Neurofibromin-deficient Schwann cells have increased lysophosphatidic acid dependent survival and migration—implications for increased neurofibroma formation during pregnancy

Glia ◽  
2007 ◽  
Vol 55 (5) ◽  
pp. 527-536 ◽  
Author(s):  
Todd D. Nebesio ◽  
Wenyu Ming ◽  
Shi Chen ◽  
Travis Clegg ◽  
Jin Yuan ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Lysophosphatidic Acid ◽  
And Migration

Lysophosphatidic acid activates satellite glia cells and Schwann cells

Glia ◽  
2019 ◽  
Vol 67 (5) ◽  
pp. 999-1012 ◽  
Author(s):  
Jan W. Robering ◽  
Lisa Gebhardt ◽  
Katharina Wolf ◽  
Helen Kühn ◽  
Andreas E. Kremer ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Lysophosphatidic Acid ◽  
Glia Cells ◽  
Satellite Glia

Reduced graphene oxide-coated electrospun fibre: effect of orientation, coverage and electrical stimulation on Schwann cells behavior

2021 ◽  
Author(s):  
Zhiqiang Huang ◽  
Manman Sun ◽  
Yanyi Li ◽  
Zhenzhao Guo ◽  
Hong Li
Keyword(s):  
Graphene Oxide ◽  
Electrical Stimulation ◽  
Reduced Graphene Oxide ◽  
Schwann Cells ◽  
Electrospun Fibre ◽  
Fibrous Scaffold ◽  
Reduced Graphene ◽  
And Migration

A conductive fibrous scaffold with typical aligned topography is beneficial for the adhesion, proliferation, NGF secretion and migration of Schwann cells under electrical stimulation.

Essential Role of Src Suppressed C Kinase Substrates in Schwann Cells Adhesion, Spreading and Migration

2008 ◽  
Vol 34 (5) ◽  
pp. 1002-1010 ◽  
Author(s):  
Meijuan Yan ◽  
Chun Cheng ◽  
Jing Jiang ◽  
Yonghua Liu ◽  
Ying Gao ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Essential Role ◽  
And Migration ◽  
Kinase Substrates

In Vitro Evaluation of the Growth and Migration of Schwann Cells on Electrospun Silk Fibroin Nanofibers

2011 ◽  
Vol 175-176 ◽  
pp. 220-223 ◽  
Author(s):  
Ai Jun Hu ◽  
Bao Qi Zuo ◽  
Feng Zhang ◽  
Qing Lan ◽  
Huan Xiang Zhang
Keyword(s):  
Tissue Engineering ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Silk Fibroin ◽  
Nerve Tissue ◽  
Nerve Tissue Engineering ◽  
And Migration ◽  
Silk Fibroin Nanofibers

Schwann cells (SCs) are primary structural and functional cells in peripheral nervous system and play a crucial role in peripheral nerve regeneration. Current challenge in peripheral nerve tissue engineering is to produce an implantable scaffold capable of bridging long nerve gaps and assist Scs in directing the growth of regenerating axons in nerve injury recovery. Electrospun silk fibroin nanofibers, fabricated for the cell culture in vitro, can provide such experiment support. Silk fibroin scaffolds (SFS) were fabricated with formic acid (FA), and the average fiber diameter was 305 ± 24 nm. The data from microscopic, immunohistochemical and scanning electron micrograph confirmed that the scaffold was beneficial to the adherence, proliferation and migration of SCs without exerting any significant cytotoxic effects on their phenotype. Thus, providing an experimental foundation accelerated the formation of bands of Bünger to enhance nerve regeneration. 305 nm SFS could be a candidate material for nerve tissue engineering.

scholarly journals ANXA1 directs Schwann cells proliferation and migration to accelerate nerve regeneration through the FPR2/AMPK pathway

2020 ◽  
Vol 34 (10) ◽  
pp. 13993-14005 ◽  
Author(s):  
Wenzheng Xia ◽  
Jin Zhu ◽  
Xueyi Wang ◽  
Yinda Tang ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Nerve Regeneration ◽  
Schwann Cells ◽  
Ampk Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Lysophosphatidic Acid Inhibits Simvastatin-Induced Myocytoxicity by Activating LPA Receptor/PKC Pathway

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1529 ◽  
Author(s):  
Kyung-Jong Won ◽  
Yu-Jin Goh ◽  
Sung-Hee Hwang
Keyword(s):  
Muscle Damage ◽  
Lysophosphatidic Acid ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Cell Toxicity ◽  
Xtt Assay ◽  
Lpa Receptor ◽  
L6 Cells ◽  
Kinase C ◽  
And Migration ◽  
Induced Apoptosis

Statins such as simvastatin have many side effects, including muscle damage, which is known to be the most frequent undesirable side effect. Lysophosphatidic acid (LPA), a kind of biolipid, has diverse cellular activities, including cell proliferation, survival, and migration. However, whether LPA affects statin-linked muscle damage has not been reported yet. In the present study, to determine whether LPA might exert potential protective effect on statin-induced myocyotoxicity, the effect of LPA on cytotoxicity in rat L6 myoblasts exposed to simvastatin was explored. Viability and apoptosis of rat L6 myoblasts were detected via 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5- [(phenylamino)carbonyl]-2H-tetrazolium hydroxide (XTT) assay and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively. Protein expression levels were detected via Western blotting. Simvastatin decreased viability of L6 cells. Such decrease in viability was recovered in the presence of LPA. Treatment with LPA suppressed simvastatin-induced apoptosis in L6 cells. In addition, treatment with LPA receptor inhibitor Ki16425, protein kinase C (PKC) inhibitor GF109203X, or intracellular calcium chelator BAPTA-AM attenuated the recovery effect of LPA on simvastatin-induced L6 cell toxicity. These findings indicate that LPA may inhibit simvastatin-induced toxicity in L6 cells probably by activating the LPA receptor-PKC pathway. Therefore, LPA might have potential as a bioactive molecule to protect muscles against simvastatin-induced myotoxicity.

scholarly journals Expression and Function of Lysophosphatidic Acid LPA1 Receptor in Prostate Cancer Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4883-4892 ◽  
Author(s):  
Rishu Guo ◽  
Elizabeth A. Kasbohm ◽  
Puneeta Arora ◽  
Christopher J. Sample ◽  
Babak Baban ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Lysophosphatidic Acid ◽  
Cell Cycle Progression ◽  
Receptor Activation ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
And Migration

The bioactive phospholipid lysophosphatidic acid (LPA) promotes cell proliferation, survival, and migration by acting on cognate G protein-coupled receptors named LPA1, LPA2, and LPA3. We profiled gene expression of LPA receptors in androgen-dependent and androgen-insensitive prostate cancer cells and found that LPA1 gene is differentially expressed in androgen-insensitive and LPA-responsive but not androgen-dependent and LPA-resistant cells. In human prostate specimens, expression of LPA1 gene was significantly higher in the cancer compared with the benign tissues. The androgen-dependent LNCaP cells do not express LPA1 and do not proliferate in response to LPA stimulation, implying LPA1 transduces cell growth signals. Accordingly, stable expression of LPA1 in LNCaP cells rendered them responsive to LPA-induced cell proliferation and decreased their doubling time in serum. Implantation of LNCaP-LPA1 cells resulted in increased rate of tumor growth in animals compared with those tumors that developed from the wild-type cells. Growth of LNCaP cells depends on androgen receptor activation, and we show that LPA1 transduces Gαi-dependent signals to promote nuclear localization of androgen receptor and cell proliferation. In addition, treatment with bicalutamide inhibited LPA-induced cell cycle progression and proliferation of LNCaP-LPA1 cells. These results suggest the possible utility of LPA1 as a drug target to interfere with progression of prostate cancer.

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