Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth

This study evaluates the proliferative effects of danshen and its monomer extract, tanshinone IIA, on Schwann cell proliferation. A piece of silicone rubber was guided across a 15-mm gap in the sciatic nerve of a rat. This nerve gap was then filled with different concentrations of danshen (0–100 mg/mL). The results showed that danshen increased the expressions of uPA, cyclin D1, E and ERK, JNK, and P38 MAP kinases via the FGF-2 signaling pathway in a dose-dependent manner. RSC96, Schwann cells were also administered with danshen (0, 20, 40, 60, 80, and 100 μg/mL) and tanshinone IIA (0, 2, 4, 6, 8, and 10 μg/mL). In lower concentrations, danshen and tanshinone IIA exhibited an apparent effect on Schwann cells. Similar effects were also demonstrated in the FGF-2-uPA regulating cascade and cell cycle proliferative protein results. Schwann cell migration was elevated as well. We used MAPK-signaling chemical inhibitors and identified the proliferative effects of danshen and tanshinone IIA as MAPK-signaling dependent. The results from thein vitrosystems indicate that danshen and tanshinone IIA can be used to induce Schwann cell proliferation, andin vivoresults potentially suggest that danshen and tanshinone IIA might enhance neuron regeneration.

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Schwann Cell Proliferation In Vitro.

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1986.tb48072.x ◽

1986 ◽

Vol 486 (1 Neurofibromat) ◽

pp. 170-181 ◽

Cited By ~ 21

Author(s):

NANCY RATNER ◽

RICHARD P. BUNGE ◽

LUIS GLASER

Keyword(s):

Cell Proliferation ◽

Schwann Cell ◽

Proliferation In Vitro

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Optogenetic stimulation promotes Schwann cell proliferation, differentiation, and myelination in vitro

Scientific Reports ◽

10.1038/s41598-019-40173-w ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 8

Author(s):

Kyuhwan Jung ◽

Ji Hye Park ◽

Sung-Yon Kim ◽

Noo Li Jeon ◽

Sung-Rae Cho ◽

...

Keyword(s):

Cell Proliferation ◽

Schwann Cell ◽

Optogenetic Stimulation

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Cyclic AMP and calcium as potential mediators of stimulation of cultured Schwann cell proliferation by axolemma-enriched and myelin-enriched membrane fractions

Biochemical and Biophysical Research Communications ◽

10.1016/0006-291x(84)90485-6 ◽

1984 ◽

Vol 122 (1) ◽

pp. 373-380 ◽

Cited By ~ 38

Author(s):

James H. Meador-Woodruff ◽

Brenda L. Lewis ◽

George H. DeVries

Keyword(s):

Cell Proliferation ◽

Cyclic Amp ◽

Schwann Cell ◽

Stimulation Of

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Coordinate control of axon defasciculation and myelination by laminin-2 and -8

The Journal of Cell Biology ◽

10.1083/jcb.200411158 ◽

2005 ◽

Vol 168 (4) ◽

pp. 655-666 ◽

Cited By ~ 99

Author(s):

Dongren Yang ◽

Jesse Bierman ◽

Yukie S. Tarumi ◽

Yong-Ping Zhong ◽

Reshma Rangwala ◽

...

Keyword(s):

Cell Proliferation ◽

Schwann Cell ◽

Schwann Cells ◽

Dominant Role ◽

Pathogenic Mechanism ◽

Structural Defects ◽

Autocrine Factors ◽

Coordinate Control

Schwann cells form basal laminae (BLs) containing laminin-2 (Ln-2; heterotrimer α2β1γ1) and Ln-8 (α4β1γ1). Loss of Ln-2 in humans and mice carrying α2-chain mutations prevents developing Schwann cells from fully defasciculating axons, resulting in partial amyelination. The principal pathogenic mechanism is thought to derive from structural defects in Schwann cell BLs, which Ln-2 scaffolds. However, we found loss of Ln-8 caused partial amyelination in mice without affecting BL structure or Ln-2 levels. Combined Ln-2/Ln-8 deficiency caused nearly complete amyelination, revealing Ln-2 and -8 together have a dominant role in defasciculation, and that Ln-8 promotes myelination without BLs. Transgenic Ln-10 (α5β1γ1) expression also promoted myelination without BL formation. Rather than BL structure, we found Ln-2 and -8 were specifically required for the increased perinatal Schwann cell proliferation that attends myelination. Purified Ln-2 and -8 directly enhanced in vitro Schwann cell proliferation in collaboration with autocrine factors, suggesting Lns control the onset of myelination by modulating responses to mitogens in vivo.

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