MICE ; COMPLEX ; FAMILY ; MEMBER ; MEMBERS ; knockout ; MOUSE ; NO ; IDENTIFICATION ; PROMOTER ; PLASMA ; MEMBRANE ; inactivation ; ADHESION ; CELL-ADHESION ; PLASMA-MEMBRANE ; Jun ; beta-catenin ; CRE RECOMBINASE ; PROTEIN INTERACTIONS ; CATENIN ; FOLLICLE ; E-cadherin ; ENDOCRINE ; FAMILIES ; INCREASE ; ADHESION MOLECULE UVOMORULIN ; GLAND ; cell adhesion ; development ; KNOCKOUT MICE ; ADHERENS JUNCTIONS ; USA ; LOSSES ; BARRIER ; CDNA CLONING ; MAINTENANCE ; Cre-loxP system ; FOLLICULAR CELLS ; KSP-CADHERIN ; SHAPE
    Abstract: We have conditionally inactivated the E-cadherin gene in the thyroid follicular cells of mouse embryo to unravel its role in thyroid development. We used the Cre-loxP system in which the Cre-recombinase was expressed under the control of the tissue-specific thyroglobulin promoter that becomes active at embryonic d 15. At postnatal d 7, thyroid follicle lumens in the knockout mice were about 30% smaller with respect to control mice and had an irregular shape. E-cadherin was almost completely absent in thyrocytes, beta-catenin was significantly reduced, whereas no change in gamma-catenin was detected. alpha-Catenin was also reduced on the cell plasma membrane. Despite the dramatic loss of E-cadherin and beta-catenin, cell-cell junctions were not affected, the distribution of tight junction proteins was unaltered, and no increase of thyroglobulin circulating in the blood was observed. In addition, we found that other members of the cadherin family, the R-cadherin and the Ksp-cadherin, were expressed in thyrocytes and that their membrane distribution was not altered in the E-cadherin conditional knockout mouse. Our results indicate that E-cadherin has a role in the development of the thyroid gland and in the expression of beta-catenin, but it is not essential for the maintenance of follicular cell adhesion
    Type of Publication: Journal article published
    PubMed ID: 17347311
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  • 2
    Keywords: CELLS ; EXPRESSION ; proliferation ; CELL-PROLIFERATION ; IN-VIVO ; KINASE ; DEATH ; DIFFERENTIATION ; MICE ; SUPPRESSION ; ASSOCIATION ; MOUSE ; TRANSGENIC MICE ; MEMBRANE ; EXTRACELLULAR-MATRIX ; BETA ; ADHESION ; EPITHELIAL-CELLS ; Jun ; INTEGRIN ; MORPHOGENESIS ; signaling ; INTEGRATION ; MATRIX ; ASSOCIATIONS ; RE ; BASEMENT-MEMBRANE ; extracellular matrix ; interaction ; GLAND ; cell proliferation ; SWITZERLAND ; MDA-MB-231 breast cancer cells ; beta 1 integrin ; mammary gland ; focal adhesion kinase ; p21(Cip1)
    Abstract: Integrin - extracellular matrix interactions play important roles in the coordinated integration of external and internal cues that are essential for proper development. To study the role of beta 1 integrin in the mammary gland, Itg beta 1(flox/flox) mice were crossed with WAPiCre transgenic mice, which led to specific ablation of beta 1 integrin in luminal alveolar epithelial cells. In the beta 1 integrin mutant mammary gland, individual alveoli were disorganized resulting from alterations in cell - basement membrane associations. Activity of focal adhesion kinase (FAK) was also decreased in mutant mammary glands. Luminal cell proliferation was strongly inhibited in beta 1 integrin mutant glands, which correlated with a specific increase of p21(Cip1) expression. In a p21(Cip1) null background, there was a partial rescue of BrdU incorporation, providing in vivo evidence linking p21(Cip1) to the proliferative defect observed in beta 1 integrin mutant glands. A connection between p21(Cip1) and beta 1 integrin as well as FAK was also established in primary mammary cells. These results point to the essential role of beta 1 integrin signaling in mammary epithelial cell proliferation
    Type of Publication: Journal article published
    PubMed ID: 15889143
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  • 3
    Keywords: CELLS ; proliferation ; DIFFERENTIATION ; HEALTH ; BONE-FORMATION ; OSTEOPOROSIS ; POSTMENOPAUSAL WOMEN ; RANDOMIZED CONTROLLED-TRIAL ; RECEPTOR-ALPHA ; CANCELLOUS BONE
    Abstract: Postmenopausal osteoporosis is characterized by declining estrogen levels, and estrogen replacement therapy has been proven beneficial for preventing bone loss in affected women. While the physiological functions of estrogen in bone, primarily the inhibition of bone resorption, have been studied extensively, the effects of pharmacological estrogen administration are still poorly characterized. Since elevated levels of follicle-stimulating hormone (FSH) have been suggested to be involved in postmenopausal bone loss, we investigated whether the skeletal response to pharmacological estrogen administration is mediated in a FSH-dependent manner. Therefore, we treated wildtype and FSHbeta-deficicent (Fshb(-/-)) mice with estrogen for 4 weeks and subsequently analyzed their skeletal phenotype. Here we observed that estrogen treatment resulted in a significant increase of trabecular and cortical bone mass in both, wildtype and Fshb(-/-) mice. Unexpectedly, this FSH-independent pharmacological effect of estrogen was not caused by influencing bone resorption, but primarily by increasing bone formation. To understand the cellular and molecular nature of this osteo-anabolic effect we next administered estrogen to mouse models carrying cell specific mutant alleles of the estrogen receptor alpha (ERalpha). Here we found that the response to pharmacological estrogen administration was not affected by ERalpha inactivation in osteoclasts, while it was blunted in mice lacking the ERalpha in osteoblasts or in mice carrying a mutant ERalpha incapable of DNA binding. Taken together, our findings reveal a previously unknown osteo-anabolic effect of pharmacological estrogen administration, which is independent of FSH and requires DNA-binding of ERalpha in osteoblasts.
    Type of Publication: Journal article published
    PubMed ID: 23209701
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  • 4
    Keywords: APOPTOSIS ; CELLS ; IN-VIVO ; PATHWAY ; PATHWAYS ; GENE ; GENE-EXPRESSION ; PROTEIN ; DIFFERENTIATION ; EPITHELIA ; TISSUE ; MICE ; TRANSDUCTION ; ACTIVATION ; TISSUES ; GROWTH-FACTOR RECEPTOR ; signal transduction ; MOUSE ; DISRUPTION ; SIGNAL-TRANSDUCTION ; SIGNALING PATHWAY ; SIGNALING PATHWAYS ; EXTRACELLULAR-MATRIX ; BETA ; ADHESION ; EPITHELIAL-CELLS ; INTEGRIN ; TYROSINE PHOSPHORYLATION ; INITIATION ; MORPHOGENESIS ; signaling ; MATRIX ; DEFICIENCY ; PROGRAM ; RE ; MAMMARY-GLAND ; extracellular matrix ; GLAND ; development ; INTEGRINS ; beta 1 integrin ; EPITHELIUM ; mammary gland ; LACTATION ; CYTOPLASMIC DOMAIN ; GENETIC-EVIDENCE ; GLAND DEVELOPMENT ; RECONSTITUTED BASEMENT-MEMBRANE ; STAT5
    Abstract: Integrin-mediated adhesion regulates the development and function of a range of tissues; however, little is known about its role in glandular epithelium. To assess the contribution of beta 1 integrin, we conditionally deleted its gene in luminal epithelia during different stages of mouse mammary gland development and in cultured primary mammary epithelia. Loss of beta 1 integrin in vivo resulted in impaired alveologenesis and lactation. Cultured beta 1 integrin-null cells displayed abnormal focal adhesion function and signal transduction and could not form or maintain polarized acini. In vivo, epithelial cells became detached from the extracellular matrix but remained associated with each other and did not undergo overt apoptosis. beta 1 integrin-null mammary epithelial cells did not differentiate in response to prolactin stimulation because of defective Stat5 activation. In mice where beta 1 integrin was deleted after the initiation of differentiation, fewer defects in alveolar morphology occurred, yet major deficiencies were also observed in milk protein and milk fat production and Stat5 activation, indicating a permissive role for beta 1 integrins in prolactin signaling. This study demonstrates that beta 1 integrin is critical for the alveolar morphogenesis of a glandular epithelium and for maintenance of its differentiated function. Moreover, it provides genetic evidence for the cooperation between integrin and cytokine signaling pathways
    Type of Publication: Journal article published
    PubMed ID: 16301336
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  • 5
    Keywords: brain ; RECEPTOR ; CELLS ; EXPRESSION ; CELL ; Germany ; SYSTEM ; SITE ; SITES ; GENE ; MICE ; FAMILY ; animals ; CONTRAST ; cell cycle ; CELL-CYCLE ; CYCLE ; MEMBER ; DELETION ; MOUSE ; MUTANT ; NERVOUS-SYSTEM ; PERFORMANCE ; NUMBER ; LINE ; inactivation ; PROGENITOR CELLS ; ABNORMALITIES ; CRE RECOMBINASE ; RE ; FAMILIES ; LEADS ; MICE LACKING ; CRE ; DEFECTS ; neurogenesis ; NUCLEAR ; function ; DEFECT ; progenitor cell ; animal ; RETINAL DEGENERATION ; NULL MICE ; PROGENITOR-CELL ; AGGRESSION ; aggressiveness ; ANXIETY ; blindness ; conditional mutant ; learning and memory ; RADIAL GLIA ; TLX
    Abstract: During embryogenesis, tailless, an orphan member of the nuclear receptor family, is expressed in the germinal zones of the brain and the developing retina, and is involved in regulating the cell cycle of progenitor cells. Consequently, a deletion of the tailless gene leads to decreased cell number with associated anatomical defects in the limbic system, the cortex and the eye. These structural abnormalities are associated with blindness, increased aggressiveness, poor performance in learning paradigms and reduced anxiousness. In order to assess the contribution of blindness to the behavioural changes, we established tailless mutant mice with intact visual abilities. We generated a mouse line in which the second exon of the tailless gene is flanked by loxP sites and crossed these animals with a transgenic line expressing the Cre recombinase in the neurogenic area of the developing brain, but not in the eye. The resulting animals have anatomically indistinguishable brains compared with tailless germline mutants, but are not blind. They are less anxious and much more aggressive than controls, like tailless germline mutants. In contrast to germline mutants, the conditional mutants are not impaired in fear conditioning. Furthermore, they show good performance in the Morris water-maze despite severely reduced hippocampal structures. Thus, the pathological aggressiveness and reduced anxiety found in tailless germline mutants are due to malformations caused by inactivation of the tailless gene in the brain, but the poor performance of tailless null mice in learning and memory paradigms is dependent on the associated blindness
    Type of Publication: Journal article published
    PubMed ID: 17953618
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  • 6
    Keywords: RECEPTOR ; CELLS ; GROWTH ; CELL ; Germany ; PATHWAY ; MICE ; MECHANISM ; TARGET ; TRANSGENIC MICE ; hormone ; SUBUNIT ; SIGNALING PATHWAY ; EPITHELIAL-CELLS ; DIET ; PROTEIN-KINASE-C ; SUBUNITS ; TARGETS ; CYCLIC-AMP ; ALPHA-SUBUNIT ; EFFECTOR ; LACKING ; signaling ; DEFICIENCY ; ADULT ; secretion ; regulation ; GLAND ; cell proliferation ; development ; USA ; function ; PREVENTS ; MEDICINE ; FOLLICULAR CELLS ; PHOSPHOLIPASE-C ; STIMULATING HORMONE ; THYROTROPIN RECEPTOR
    Abstract: The function of the adult thyroid is regulated by thyroid-stimulating hormone (TSH), which acts through a G protein-coupled receptor. Overactivation of the TSH receptor results in hyperthyroidisin and goiter. The G(s)-mediated stimulation of adenylyl cyclase-dependent cAMP formation has been regarded as the principal intracellular signaling mechanism mediating the action of TSH. Here we show that the G(q)/G(11)-mediated signaling pathway plays an unexpected and essential role in the regulation of thyroid function. Mice lacking the a subunits of G(q) and G(11) specifically in thyroid epithelial cells showed severely reduced iodine organification and thyroid hormone secretion in response to TSH, and many developed hypothyroidism within months after birth. In addition, thyrocyte-specific: G alpha(q)/G alpha(11)-deficient mice lacked the normal proliferative thyroid response to TSH or goitrogenic diet, indicating an essential role of this pathway in the adaptive growth of the thyroid gland. Our data suggest that G(q)/G(11) and their downstream effectors are promising targets to interfere with increased thyroid function and growth
    Type of Publication: Journal article published
    PubMed ID: 17694176
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