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- 저자 : ( Jeffrey A Golden ) (검색결과 2 건)
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RET signaling is required for survival and normal function of nonpeptidergic nociceptors.
Golden, Judith P,Hoshi, Masato,Nassar, Mohammed A,Enomoto, Hideki,Wood, John N,Milbrandt, Jeffrey,Gereau, Robert W,Johnson, Eugene M,Jain, Sanjay The Society 2010 The Journal of neuroscience Vol.30 No.11
<P>Small unmyelinated sensory neurons classified as nociceptors are divided into two subpopulations based on phenotypic differences, including expression of neurotrophic factor receptors. Approximately half of unmyelinated nociceptors express the NGF receptor TrkA, and half express the GDNF family ligand (GFL) receptor Ret. The function of NGF/TrkA signaling in the TrkA population of nociceptors has been extensively studied, and NGF/TrkA signaling is a well established mediator of pain. The GFLs are analgesic in models of neuropathic pain emphasizing the importance of understanding the physiological function of GFL/Ret signaling in nociceptors. However, perinatal lethality of Ret-null mice has precluded the study of the physiological role of GFL/Ret signaling in the survival, maintenance, and function of nociceptors in viable mice. We deleted Ret exclusively in nociceptors by crossing nociceptor-specific Na(v)1.8 Cre and Ret conditional mice to produce Ret-Na(v)1.8 conditional knock-out (CKO) mice. Loss of Ret exclusively in nociceptors results in a reduction in nociceptor number and size, indicating that Ret signaling is important for the survival and trophic support of these cells. Ret-Na(v)1.8 CKO mice exhibit reduced epidermal innervation but normal central projections. In addition, Ret-Na(v)1.8 CKO mice have increased sensitivity to cold and increased formalin-induced pain, demonstrating that Ret signaling modulates the function of nociceptors in vivo. Enhanced inflammation-induced pain may be mediated by decreased prostatic acid phosphatase (PAP), as PAP levels are markedly reduced in Ret-Na(v)1.8 CKO mice. The results of this study identify the physiological role of endogenous Ret signaling in the survival and function of nociceptors.</P>
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( Eun Kyung Kim ),( Seung Ick Cha ),( Aaron V Schroeder ),( Jasleen Kukreja ),( Kirk D Jones ),( Jeffrey A Golden ),( Michael A Matthay ),( David J Erle ),( Harold R Collard ),( Paul J Wolters ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Background: The prevalence of idiopathic pulmonary fibrosis (IPF) increases with age. Recent reports have demonstrated that mutations in TERT or TERC and short telomeres are risk factors for the development of IPF. Because short telomeres induce cellular senescence, these findings suggest senescence may occur in IPF lung. Methods: To evaluate for cellular senescence, we compared microRNA (miRNA) expression by miRNA arrays in type II epi-thelial cells. Senescence-associated β-galactosidase staining and immunohistochemical detection of p16, p21 and p53 were examined in sections of lung obtained from IPF patients and normal controls. Results: Expression of miR34-a, -b, and -c, which reportedly induce senescence in human epithelial cells are increased in IPF type II epithelial cells. β-Galactosidase activity is detectable on type II epithelial cells of IPF, but not normal lung. p16, p21 and p53 were detectable by immunostaining in IPF epithelial cells. Conclusions: IPF epithelial cells express several markers of senescence. These results suggest that the senescence of alveolar epithelial cells is accelerated in patients with IPF and may play a role in the pathogenesis of IPF.
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