Article
Nitric oxide in the commissural nucleus tractus solitarii regulates carotid chemoreception hyperglycemic reflex and c-Fos expression
Fecha
2004Registro en:
10.1016/j.niox.2013.12.004
Autor
Ordonez, R.M.
Espinosa, A.M.
Sanchez-Gonzalez, D.J.
Armendariz-Borunda, J.
Berumen, J.
Institución
Resumen
Asian-American (AA) variants of human papillomavirus 16 (HPV-16) are linked to a high incidence of cervical cancer in Mexico, with some evidence strongly suggesting that they are more oncogenic than European (E) variants, including their association with younger women and their higher associated risk of cervical cancer. Differences in the regulation of viral E6/E7 oncogene transcription by the E2 protein may be involved in the higher oncogenicity of AA variants. In E variants, E6/E7 oncogene transcription is repressed by the E2 protein and is frequently up-regulated by the destruction of the E2 gene during viral integration. In contrast, the E2 gene is retained in full in most AA-positive carcinomas, raising the possibility of alternative mechanisms for increasing viral oncogene transcription. The authors investigated whether the higher oncogenicity of AA variants is linked to differences in E6/E7 oncogene transcription and the mechanism of E2 deactivation. E6/E7 and E1/E2 transcripts were explored by RT-PCR in 53 HPV-16-positive cervical carcinomas, 39 retaining (20 European and 19 AA) and 14 having lost (12 European and 2 AA) the E1/E2 genes, and transcription repression activity of the AA E2 genes was tested in four cell lines that constitutively express the ?-galactosidase reporter or E6/E7 genes driven by the viral long control region. E6/E7 oncogene transcripts were found in all carcinomas, but only those positive for AA variants with E1/E2 genes had complete E2 transcripts. E2 transcripts were down-regulated by splicing in E-positive carcinomas retaining E1/E2. AA E2 genes were impaired for repression of E6/E7 oncogene transcription in vivo. These results suggest that E6/E7 oncogene expression starts earlier in AA than E variant infections, since E variants need E2 to be destroyed or down-regulated. " 2004 SGM.",,,,,,"10.1099/vir.0.19317-0",,,"http://hdl.handle.net/20.500.12104/41232","http://www.scopus.com/inward/record.url?eid=2-s2.0-18244415256&partnerID=40&md5=e67ba2ca7626b17c7f1859360cc8ffb2",,,,,,"6",,"Journal of General Virology",,"1433 1444",,"85",,"Scopus WOS",,,,,,,,,,,,"Enhanced oncogenicity of Asian-American human papillomavirus 16 is associated with impaired E2 repression of E6/E7 oncogene transcription",,"Article"
"44927","123456789/35008",,"Montero, S., Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico, Facultad de Medicina, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico; Lemus, M., Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico; Luquin, S., Departamento de Neurociencias, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Mexico; García-Estrada, J., División de Neurociencias, Centro de Investigación Biomédica de Occidente, IMSS, Guadalajara, Mexico; Melnikov, V., Facultad de Medicina, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico; Leal, C.A., División de Investigación Quirúrgica, Centro de Investigación Biomédica de Occidente, IMSS, Guadalajara, Mexico; Portilla-De Buen, E., División de Investigación Quirúrgica, Centro de Investigación Biomédica de Occidente, IMSS, Guadalajara, Mexico; Roces De Álvarez-Buylla, E., Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Ave. 25 de Julio s/n, Colima 28045, Mexico",,"Montero, S. Lemus, M. Luquin, S. García-Estrada, J. Melnikov, V. Leal, C.A. Portilla-De Buen, E. Roces De Alvarez-Buylla, E.",,"2014",,"Carotid body chemoreceptors function as glucose sensors and contribute to glucose homeostasis. The nucleus tractus solitarii (NTS) is the first central nervous system (CNS) nuclei for processing of information arising in the carotid body. Here, we microinjected a nitric oxide (NO) donor sodium nitroprusside (SNP), an NO-independent activator of the soluble guanylyl cyclase (sGC) (YC1) or an NO-synthase (NOS) inhibitor N?-nitro-l- arginine methyl ester (L-NAME) into the commissural NTS (cNTS) before carotid chemoreceptor anoxic stimulation and measured arterial glucose and the expression of Fos-like immunoreactivity (Fos-ir). Male Wistar rats (250-300 g) were anesthetized, and the carotid sinus was vascularly isolated. Either artificial cerebrospinal fluid (aCSF), SNP, YC1 or L-NAME were stereotaxically injected into the cNTS. The SNP and YC1 infused into the cNTS before carotid chemoreceptor stimulation (SNP-2 and YC1-2 groups) similarly increased arterial glucose compared to the aCSF-2 group. By contrast, infusion of L-NAME into the cNTS before carotid chemoreceptor stimulation (L-NAME-2 group) decreased arterial glucose concentration. The number of cNTS Fos-ir neurons, determined in all the groups studied except for YC1 groups, significantly increased in SNP-2 rat when compared to the aCSF-2 or SNP-2 groups. Our findings demonstrate that NO signaling, and the correlative activation of groups of cNTS neurons, plays key roles in the hyperglycemic reflex initiated by carotid chemoreceptor stimulation. " 2013 Elsevier Inc. All rights reserved.