title: Involvement of activated astrocyte and microglia of locus coeruleus in cardiac pain processing after acute cardiac injury.
abstract: OBJECTIVE
  It is still not known whether the glial cell activation of locus coeruleus (LC) is involved in the neurophysiologic mechanism of the acute phase of heart disease. The aim of this study was to investigate whether the glial cell activation of LC responds to acute cardiac injury (ACI).
  
  
  METHODS
  In this study, ACI was established by intramyocardial injection of formalin. Afterward, we analysed c-Fos, OX42, GFAP and P2X(4)R expression levels in the LC of the rats by immunofluorescence staining or Western blot analysis.
  
  
  RESULTS
  There was no significant difference in the levels of these markers in the LC between the normal control and the sham-operated groups. Following ACI, up-regulation of GFAP, OX42 and P2X(4)R expression levels were observed in locus coeruleus of the rats. The peak expression time was at hour 24. P2X(4)R was colocalized with OX42 in activated microglias, but not with GFAP in activated astrocytes. Compared with the control group, the ACI group showed a high expression level of c-Fos at hour 1 with a peak expression level at hour 2.
  
  
  CONCLUSIONS
  The results showed that LC glia cells, like neurons, could sensitively respond to cardiovascular nociception induced by ACI at different time points. Results of this study may provide insights into the role of glial activation in response to ACI and may represent a potential strategy for investigation of neurophysiologic mechanism of cardiac pain.
authors.affiliation: Department of Cardiology, Fourth Military Medical University, Xi'an, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Hexiang
authors.initials: H
authors.lastname: Cheng
authors.forename: Jinwu
authors.initials: J
authors.lastname: Chen
authors.forename: Fu
authors.initials: F
authors.lastname: Yi
authors.forename: Weijei
authors.initials: W
authors.lastname: Li
authors.forename: Ronghua
authors.initials: R
authors.lastname: Luan
authors.forename: Wenyi
authors.initials: W
authors.lastname: Guo
authors.forename: Anlin
authors.initials: A
authors.lastname: Lv
authors.forename: Zhiren
authors.initials: Z
authors.lastname: Rao
authors.forename: Haichang
authors.initials: H
authors.lastname: Wang
mesh_terms: D000208:Acute Disease; D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D039481:CD11b Antigen / Q000378:metabolism; D004195:Disease Models, Animal; D005557:Formaldehyde; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006331:Heart Diseases / Q000139:chemically induced / Q000150:complications*; D008125:Locus Coeruleus / Q000473:pathology*; D008297:Male; D017628:Microglia / Q000378:metabolism*; D010146:Pain / Q000209:etiology* / Q000473:pathology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D011921:Rats, Inbred WKY; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D058848:Receptors, Purinergic P2X4; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D039481:CD11b Antigen; D005904:Glial Fibrillary Acidic Protein; D016760:Proto-Oncogene Proteins c-fos; D018048:Receptors, Purinergic P2; D058848:Receptors, Purinergic P2X4; D005557:Formaldehyde