Co-expression of Transforming Growth Factor-β1 and Glial Cell Line–Derived Neurotrophic Factor in Vestibular Schwannoma

The shapes of different organs can be explained largely by two fundamental characteristics of their epithelial rudiments - the pattern of branching and the rate of proliferation. Glial-cell-line-derived neurotrophic factor (GDNF) has recently been implicated in the development of metanephric ureteric epithelium (Pichel, J. G., Shen, L., Sheng, H. Z., Granholm, A.-C., Drago, J., Grinberg, A., Lee, E. J., Huang, S. P., Saarma, M., Hoffer, B.J., Sariola, H. and Westphal, H. (1996). Nature 382, 73–76; Sanchez, M.P., Silos-Santiago, I., Frisen, J., He, B., Lira, S.A. and Barbacid, M. (1996). Nature 382, 70–73; Vega, Q.C., Worby, C.A., Lechner, M.S., Dixon, J.E. and Dressler, G.R. (1996). Proc. Nat. Acad. Sci. USA 93, 10657–10661). We have analysed the target cells of GDNF and the manner in which it controls ureteric development, and have compared it with other growth factors that have been associated with the regulation of branching morphogenesis, namely hepatocyte growth factor (HGF) and transforming growth factor-beta1 (TGFbeta1). We show that GDNF binds directly to the tips of ureteric bud branches, and that it has the ability to promote primary ureteric buds from various segments of Wolffian duct and to attract ureteric branches towards the source of GDNF. It increases cell adhesion, but is not obviously mitogenic for ureteric cells. The data indicate that GDNF is required primarily for bud initiation. Comparison of GDNF, HGF and TGFbeta1 suggests that the latter act later than GDNF, and may represent a partially redundant set of mesenchyme-derived growth factors that control ureteric development. Thus, GDNF is the first defined inducer in the embryonic metanephric kidney.

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Differential effects of transforming growth factor-βs and glial cell line-derived neurotrophic factor on gene expression of presenilin-1 in human post-mitotic neurons and astrocytes

Neuroscience ◽

10.1016/s0306-4522(99)00215-8 ◽

1999 ◽

Vol 93 (3) ◽

pp. 1041-1049 ◽

Cited By ~ 14

Author(s):

R.F. Ren ◽

J.J. Lah ◽

A. Diehlmann ◽

E.S. Kim ◽

D.B. Hawver ◽

...

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Cell Line ◽

Glial Cell ◽

Neurotrophic Factor ◽

Transforming Growth Factor ◽

Presenilin 1 ◽

Differential Effects

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Transforming growth factor-β1-induced N-cadherin drives cell–cell communication through connexin43 in osteoblast lineage

International Journal of Oral Science ◽

10.1038/s41368-021-00119-3 ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Yueyi Yang ◽

Wenjing Liu ◽

JieYa Wei ◽

Yujia Cui ◽

Demao Zhang ◽

...

Keyword(s):

Growth Factor ◽

Gap Junction ◽

Cell Line ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β1 ◽

Cx43 Expression ◽

Mc3t3 Cell ◽

Primary Osteoblasts ◽

Tgf Β1 ◽

Cell Cell

AbstractGap junction (GJ) has been indicated to have an intimate correlation with adhesion junction. However, the direct interaction between them partially remains elusive. In the current study, we aimed to elucidate the role of N-cadherin, one of the core components in adhesion junction, in mediating connexin 43, one of the functional constituents in gap junction, via transforming growth factor-β1(TGF-β1) induction in osteoblasts. We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43, and the enhancement of functional gap junctional intercellular communication (GJIC) triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line. Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell–cell contact. Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43. Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced. TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation, whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43. Overall, these data indicate the direct interactions between N-cadherin and Cx43, and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts.

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