Disease relevance of LOC534069

• Hearts isolated from rats exposed to hyperthermia show an initial 20-fold decrease in TGF-beta 1 and 3 mRNA levels which return to control levels by 24 h and subsequently are elevated two- to threefold above normal 48-72 h after heat shock; there is little change in TGF-beta 2 mRNA [1].
• When TGF-beta2 and the MBWE preparations were compared, on the basis of growth inhibition equivalents, MBWE protected cells against drug toxicity at concentrations an order of magnitude lower than with TGF-beta2 or A-MBWE [2].
• The objective of the current study was to determine whether TGF-alpha, TGF-beta1, and TGF-beta2 milk concentrations were altered during the course of E. coli-induced mastitis [3].
• A possible effect of transforming growth factor type-beta 2 (TGF-beta 2) on autoimmune inflammation of the peripheral nervous system (PNS) was evaluated in experimental autoimmune neuritis (EAN) in Lewis rats, a disease model of the human Guillain-Barré syndrome [4].
• In contrast, none of the four melanoma lines responded to hypothalamic preparations containing MGF that consistently produced an approximately 30-fold increase in newborn melanocyte cell yield over a 2-week period [5].

High impact information on LOC534069

• Neutralizing antisera to TGF-beta 1 and TGF-beta 2 were used to demonstrate that the majority of the activity was of the TGF-beta 2 isoform [6].
• Spontaneous production of transforming growth factor-beta 2 by primary cultures of bronchial epithelial cells. Effects on cell behavior in vitro [6].
• Two essential regions were identified by analysis of mutant constructions: one binds C/EBP-beta and the other binds MGF/STAT5 and an as-yet-unidentified binding protein [7].
• Conversely, TGF-beta 2 mRNA was not detected in T47D:A18 cells cultured under estrogenic conditions; however, message was detected after the cells were cultured under estrogen-free conditions [8].
• FP3 (0.2 microM) neutralized the activity of TGF-beta1 and TGF-beta2 in fetal bovine heart endothelial (FBHE) cell proliferation assays; FP4 was inactive in this assay [9].

Chemical compound and disease context of LOC534069

• Secondly, in a rat model for induced small intestinal damage, oral supplementation of rats exposed to methotrexate with the Transforming Growth Factor-beta2 enriched fraction significantly reduced the chemotherapy-associated weight loss and ileal villus atrophy by reducing cell proliferation in the normal stem cell population [10].
• METHODS: Fifty-one eyes with chronic macular holes (> or = 2 years' duration) were treated in a retrospective analysis of the results of vitrectomy, 16% perfluoropropane gas tamponade, and one of three adjunctive agents (bovine transforming growth factor beta-2, recombinant transforming growth factor beta-2, or autologous platelet extract) [11].

Biological context of LOC534069

• When analyzed by RT-PCR, porcine GC RNA from 1-3 mm follicles did not yield the expected 489 base pair (bp) TGF-beta 2 product but instead generated a smaller than anticipated 240 bp species; porcine testis RNA generated both the 240 and the anticipated 489 bp products [12].
• This is the first reported nucleotide sequence for porcine TGF-beta 2; it is 90% and 91% identical to murine and human TGF-beta 2 sequences, respectively [12].
• The doublet did not appear to be the result of glycosylation of a conventional 25-kDa TGF beta 2 and could be converted into the lower molecular mass form by incubation for 18 h at 37 degrees C, with pH 4.5 but not with pH 7.5 buffer; this incubation in the absence of decidual cells was not accompanied by increased immunosuppressive activity [13].
• The 180-kDa TGF-beta 1 binding protein and the 60- and 140-kDa TGF-beta 2 binding proteins can be released from the cell surface by treatment with phosphatidylinositol-specific phospholipase C, suggesting that these proteins are attached to the plasma membrane through a phosphatidylinositol anchor [14].
• OIF activity in the model used is substantially increased by addition of transforming growth factor (TGF)-beta 1 or TGF-beta 2, suggesting an important role for TGF-beta 1 and -2 in bone regeneration and repair [15].

Anatomical context of LOC534069

• Expression of transforming growth factor type III receptor in vascular endothelial cells increases their responsiveness to transforming growth factor beta 2 [16].
• TGF-beta 2.3 inhibited proliferation of mink lung epithelial cells and promoted the formation of colonies of normal rat kidney fibroblasts in culture with specific biological activity similar to those of TGF-beta 1 and TGF-beta 2 [17].
• Porcine granulosa cells do not express transforming growth factor-beta 2 (TGF-beta 2) messenger ribonucleic acid: molecular basis for their inability to produce TGF-beta activity comparable to that of rat granulosa cells [12].
• Characterization of murine pregnancy decidua transforming growth factor beta. I. Transforming growth factor beta 2-like molecules of unusual molecular size released in bioactive form [13].
• Most of the TGF-beta 2 (94%) was found in the whey fraction of colostrum [18].

Associations of LOC534069 with chemical compounds

• According to this test > 90% of total TGF-beta 2 (74.5 +/- 4.4 ng/ml) in colostrum pool was in a latent form that could be activated by acetic acid treatment, whereas the concentration of the active form was only 4.19 +/- 0.27 ng/ml [18].
• The observations provide evidence that a single treatment with exogenous TGF-beta 2 delivered in collagen/heparin sponge vehicle can accelerate repair in guinea pig dermal wounds allowed to heal by secondary intent [19].
• Northern blot analyses showed that mRNA levels for TGF-beta 2 but not for TGF-beta 1 increased in cells treated with retinol [20].
• Improved local delivery of TGF-beta2 by binding to injectable fibrillar collagen via difunctional polyethylene glycol [21].
• Treatment of the cultures with retinoic acid elevated levels of TGF-beta 2 synthesis, but not TGF-beta 1 [22].

Regulatory relationships of LOC534069

• Also, preincubation of MAC-T cells with 50 pM TGF-beta 1 or TGF-beta 2 markedly downregulated TGF-beta receptors [23].
• Transforming growth factor-beta 2 enhances the osteoinductive activity of a bovine bone-derived fraction containing bone morphogenetic protein-2 and 3 [24].

Other interactions of LOC534069

• Transfected BAECs exhibit increased responsiveness to TGF beta 2 by several different criteria including an increase in plasminogen activator inhibitor-1 protein and inhibition of migration and proliferation [16].
• RESULTS: The production of laminin and fibronectin was stimulated by treatment with TGF-beta1 or TGF-beta2 [25].
• IGF-I and platelet-derived growth factor were ineffective, whereas TGF-beta2 induced growth inhibition and cell survival, with a maximum response at 3 ng/ml [2].
• Transforming growth factor (TGF)-alpha, TGF-beta1, and TGF-beta2 are cytokines that regulate mammary gland development [26].
• In contrast, elevations in IL-1beta, IFN-gamma, TGF-alpha, TGF-beta1, TGF-beta2, sCD14, LBP, and activated complement factor 5 (C5a) were sustained for periods of >48 h [27].

Analytical, diagnostic and therapeutic context of LOC534069

• Amino acid composition and sequence analyses demonstrate that MGF is related to transforming growth factor type beta 2 [28].
• The purified MGF-a, consisting of a single band by gel electrophoresis and a single peak on an HPLC reversed-phase C-4 column, has the same specific activity as TGF-beta 2 in the fibroblast migration assay [29].
• The ELISA results were also compared with a TGF-beta 2 bioassay, the fibroblasts migration assay [18].
• Northern blotting of poly A+ RNA extracted from both homotypic and heterotypic cultures of BAE cells and SMCs revealed that BAE cells produced both TGF-beta 1 and TGF-beta 2, while SMCs produced primarily TGF-beta 1 [30].
• The ratio of TGF-beta 1:TGF-beta 2 as estimated on the basis of neutralization studies was supported by visual observation of TGF-beta 1 and TGF-beta 2 protein bands on Western blotting [31].

References