Disease relevance of Tgfb2

• Selective expression of TGF-beta2 and TGF-beta3 isoforms in early mesangioproliferative glomerulonephritis [1].
• CONCLUSIONS: Our findings suggest that TGF-beta may act in the retina as a neurotrophic agent, since TGF-beta 1 is normally transcribed in ganglion cells and TGF-beta 2 is also transcribed in ganglion cells and choriocapillaris endothelium [2].
• Although neither TGF-beta2 nor TGF-beta3 expression was affected by hypoxia, the TGF-beta type I receptor was substantially upregulated within 6 h [3].
• TGF-beta 2 was the predominant isoform of TGF-beta, and its expression was especially strong in the endothelium of the choroidal neovascularization at 2 weeks [2].
• After intraarticular injection of TGF-beta 1 or TGF-beta 2, marked swelling and erythema of the injected joints were apparent within 12-24 h [4].

High impact information on Tgfb2

• Intraarticular injection of monoclonal antibody 1D11.16, which inhibits both TGF-beta 1 and TGF-beta 2 bioactivity, into animals receiving an arthropathic dose of bacterial cell walls significantly inhibits arthritis [5].
• TGF-beta 2, a homologue of TGF-beta 1, was found to induce a similar level of synovitis and synovial hyperplasia consistent with its parallel monocyte and fibroblast chemotactic properties and ability to induce transcription and translation of monocyte/macrophage-derived growth factors [4].
• 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 [6].
• Moreover, bone resorption induced by the bone-resorbing agents IL 1 and 1,25-dihydroxyvitamin D3 was partially or completely inhibited by TGF-beta 1 and TGF-beta 2 during the second half of the 6-d incubation period [7].
• TGF-beta 2 is a closely related polypeptide that was originally isolated from bone matrix [7].

Chemical compound and disease context of Tgfb2

• It has been shown that 17beta-estradiol (E2) can prevent TGF-beta2-induced cataracts in lenses from ovariectomized female rats [8].

Biological context of Tgfb2

• We conclude that complement-mediated injury to the GEC in vivo is associated with the up-regulation of TGF-beta 2 and -beta 3 isoforms, an increase in TGF-beta 2 bioactivity, and an increase in T beta RI and T beta RII expression [9].
• IC50 values for TGF beta 1 and 2 in the 4-1 cells were at least 1/9 those of the parental cells; growth rates were reduced by 49% for TGF beta 1 and by 26% for TGF beta 2 in this clone [10].
• TGF beta 2 and -beta 3 mRNA expression decreased as a function of gestational age, whereas TGF alpha mRNA increased [11].
• However, specific genes, including TGF-beta2, may be altered and effect cell death mechanisms after TBI [12].
• The most pronounced changes in TGF-beta1 and TGF-beta2 immunoreactivity occurred during spermatogenesis [13].

Anatomical context of Tgfb2

• The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2 [14].
• Antibodies to TGF-beta1, TGF-beta2, TGF-betaRI and TGF-betaRII stained blood vessels intensively, already at the early onset of inflammation, whereas the synovial lining layer and chondrocytes expressed strong immunoreactivity later on in the inflammatory process [15].
• 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].
• Although TGF-beta2-triggered germ cell death also was significantly reduced by rLAP-TGF-beta1, inhibition was not maximal [16].
• The biological activity of TGF-beta could be inhibited by neutralizing antibodies against TGF-beta1 (spermatocytes and round spermatids) and TGF-beta2 (round and elongating spermatids) [13].

Associations of Tgfb2 with chemical compounds

• Previously we have shown that dexamethasone and transforming growth factor-beta 2 (TGF-beta 2) suppress sPLA2 protein synthesis and enzyme activity induced by cytokines and forskolin [17].
• Basal expression of TGF beta 2 diminished under conditions of vitamin A deficiency [18].
• We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF beta 2 in the vitamin A-deficient rat [18].
• Cells expressing the TGF-beta1, TGF-beta2, or TGF-beta3 transcripts were identified by in situ hybridization with digoxigenin-labeled riboprobes [19].
• Results indicated that the presence of TGF-beta 1 and TGF-beta 2 were associated with developing coronal and frontonasal sutures, and that the continued presence of these factors was associated with osseous obliteration of the frontonasal suture [20].

Physical interactions of Tgfb2

• The transforming growth factor-beta (TGF-beta) receptor type III is a low abundance cell surface component that binds TGF-beta 1 and TGF-beta 2 with high affinity and specificity, and is present in many mammalian and avian cell types [21].
• A comparable decrease in PTHrP binding was only observed after 24 h of incubation with 100 pM TGF beta 2 [22].

Regulatory relationships of Tgfb2

• Here we report that transforming growth factor beta 2 (TGF beta 2) dose-dependently inhibits IL-1 beta- and TNF alpha-stimulated cGMP formation in mesangial cells [23].
• Furthermore, TGF-beta 2 induced a sustained activation of p44mapk under these conditions, lasting for at least 90 min after initial growth factor treatment [24].
• TGF beta 1 or TGF beta 2 reduced both basal and Ca(2+)-stimulated PRL mRNA levels [25].
• Exposure of rat glomerular mesangial cells to transforming growth factor beta 2 (TGF beta 2) stimulates a biphasic mitogen-activated protein kinase (MAP kinase) activation [26].

Other interactions of Tgfb2

• In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta [14].
• 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 [11].
• Transforming growth factor (TGF) beta 1, TGF beta 2 and TGF beta 3 equipotently attenuated the IL-1 beta- and forskolin-induced elevation of PLA2 mRNA, as well as PLA2 synthesis and secretion [27].
• We report here that, whereas TGF beta 2 potentiates the IL-1 beta- and TNF alpha-evoked PGE2 production, it strongly inhibits the phospholipase A2 secretion induced by both cytokines [28].
• The activity cross-reacted to antisera specific for TGF-beta 1, beta 2 and for TGF-beta 2 exclusively, but not with antisera to rat interferon (alpha-beta) or rat interleukin 6 [29].

Analytical, diagnostic and therapeutic context of Tgfb2

• The TGF-beta bioactivity dramatically increased in the transplanted allografts during the chronic rejection process compared to the normal hearts, and so did the immunostaining as well as the mRNA levels for TGF-beta 1 and, to a lesser extent, the immunostaining for TGF-beta 2 [30].
• We have examined both how the molecular phenotype of Schwann cells in vitro is regulated by transforming growth factor beta (TGF-beta), using immunohistochemistry and immunoblotting, and the distribution of TGF-beta 2 and 3 in embryonic and mature nerves and ganglia, using immunohistochemistry and in situ hybridisation [31].
• No significant TGF-beta2 or TGF-beta3 protein expression was observed either in the trauma induced group or in the control group [32].
• Additionally, matrix-grafted and host bladders were processed for analysis of mRNA expression of transforming growth factor (TGF)-alpha, TGF-beta1, TGF-beta2, and TGF-beta3 by reverse transcriptase polymerase chain reaction [33].
• No expression of TGF-beta2 was evident either by immunohistochemistry or Northern blot analysis [34].

References