期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 33, 页码 8417-8427出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1578-06.2006
关键词
Schwann cell; proliferation; death; TGF beta; neuregulin; CRE recombinase
资金
- Telethon [GGP030074] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
During development, Schwann cell numbers are precisely adjusted to match the number of axons. It is essentially unknown which growth factors or receptors carry out this important control in vivo. Here, we tested whether the type II transforming growth factor (TGF)beta receptor has a role in this process. We generated a conditional knock-out mouse in which the type II TGF beta receptor is specifically ablated only in Schwann cells. Inactivation of the receptor, evident at least from embryonic day 18, resulted in suppressed Schwann cell death in normally developing and injured nerves. Notably, the mutants also showed a strong reduction in Schwann cell proliferation. Consequently, Schwann cell numbers in wild-type and mutant nerves remained similar. Lack of TGF beta signaling did not appear to affect other processes in which TGF beta had been implicated previously, including myelination and response of adult nerves to injury. This is the first in vivo evidence for a growth factor receptor involved in promoting Schwann cell division during development and the first genetic evidence for a receptor that controls normal developmental Schwann cell death.
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