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Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death.
Pathological examination revealed an excessive inflammatory response with massive infiltration of lymphocytes and macrophages in many organs, but primarily in heart and lungs, which suggests a prominent role for TGF-beta 1 in homeostatic regulation of immune cell proliferation and extravasation into tissues. Expand
Smad3 is key to TGF-beta-mediated epithelial-to-mesenchymal transition, fibrosis, tumor suppression and metastasis.
Focusing on models involving epithelial-to-mesenchymal transition (EMT), including injury to the lens and retina of the eye and to the kidney, it is found that loss of Smad3 blocks EMT and attenuates development of fibrotic sequelae. Expand
Smad3 as a mediator of the fibrotic response
  • K. Flanders
  • Medicine, Biology
  • International journal of experimental pathology
  • 1 April 2004
It is shown that inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation‐induced fibrosis. Expand
Smad3 signaling is required for epithelial-mesenchymal transition of lens epithelium after injury.
It is shown that EMT of primary lens epithelial cells in vitro depends on TGF-beta expression and that injury-induced EMT in vivo depends, more specifically, on signaling via Smad3. Expand
Increased production and immunohistochemical localization of transforming growth factor-beta in idiopathic pulmonary fibrosis.
Examination of lung sections of patients with advanced idiopathic pulmonary fibrosis demonstrated a marked and consistent increase in TGF-beta production in epithelial cells and macrophages when compared to patients with nonspecific inflammation and those with no inflammation or fibrosis. Expand
Evidence that transforming growth factor-β is a hormonally regulated negative growth factor in human breast cancer cells
In MCF-7 cells, TGF-beta is a hormonally regulated growth inhibitor with possible autocrine and paracrine functions in breast cancer cells, and growth inhibition is reversed with anti-TGF- beta antibodies. Expand
TGF-beta 1, but not TGF-beta 2 or TGF-beta 3, is differentially present in epithelial cells of advanced pulmonary fibrosis: an immunohistochemical study.
While TGF-beta 1 is expressed in epithelial cells of fibrotic lungs where the presence of T GF- beta 1 is not disease-specific but an indication of the chronicity of the injury, the findings suggest that TGFs 2 and 3 are ubiquitously expressed in the lung. Expand
Inducible nitric oxide synthase in tangle-bearing neurons of patients with Alzheimer's disease
Human neurons can express NOS2 in vivo, and the high-output pathway of NO production may contribute to pathogenesis in AD. Expand
Regulated expression and growth inhibitory effects of transforming growth factor-beta isoforms in mouse mammary gland development.
Striking differences in patterns of gene expression and in the distribution of immunoreactive peptides suggest that TGF-beta isoforms may have distinct roles in mammary growth regulation, morphogenesis and functional differentiation. Expand
A Flexible Reporter System for Direct Observation and Isolation of Cancer Stem Cells
A flexible lentiviral-based reporter system that allows direct visualization of cancer stem cells based on functional properties and the spatial distribution of CSCs can be assessed in settings that retain microenvironmental and structural cues, and CSC plasticity and response to therapeutics can be monitored in real time. Expand