Cardiac NGF and GDNF expression during Trypanosoma cruzi infection in rats.
In rats, autonomic nerve endings are damaged during Trypanosoma cruzi-induced myocarditis. Gradual recovery occurs after the acute phase. The present work shows the cardiac levels of glial cell line-derived neurotrophic factor (GDNF) and nerve growth factor (NGF), and their cellular sources during T. cruzi infection in rats. Atrial and ventricular NGF levels (ELISA) increased significantly at day 20 post inoculation, the time-point of maximal sympathetic denervation. ELISA failed to show significant increase of cardiac GDNF levels. However immunohistochemistry showed a significant increase of anti-GDNF gold particles over atrial granules at day 20. Light microscopy showed stronger NGF immunostaining in atrial cardiomyocytes and several blood capillaries. In situ hybridization showed NGF and GDNF mRNAs in atrial and ventricular myocytes of both infected and uninfected animals. Endothelial cells exhibited NGF mRNA and protein only in infected rats. No evidence of neurotrophic factor expression by the infiltrating mononuclear cells was found. This is the first report on neurotrophic factor expression during T. cruzi infection. Our findings indicate an important role for NGF in the regenerative phenomena subsequent to a myocarditis able to damage sympathetic nerve endings, with preservation of preterminals and nerve trunks. GDNF could have a minor or a more transient participation.
Martinelli
Patrícia Massara
PM
Department of Morphology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, 31270-901, Belo Horizonte, MG, Brazil.
Camargos
Elizabeth Ribeiro da Silva
ER
Azevedo
Andréa Alves
AA
Chiari
Egler
E
Morel
Gérard
G
Machado
Conceição Ribeiro da Silva
CR
D000818:Animals; D002598:Chagas Cardiomyopathy / Q000378:metabolism*; D003289:Convalescence; D018450:Disease Progression; D004727:Endothelium / Q000378:metabolism; D051100:Glial Cell Line-Derived Neurotrophic Factor / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D006321:Heart / Q000294:innervation*; D006325:Heart Atria / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism; D007124:Immunoenzyme Techniques; D017403:In Situ Hybridization; D016253:Microscopy, Immunoelectron; D009205:Myocarditis / Q000378:metabolism* / Q000469:parasitology; D009206:Myocardium / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology*; D009411:Nerve Endings / Q000378:metabolism / Q000473:pathology; D020932:Nerve Growth Factor / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D009416:Nerve Regeneration; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017779:Sympathetic Fibers, Postganglionic / Q000473:pathology / Q000502:physiology*
D051100:Glial Cell Line-Derived Neurotrophic Factor; D012333:RNA, Messenger; D020932:Nerve Growth Factor