====== Transforming growth factor Beta ======

[[Transforming growth factor]]-βs (TGF-βs) are a group of multifunctional proteins that have neuroprotective roles in various experimental models. 

Transforming [[growth factor beta]] (TGFβ) [[signalling cascade]] has been implicated in enhancing neuronal excitability and excitatory synaptogenesis following blood brain barrier (BBB) damage and inflammation.
===== Importance =====

[[Transforming growth factor]] Beta ([[TGFβ]]) is upregulated in Marfan's syndrome and some human cancers, and play crucial roles in tissue regeneration, cell differentiation, embryonic development, and regulation of the immune system, promotes the growth of [[glioma cell]]s, and correlate with the degree of malignancy of [[glioma]]s. However, the molecular mechanisms involved in the malignant function of TGF-β are not fully elucidated. 

Isoforms of transforming growth factor-beta (TGF-β1) are also thought to be involved in the pathogenesis of pre-eclampsia. 

see [[Transforming growth factor beta receptor]]

see [[Transforming growth factor beta signaling pathway]]

Intrathecal injections of TGF-β1 significantly inhibit [[neuropathy]]-induced thermal [[hyperalgesia]], spinal [[microglia]] and [[astrocyte]] activation, as well as upregulation of [[tumor necrosis factor]]-α. However, additional cellular mechanisms for the antinociceptive effects of TGF-β1, such as the [[mitogen activated protein kinase]] (MAPK) pathway, have not been elucidated. During persistent pain, activation of MAPKs, especially p38 and extracellular signal-regulated kinase (ERK), have crucial roles in the induction and maintenance of pain hypersensitivity, via both nontranscriptional and transcriptional regulation. 
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TGF-β-induced epithelial-mesenchymal transition (EMT) plays an important role in tumor progression. 

Ling et al., assessed whether the TGF-β-induced EMT contributed to [[vasculogenic mimicry]] (VM) formation in glioma, they established an SHG44 cell line stably transfected with TGF-β cDNA loaded lentivirus. SB203580 was employed to inhibit the TGF-β-induced EMT. The results showed that the VM forming ability of cells could be improved by TGF-β over-expression. The migration and invasion capabilities of cells were also enhanced due to EMT. SB203580 was able to weaken cell migration, invasion and VM forming abilities via blocking p38/MAPK signaling pathways, but it had tiny influence on MMP/LAMC2 chain. Consequently, we concluded that EMT inhibition via p38/MAPK signaling pathways would partly impair TGF-β-induced VM formation in glioma
((Ling G, Ji Q, Ye W, Ma D, Wang Y. Epithelial-mesenchymal transition regulated 
by p38/MAPK signaling pathways participates in vasculogenic mimicry formation in 
SHG44 cells transfected with TGF-β cDNA loaded lentivirus in vitro and in vivo.
Int J Oncol. 2016 Oct 7. doi: 10.3892/ijo.2016.3724. PubMed PMID: 27748800.
)).
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====Types====

[[Transforming growth factor beta 1]]

TGFβ2

[[Transforming growth factor beta 3]]
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Guo et al. showed that TGF-β induced the downregulation of [[MST1]] expression in U87 and U251 glioma cells. Treatment of glioma cells with the DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-AzadC) prevented the loss of MST1 expression. Addition of 5-AzadC also reduced the TGF-β-stimulated proliferation, migration and invasiveness of glioma cells. Furthermore, Knockdown of DNMT1 upregulated MST1 expression in gliomas cells. In addition, the inhibition of DNMT1 blocked TGF-β-induced proliferation, migration and invasiveness in glioma cells. These results suggest that TGF-β promotes glioma malignancy through DNMT1-mediated loss of MST1 expression
((Guo Z, Li G, Bian E, Ma CC, Wan J, Zhao B. TGF-β-mediated repression of MST1
by DNMT1 promotes glioma malignancy. Biomed Pharmacother. 2017 Aug 9;94:774-780. 
doi: 10.1016/j.biopha.2017.07.081. [Epub ahead of print] PubMed PMID: 28802229.
)).