The 1st International standard for transforming growth factor-β3 (TGF-β3)

Wadhwa, Meenu; Dilger, Paula; Hamill, Michelle; Bending, David; Gibbs, Sarah; Wu, Guoping; Read, Jo; Wyss‐Coray, Tony; Zhang, Hui; Little, John A.; Getliffe, Katherine M.; Gao, Kai; Wang, Weihong; Bender, David; Bird, Christopher; Heath, Alan; Cooke, Anne; Thorpe, Robin

doi:10.1016/j.jim.2012.03.002

Cited by 2 publications

(3 citation statements)

References 20 publications

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“…TGF-b3 released by lactotrophic cells in adequate amounts stimulates the function of folliculotrophic cells that reversibly stimulate lactotrophic cells, which is regarded as one of the mechanisms promoting TGF-b3 involvement in developing prolactinoma. TGF-b3 and TGF-b2 isoforms occur in glial and microglial cells, as well as in astrocytes and oligodendrocytes [40]. Moreover, TGF-b3 is an important regulator of neuron differentiation, a neurite stimulator and cofactor of neurotrophic factors, e.g.…”

Section: Tgf-b3mentioning

confidence: 99%

The Role of the TGF-SMAD Signalling Pathway in the Etiopathogenesis of Severe Asthma

Koćwin

Jonakowski

Przemęcka

et al. 2016

Advances in Respiratory Medicine

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Asthma is a chronic inflammatory heterogeneous disease of the lower respiratory tract characterised by the occurrence of bronchial hyper-responsiveness and paroxysmal, changeable bronchial obstruction. Transforming growth factor-beta (TGF-b) is one of the cytokines involved in mediating airway inflammation and remodelling. The level of TGF-b1 gene expression correlates with severity of symptoms. Alterations in the main SMAD signal transmission, overexpression of TGF-b genes and changes in the transcriptome cause excessive secretion of TGF-b and its increased expression in target cells, which clinically induces a moderate-severe or severe course of asthma as well as an earlier and faster disease progression. Knowledge of these processes allows clinicians to assess immune responses in patients, which affects adequate disease control and prevention of remodelling.

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Section: Tgf-b3mentioning

confidence: 99%

The Role of the TGF-SMAD Signalling Pathway in the Etiopathogenesis of Severe Asthma

Koćwin

Jonakowski

Przemęcka

et al. 2016

Advances in Respiratory Medicine

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“…Based on currently available data, it is reasonable to hypothesize that administration of acute low doses of exogenous TGF‐β3 is unlikely to affect tumor initiation or progression . Moreover, the preparation coded 09/234 was established by the WHO Expert Committee on Biological Standardization (ECBS) as the WHO 1st IS for human TGF‐β3 with an assigned value for TGF‐β3 activity of 19,000 IU/ampoule . That is the reason we chose TGF‐β3 as the cytokine for our study to prevent adhesion formation.…”

Section: Discussionmentioning

confidence: 99%

“…21 Moreover, the preparation coded 09/234 was established by the WHO Expert Committee on Biological Standardization (ECBS) as the WHO 1st IS for human TGF-b3 with an assigned value for TGF-b3 activity of 19,000 IU/ ampoule. 22 That is the reason we chose TGF-b3 as the cytokine for our study to prevent adhesion formation. To protect TGF-b3 from proteolysis and antibody neutralization and to maintain its activity for the required period of time, normally suitable carriers for delivery of TGF-b3 are required.…”

Section: Discussionmentioning

confidence: 99%

A new TGF‐β3 controlled‐released chitosan scaffold for tissue engineering synovial sheath

Jiang

Wang

et al. 2013

J Biomedical Materials Res

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The post-operative outcome of flexor tendon healing remains limited by flexor tendon adhesion that reduces joint range of motion. Despite improvement in different methods, peritendinous adhesion formation continues to present a formidable challenge. Recent studies showed that transforming growth factor-β3 (TGF-β3) may be the key factor to reducing adhesion formation in skin or tendon. In this study, we designed a novel type of tissue engineering synovial sheath containing TGF-β3, to prevent flexor tendon adhesion. First, to achieve a stable release of TGF-β3, chitosan microspheres, prepared by crosslinking-emulsion, were used for the delivery of TGF-β3. Second, a three-dimensional chitosan scaffold was prepared by lyophilization, and TGF-β3 microspheres were carefully introduced into the scaffold. Then, synovial cells were cultured and then seeded into the TGF-β3 loaded scaffold to produce TGF-β3 controlled-released tissue engineering synovial sheath. Tests clearly demonstrated that the scaffold has good structure and compatibility with cells. These results expand the feasibility of combinative strategies of controlled protein release and tissue-engineered synovial sheath formation. Application of this scaffold to tendon repair sites may help to prevent adhesion of tendon healing.

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The 1st International standard for transforming growth factor-β3 (TGF-β3)

Cited by 2 publications

References 20 publications

The Role of the TGF-SMAD Signalling Pathway in the Etiopathogenesis of Severe Asthma

The Role of the TGF-SMAD Signalling Pathway in the Etiopathogenesis of Severe Asthma

A new TGF‐β3 controlled‐released chitosan scaffold for tissue engineering synovial sheath

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