Sympathetic nerve sprouting after orthotopic heart transplantation

Kim, Dave T.; Luthringer, Daniel; Lai, Angela; Suh, Gina A.; Czer, L.; Chen, Lan S.; Chen, Peng Sheng; Fishbein, Michael C.

doi:10.1016/j.healun.2003.10.005

Cited by 28 publications

(24 citation statements)

References 24 publications

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“…It was perceived by some researchers that cardiac nerve sprouting potentially mediated electrophysiological turbulence resulting in malignant cardiac arrhythmia (Cao et al 2000), whereas other scholars precluded higher incidences of arrhythmia via studies of nerve sprouting alone or in combination with a pacemaker (Kim et al 2004). The gap junction was generally referred to as an essential marker for effective treatment of cellular cardiomyoplasty (Valiunas et al 2004), rendering that differentiation from ADSCs to cardiomyocytes might be insufficient for functional improvement.…”

Section: Discussionmentioning

confidence: 99%

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Yang

Liu

et al. 2012

Tohoku J. Exp. Med.

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Adipose tissue-derived stem cells (ADSCs) are a promising source of autologous stem cells that are used for regeneration and repair of infracted heart. However, the efficiency of their transplantation is under debate. One of the possible reasons for marginal improvement in ADSCs transplantation is the significant cell death rate of implanted cells after being grafted into injured heart. Therefore, overcoming the poor survival rate of implanted cells may improve stem cell therapy. Due to limited improvement concerning direct stem cell therapy, gene-transfer methods are used to enhance cellular cardiomyoplasty efficacy. Heme oxygenase-1 (HO-1) can provide various types of cells with protection against oxidative injury and apoptosis. However, exact effects of autologous ADSCs combined with HO-1 on cardiac performance remains unknown. In this study, rabbits were treated with ADSCs transduced with HO-1 (HO-1-ADSCs), treated with non-transduced ADSCs, or injected with phosphate buffered saline 14 days after experimental myocardial infarction was induced, when autologous ADSCs were obtained simultaneously. Four weeks after injection, echocardiography showed significant improvements for cardiac functions and left ventricular dimensions in HO-1-ADSCs-treated animals. Structural consequences of transplantation were determined by detailed histological analysis, which showed differentiation of HO-1-ADSCs to cardiomyocyte-like tissues and lumen-like structure organizations. Apart from improvement in angiogenesis and scar areas, more connexin 43-positive gap junction and greater tyrosine hydroxylase-positive cardiac sympathetic nerves sprouting were observed in the HO-1-ADSCs-treated group compared with ADSCs group. These data suggest that the transplantation of autologous ADSCs combined with HO-1 transduction is a feasible and efficacious method for improving infarcted myocardium.

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Section: Discussionmentioning

confidence: 99%

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Yang

Liu

et al. 2012

Tohoku J. Exp. Med.

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“…This limited reinnervation may affect the cardiac calcium homeostasis . There was also transmural heterogeneity of nerve distribution in allograft hearts . The retention of 11 C‐ meta ‐hydroxyephedrine (HED), which is a norepinephrine (NE) analogue, showed heterogeneous “patchy” reinnervation in some HTx recipients, whereas control subjects showed homogeneous retention in the entirety of the left ventricle .…”

Section: Cardiac Reinnervationmentioning

confidence: 99%

“…Cardiac denervation causes loss of afferent nerves in the myocardium,which is hypothesized to impair the reflex responses of the sensory endings of the cardiopulmonary region . Cardiac denervation occurs in the context of a variable background of nerve density in the donor heart: it has been observed that nerve density differs greatly in all areas of the allograft . There was also a significant decrease in total nerve density in cardiac allografts after HTx …”

Section: Introductionmentioning

confidence: 99%

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Early Denervation and Later Reinnervation of the Heart Following Cardiac Transplantation: A Review

Awad

Czer

Hou

et al. 2016

JAHA

105

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“…Imaging studies showing reinnervation of transplanted hearts are complemented by functional responses to exercise (Wilson et al, 2000) and functional responses to drugs that cause NE release or block NE receptors (Bengel et al, 2004). Finally, sympathetic reinnervation of transplants was confirmed post-mortem by tyrosine hydroxylase (TH) staining (Kim et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

Infarct-Derived Chondroitin Sulfate Proteoglycans Prevent Sympathetic Reinnervation after Cardiac Ischemia-Reperfusion Injury

Gardner

Habecker

2013

J. Neurosci.

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Sympathetic nerve can regenerate after injury to re-innervate target tissues. Sympathetic regeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac infarct remained denervated following ischemia-reperfusion (I-R). We used mice to ask if the lack of sympathetic regeneration into the scar was due to blockade by inhibitory extracellular matrix within the infarct. We found that chondroitin sulfate proteoglycans (CSPGs) were present in the infarct after I-R, but not after chronic ischemia, and that CSPGs caused inhibition of sympathetic axon outgrowth in vitro. Ventricle explants after I-R and chronic ischemia stimulated sympathetic axon outgrowth that was blocked by NGF antibodies. However, growth in I-R co-cultures was asymmetrical, with axons growing toward the heart tissue consistently shorter than axons growing in other directions. Growth toward I-R explants was rescued by adding chondroitinase ABC (ChABC) to the co-cultures, suggesting that I-R infarct-derived CSPGs prevented axon extension. Sympathetic ganglia lacking Protein Tyrosine Phosphatase Sigma (PTPRS) were not inhibited by CSPGs or I-R explants in vitro, suggesting PTPRS is the major CSPG receptor in sympathetic neurons. To test directly if infarct-derived CSPGs prevented cardiac reinnervation, we carried out ischemia-reperfusion in ptprs-/- and ptprs+/- mice. Cardiac infarcts in ptprs-/- mice were hyperinnervated, while infarcts in ptprs+/- littermates were denervated, confirming that CSPGs prevent sympathetic reinnervation of the cardiac scar after I-R. This is the first example of CSPGs preventing sympathetic reinnervation of an autonomic target following injury, and may have important consequences for cardiac function and arrhythmia susceptibility after myocardial infarction.

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Sympathetic nerve sprouting after orthotopic heart transplantation

Cited by 28 publications

References 24 publications

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Early Denervation and Later Reinnervation of the Heart Following Cardiac Transplantation: A Review

Infarct-Derived Chondroitin Sulfate Proteoglycans Prevent Sympathetic Reinnervation after Cardiac Ischemia-Reperfusion Injury

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