Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation

Shengmei Zhou, Ji Min Cao, Moshe Swissa, Ignacio Gonzalez-Gomez, Che Ming Chang, Kai Chien, Yasushi Miyauchi, Katherine J. Fu, Johnny Yi, Kamlesh Asotra, Hrayr S. Karagueuzian, Michael C. Fishbein, Peng Sheng Chen, Lan S. Chen

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Introduction: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. Methods and Results: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. Conclusion: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart.

Original languageEnglish (US)
Pages (from-to)430-437
Number of pages8
JournalJournal of Cardiovascular Electrophysiology
Volume15
Issue number4
DOIs
StatePublished - Apr 1 2004
Externally publishedYes

Fingerprint

Nerve Growth Factor Receptor
Nerve Growth Factor
Myocardium
Stellate Ganglion
Protein-Tyrosine Kinases
Electric Stimulation
Canidae
Schwann Cells
Receptor Protein-Tyrosine Kinases
Axons
Cardiac Arrhythmias
Neurons
Control Groups
Growth

Keywords

  • Nerve growth factor
  • p75NTR
  • Sudden cardiac death
  • Sympathetic nerve
  • TrkA

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation. / Zhou, Shengmei; Cao, Ji Min; Swissa, Moshe; Gonzalez-Gomez, Ignacio; Chang, Che Ming; Chien, Kai; Miyauchi, Yasushi; Fu, Katherine J.; Yi, Johnny; Asotra, Kamlesh; Karagueuzian, Hrayr S.; Fishbein, Michael C.; Chen, Peng Sheng; Chen, Lan S.

In: Journal of Cardiovascular Electrophysiology, Vol. 15, No. 4, 01.04.2004, p. 430-437.

Research output: Contribution to journalArticle

Zhou, S, Cao, JM, Swissa, M, Gonzalez-Gomez, I, Chang, CM, Chien, K, Miyauchi, Y, Fu, KJ, Yi, J, Asotra, K, Karagueuzian, HS, Fishbein, MC, Chen, PS & Chen, LS 2004, 'Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation', Journal of Cardiovascular Electrophysiology, vol. 15, no. 4, pp. 430-437. https://doi.org/10.1046/j.1540-8167.2004.03517.x
Zhou, Shengmei ; Cao, Ji Min ; Swissa, Moshe ; Gonzalez-Gomez, Ignacio ; Chang, Che Ming ; Chien, Kai ; Miyauchi, Yasushi ; Fu, Katherine J. ; Yi, Johnny ; Asotra, Kamlesh ; Karagueuzian, Hrayr S. ; Fishbein, Michael C. ; Chen, Peng Sheng ; Chen, Lan S. / Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation. In: Journal of Cardiovascular Electrophysiology. 2004 ; Vol. 15, No. 4. pp. 430-437.
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abstract = "Introduction: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. Methods and Results: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. Conclusion: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart.",
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T1 - Low-affinity nerve growth factor receptor p75NTR immunoreactivity in the myocardium with sympathetic hyperinnervation

AU - Zhou, Shengmei

AU - Cao, Ji Min

AU - Swissa, Moshe

AU - Gonzalez-Gomez, Ignacio

AU - Chang, Che Ming

AU - Chien, Kai

AU - Miyauchi, Yasushi

AU - Fu, Katherine J.

AU - Yi, Johnny

AU - Asotra, Kamlesh

AU - Karagueuzian, Hrayr S.

AU - Fishbein, Michael C.

AU - Chen, Peng Sheng

AU - Chen, Lan S.

PY - 2004/4/1

Y1 - 2004/4/1

N2 - Introduction: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. Methods and Results: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. Conclusion: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart.

AB - Introduction: We previously demonstrated the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia. Nerve growth factor (NGF) regulates myocardial sympathetic innervation. However, it is unclear whether the NGF high-affinity receptor tyrosine kinase A (TrkA) and the NGF low-affinity receptor p75NTR are altered in the state of sympathetic hyperinnervation in the heart. The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation. Methods and Results: Myocardial sympathetic hyperinnervation was induced by local infusion of NGF into myocardium or left stellate ganglia, or chronic subthreshold electric stimulation to the left stellate ganglia. The results showed that TrkA immunoreactivity was absent in the myocardium. Low-affinity receptor p75NTR immunoreactivity was present in axons, Schwann cells, and interstitial cells of sympathetic nerves, as well as in interstitial cells of the myocardium. The density of p75NTR immunolabeled myocardial interstitial cells at the NGF infusion site was lower than that at the site remote from NGF infusion, yet the sympathetic nerve density was higher at the infusion site than the remote area. The density of p75NTR also was lower in the myocardium with high sympathetic nerve density, induced by NGF infusion or chronic electric stimulation of the left stellate ganglia, compared to control groups. Conclusion: The data indicate that p75NTR may be the main NGF receptor in the myocardium, and p75NTR immunopositive interstitial cells may have a role in regulating sympathetic nerve growth in canine heart.

KW - Nerve growth factor

KW - p75NTR

KW - Sudden cardiac death

KW - Sympathetic nerve

KW - TrkA

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