Showing papers by "Kathleen C. Flanders published in 1995"
TL;DR: Increased expression of TGF-beta 2 in large, tangle-bearing neurons with widespread staining of glia in NDAD and FAD-14 patients compared with control cases, suggesting selective induction of T GF- beta 2 may occur in ND AD and Fad-14.
Abstract: We compared immunohistochemical expression of the transforming growth factor-betas (TGF-beta 1, TGF-beta 2, and TGF-beta 3) using brain tissue from patients with nondominantly inherited Alzheimer's disease (NDAD) (n = 9), autosomal dominantly inherited Alzheimer's disease with linkage to 14q24.3 (FAD-14) (n = 4), and cognitively normal controls (n = 10) to determine whether their pathologic changes are associated with an altered distribution of the TGF-betas. We found increased expression of TGF-beta 2 in large, tangle-bearing neurons with widespread staining of glia in NDAD and FAD-14 patients compared with control cases. This result was confirmed with sandwich ELISA assays of brain tissue, which showed TGF-beta 2 levels in AD and NDAD to average 3.2 times the average level of control cases. Despite proximity of TGF-beta 1 and TGF-beta 3 to the sites of susceptibility loci on chromosomes 19 and 14, we did not find that TGF-beta 1 and TGF-beta 3 were selectively altered in any AD subtypes. However, selective induction of TGF-beta 2 may occur in NDAD and FAD-14.
163 citations
Journal Article•
TL;DR: It is confirmed that prostate cancer exhibits enhanced intracellular and extracellular accumulation of TGF-beta 1 relative to normal prostate tissue and benign prostatic hyperplasia and in primary tumors without metastasis.
113 citations
TL;DR: It is found that treatment of primary cultures of neonatal rat cardiomyocytes or cardiac fibroblasts with TGF-beta 1, 2, or 3 results in increased expression of TGRD 1,2, and 3 mRNA, and exogenous administration of T GF-beta decreases cardiac damage following ischemic injury in rats.
55 citations
TL;DR: It is concluded that induction of TGF-beta 2 may be an intrinsic part of the processes that underlie NFT formation and reactive gliosis in a variety of neurodegenerative diseases.
47 citations
TL;DR: It is found that TGF β1 RNA transcript levels were reduced following exposure to RA excess, and this results indicate that retinoids are capable of differentially regulating T GF β isoforms through mechanisms involving different stages in the process of TGFβ synthesis and secretion.
Abstract: In a previous study we investigated the effects of RA excess on TGF β protein localization in early postimplantation stages of mouse development. Here we extend this investigation by comparing the effects of retinoid deficiency with those of excess, and by comparing the effects of altered retinoid status on TGF β protein and RNA transcript distribution. In vitamin A-deficient embryos, TGF β1 RNA and protein distribution were both unaltered compared with controls; conversely, TGF β2 protein levels were reduced while RNA levels remained normal. In RA-treated embryos, the previous study showed that intracellular TGF β1 levels were decreased, while those of extracellular TGF β1 were initially decreased but subsequently increased; here we found that TGF β1 RNA transcript levels were reduced following exposure to RA excess. TGF β2 showed a clear disparity between the effects of RA excess on protein and RNA transcript levels: RNA transcript distribution was unchanged or showed a slight increase in RA-treated embryos, whereas the previous results showed greatly reduced protein levels. The new results provide further evidence for interaction between retinoids and TGF βs during mouse development, and indicate that retinoids are capable of differentially regulating TGF β isoforms through mechanisms involving different stages in the process of TGF β synthesis and secretion. The long-term nature of the effects of transient exposure to RA excess suggests that the mechanisms of RA-TGF β interaction may be indirect.
17 citations
TL;DR: These studies indicate that, in the uteri of oophorectomized rats, tamoxifen exerts estrogen-like effects on a peptide previously implicated in the control of cellular growth and differentiation.
17 citations
Journal Article•
16 citations