title: Gene expression profiles of major cytokines in the nucleus tractus solitarii of the spontaneously hypertensive rat.
abstract: Since the nucleus of the solitary tract (NTS) is a pivotal region for regulating the set-point of arterial pressure, we proposed a role for it in the development of neurogenic hypertension. Recent studies have suggested that pro-inflammatory molecules are highly expressed in the NTS of an animal model of human essential hypertension--the spontaneously hypertensive rat (SHR), compared to normotensive Wistar-Kyoto rat (WKY). Based on this evidence, we hypothesized that inflammatory mediators such as cytokines are up-regulated in the hypertensive NTS. In the present study, we have assessed the level of gene expression of some cytokines in the NTS of SHR compared to WKY. In addition, for further confirmation of abnormal inflammatory condition within the NTS of SHR, we identified gene expression levels of an inflammatory marker, glycoprotein-39 (gp39) precursor, which is homologous to chitinase 3-like protein 1, human cartilage-gp39 or YKL40. The NTS was micro-dissected from 15-week-old male SHR and WKY rats. Total RNA was extracted and quantitative RT-PCR was performed. Gene expression of gp39 precursor and monocyte chemoattractant protein-1 were higher in the NTS of SHR while inter-leukin-6 was lower in the NTS of SHR compared to the WKY. In contrast, there were no significant differences in the expression of other cytokines including: inter-leukin-1 beta, tumor necrosis factor-alpha and transforming growth factor beta 1. These data together with our previous published finding of an over expression of junctional adhesion molecule-1 suggest that the NTS of the SHR exhibits a specific inflammatory state.
authors.affiliation: Department of Physiology, Wakayama Medical University School of Medicine, 811-1, Kimiidera, Wakayama City 641-8509, Japan. h-waki@wakayama-med.ac.jp
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Waki
authors.forename: Sabine S
authors.initials: SS
authors.lastname: Gouraud
authors.forename: Masanobu
authors.initials: M
authors.lastname: Maeda
authors.forename: Julian F R
authors.initials: JF
authors.lastname: Paton
mesh_terms: D000818:Animals; D023201:CD40 Ligand / Q000235:genetics; D018932:Chemokine CCL2 / Q000235:genetics; D016207:Cytokines / Q000235:genetics*; D004195:Disease Models, Animal; D004660:Encephalitis / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000276:immunology; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006973:Hypertension / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology; D015850:Interleukin-6 / Q000235:genetics; D008297:Male; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017552:Solitary Nucleus / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D012333:RNA, Messenger; D023201:CD40 Ligand