Disease relevance of Tgfb3

• Selective expression of TGF-beta2 and TGF-beta3 isoforms in early mesangioproliferative glomerulonephritis [1].
• These findings are consistent with the idea that GDNF, TGF beta 2, and TGF beta 3 are physiological survival factors for developing midbrain dopaminergic neurons and may have applications as therapeutics for Parkinson's disease, a neurodegenerative disorder of dopaminergic neurons [2].
• The three mammalian transforming growth factor (TGF)-beta isoforms (TGF-beta1, TGF-beta2, and TGF-beta3) differ in their putative roles in radiation-induced fibrosis in intestine and other organs [3].
• The purpose of this study was to characterize the expression of all three isoforms in nephrotoxic nephritis (NTN) in rats and to determine the effect of TGF-beta3 infusions on injury because of its reported combined anti-inflammatory and antifibrotic effects [4].
• Infusions of TGF-beta3 did not reduce proteinuria over seven days after the induction of nephritis [4].

Psychiatry related information on Tgfb3

• After injection of TGF-beta3 into the cisterna magna of the rat, spontaneous motor activity decreased significantly for 1 h [5].

High impact information on Tgfb3

• Furthermore, we find that TGF beta 2, TGF beta 3, and GDNF are expressed sequentially as local and target-derived trophic factors and that subpopulations of dopaminergic neurons projecting to distinct targets have access to only one of these factors [2].
• We report here that transforming growth factors (TGFs) TGF beta 2 and TGF beta 3, which are distantly related to GDNF, also prevent the death of cultured rat embryonic midbrain dopaminergic neurons at picomolar concentrations [2].
• We investigated the effects of intracerebral administration of GDNF and TGF-beta 3 on the delayed cell death of the dopamine neurons in the rat substantia nigra following 6-hydroxydopamine lesions of dopaminergic terminals in the striatum [6].
• Scatchard analysis of receptor competition studies indicated the presence of high-affinity binding sites for TGF-beta 3 in the picomolar range [7].
• In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity [7].

Biological context of Tgfb3

• Radiation-induced alterations in rat mesangial cell Tgfb1 and Tgfb3 gene expression are not associated with altered secretion of active Tgfb isoforms [8].
• Continuous administration of TGF-beta 3, starting on the day of lesion surgery, did not affect nigral cell death or atrophy [6].
• Our results implicate increased TGF-beta 1, -beta 2, and decreased TGF-beta 3 expression, as well as increased type I and II receptor expression in late gestation fetal scar formation [9].
• Analysis of DNA sequence homology suggested that this cDNA encodes the rat transforming growth factor-beta 3 (TGF beta 3) [10].
• However, TGF-beta3 selectively disrupts Sertoli-germ cell adhesion in the seminiferous epithelium to facilitate germ cell migration without compromising BTB when TbetaRI interacts only with adaptor CD2AP [11].

Anatomical context of Tgfb3

• Both quiescent and irradiated rat mesangial cells secreted active Tgfb as primarily the Tgfb3 isoform [8].
• These results demonstrate for the first time that the TGF-beta3/p38 MAP kinase signaling pathway is being used to regulate both TJ and AJ dynamics in the testis, mediated by the effects of TGF-beta3 on TJ- and AJ-integral membrane proteins and adaptors, but not protease inhibitors [12].
• Also, it was found that recombinant TGF-beta3 added to Sertoli cells cultured in vitro at 1.2 x 10(6) cells/cm(2) on Matrigel-coated bicameral units perturbed the inter-Sertoli TJ permeability barrier dose-dependently [13].
• TGF-beta3 regulates the blood-testis barrier dynamics via the p38 mitogen activated protein (MAP) kinase pathway: an in vivo study [14].
• Interestingly, TGF-beta3 only stained macrophage-like cells and chondrocytes in the synovia [15].

Associations of Tgfb3 with chemical compounds

• Estradiol and TGF-beta3, either alone or in combination, increased the levels of active Ras [16].
• Ethanol and TGF-beta3, either alone or in combination, increased the levels of active Ras [17].
• Treatment with retinoic acid caused a rapid and transient induction of TGF beta 2 and TGF beta 3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa [18].
• Maternal administration of dexamethasone also enhanced mRNA expression of TGF beta 3 in fetal lung fibroblasts [10].
• Exposure of fetal lung fibroblasts to cortisol increased TGF beta 3 mRNA expression in a time- and dose-dependent manner [10].

Regulatory relationships of Tgfb3

• Estradiol and TGF-beta3 alone moderately activated MAPK p44/42; together they produced marked activation of MAPK p44/42 [16].
• In transdifferentiating rat hepatic stellate cells (HSC) the TGF-beta 1-mRNA was found to be the predominant isoform expressed followed by TGF-beta 3 and low amounts of TGF-beta 2-mRNA [19].
• Also, neutralizing antibodies to TGF-beta 3 blocked the cortisol-stimulated TE mRNA expression [20].
• However, TGF-beta 3 did inhibit the increase of SP-B, SP-C mRNA levels caused by dexamethasone (100 nmol/L), in a dose-dependent manner [21].

Other interactions of Tgfb3

• This result clearly illustrates that CdCl(2) mediates its BTB disruptive effects via the TGF-beta3/p38 MAP kinase signaling pathway [12].
• TGF-beta 3 staining was increased at day 10 only, and TGF-beta 1 was unchanged [22].
• We found that TGF-beta3 and estradiol alone moderately increased cell content and release of bFGF from FS cells; but together, they markedly increased the peptide [16].
• Astroglial cells from all brain regions showed a slight FGF-mediated increase in 5-bromo-2'-desoxy-uridine (BrdU) incorporation, which was abolished upon co-treatment with TGF-beta3 [23].
• In bladders subjected to partial urethral outlet obstruction, there was a 2-fold increase in mRNA for TGF beta 2, a 5-fold increase in TGF beta 3, and a 10-fold increase TGF alpha mRNA [24].

Analytical, diagnostic and therapeutic context of Tgfb3

• The steady-state messenger RNA levels of basic fibroblast growth factor (bFGF), transforming growth factor (TGF)-beta2, and TGF-beta3 at different time points were assessed by semiquantitative RT-PCR [13].
• In marked contrast, in the one-shot model, TGF-beta2 and TGF-beta3 stainings increased rapidly, yet transiently, throughout affected glomeruli, followed by more sustained staining in glomerular epithelial cells [1].
• Levels of mRNA expression of TGF-beta1 and TGF-beta3 were measured by Northern blot hybridization [25].
• No significant TGF-beta2 or TGF-beta3 protein expression was observed either in the trauma induced group or in the control group [26].
• In this paper, the cellular locations of TGF-beta2 and TGF-beta3 in freeze-lesioned skeletal muscle were examined using immunohistochemistry [27].

References