Spatial distribution of nerve sprouting after myocardial infarction in mice

Oh, Yong Seog; Jong, Ambrose; Kim, Dave T.; Li, Hongmei; Wang, Charles; Zemljic-Harpf, Alice; Ross, Robert S.; Fishbein, Michael C.; Chen, Peng Sheng; Chen, Lan S.

doi:10.1016/j.hrthm.2006.02.005

Cited by 68 publications

(61 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The same group reported that, in rats infected with Trypanosoma cruzi (Chagas disease), gold particles showing existence of GDNF in atrial granules increased transiently at the time of maximal autonomic denervation (15). On the other hand, in a mouse model of myocardial infarction and subsequent sympathetic nerve sprouting, myocardial gene expression of GDNF (estimated by DNA microarray) was, unlike NGF, virtually unchanged (16). In humans, cardiac expression of GDNF is limited to the embryonic and early post-natal stage, whereas NGF (estimated by DNA microarray) is abundantly expressed in the adult heart (18).…”

Section: Discussionmentioning

confidence: 99%

Glial cell line-derived neurotrophic factor (GDNF) enhances sympathetic neurite growth in rat hearts at early developmental stages

Miwa¹,

Lee²,

Takagishi³

et al. 2010

Biomed. Res.

View full text Add to dashboard Cite

Molecular signaling of sympathetic innervation of myocardium is an unresolved issue. The purpose of this study was to investigate the effect of neurotrophic factors on sympathetic neurite growth towards cardiomyocytes. Cardiomyocytes (CMs) and sympathetic neurons (SNs) were isolated from neonatal rat hearts and superior cervical ganglia, and were co-cultured, either in a random or localized way. Neurite growth from SNs toward CMs was assessed by immunohistochemistry for neurofilament M and α-actinin in response to neurotrophic factors-nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF) and a chemical repellent, semaphorin 3A. As a result, GDNF as well as NGF and BDNF stimulated neurite growth. GDNF enhanced neurite outgrowth even under the NGF-depleted culture condition, excluding an indirect effect of GDNF via NGF. Quantification of mRNA and protein by real-time PCR and immunohistochemistry at different developmental stages revealed that GDNF is abundantly expressed in the hearts of embryos and neonates, but not in adult hearts. GDNF plays an important role in inducing cardiac sympathetic innervation at the early developmental stages. A possible role in (re)innervation of injured or transplanted or cultured and transplanted myocardium may deserve investigation.

show abstract

Section: Discussionmentioning

confidence: 99%

Glial cell line-derived neurotrophic factor (GDNF) enhances sympathetic neurite growth in rat hearts at early developmental stages

Miwa¹,

Lee²,

Takagishi³

et al. 2010

Biomed. Res.

View full text Add to dashboard Cite

show abstract

“…Nerve sprouting, which resulted in sympathetic (but not parasympathetic) hyperinnervation, was greater in the outer loop of the heart. The difference in the outer and inner loops started within 3 hours and persisted for 2 months after myocardial infarction ( Figure 4) (Oh et al, 2006). Fig.…”

Section: Sympathetic Neural Remodeling After Myocardial Infarctionmentioning

confidence: 91%

“…The nerve fiber regeneration process is triggered by up-regulation of nerve growth factor or other neurotrophic factor genes in the non-neuronal cells around the site of injury. Upregulation of nerve growth factor was more prominent in the area near the infarct than in the area remote to the infarct (Oh et al, 2006). Nerve growth factor mRNA was significantly up-regulated within 3 hours after myocardial infarction and persisted for 1 month in both the infarcted myocardium and the noninfarcted left ventricular free wall (Oh et al, 2006;Zhou et al, 2004).…”

Section: Mechanisms Of Sympathetic Neural Remodeling After Myocardialmentioning

confidence: 93%

“…The density of nerve fibers immunopositive for Growth-associated protein-43 upregulated after myocardial infarction at different periods, indicating nerve fibers undergoing sprouting activity shortly after myocardial infarction (Oh et al, 2006;Zhou et al, 2004). However, sprouting nerve fibers may regress unless nerve terminals can form synaptic contacts with target cells.…”

Section: Sympathetic Neural Remodeling After Myocardial Infarctionmentioning

confidence: 99%

“…More nerve fibers are present in the outer loop than the inner loop. Arrows point to brown nerve twigs (20×objective) (Oh et al, 2006). Necrotic injury to the rat myocardium results in denervation followed by proliferative regeneration of schwann cells and axons (Nori et al, 1995).…”

Section: Sympathetic Neural Remodeling After Myocardial Infarctionmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

Zhong¹,

Li²,

Ke³

et al. 2012

Advances in Electrocardiograms - Clinical Applications

View full text Add to dashboard Cite

Transplantation of iPSc Ameliorates Neural Remodeling and Reduces Ventricular Arrhythmias in a Post‐Infarcted Swine Model

Zhang

Song

et al. 2014

J of Cellular Biochemistry

View full text Add to dashboard Cite

Neural remodeling after myocardial infarction (MI) may cause malignant ventricular arrhythmia, which is the main cause of sudden cardiac death following MI. Herein, we aimed to examine whether induced pluripotent stem cells (iPSc) transplantation can ameliorate neural remodeling and reduce ventricular arrhythmias (VA) in a post-infarcted swine model. Left anterior descending coronary arteries were balloon-occluded to generate MI. Animals were then divided into Sham, PBS control, and iPS groups. Dynamic electrocardiography programmed electric stimulation were performed to evaluate VA. The spatial distribution of vascularization, Cx43 and autonomic nerve regeneration were evaluated by immunofluorescence staining. Associated protein expression was detected by Western blotting. Likewise, we measured the enzymatic activities of superoxide dismutase and content of malondialdehyde. Six weeks later, the number of blood vessels increased significantly in the iPSc group. The expression of vascular endothelial growth factor and connexin 43 in the iPS group was significantly higher than the PBS group; however, the levels of nerve growth factor and tyrosine hydroxylase were lower. The oxidative stress was ameliorated by iPSc transplantation. Moreover, the number of sympathetic nerves in the iPSc group was reduced, while the parasympathetic nerve fibers had no obvious change. The transplantation of iPSc also significantly decreased the low-/high-frequency ratio and arrhythmia score of programmed electric stimulation-induced VA. In conclusion, iPSc intramyocardial transplantation reduces vulnerability to VAs, and the mechanism was related to the remodeling amelioration of autonomic nerves and gap junctions. Moreover, possible mechanisms of iPSc transplantation in improving neural remodeling may be related to attenuated oxidative stress and inflammatory response.

show abstract

Spatial distribution of nerve sprouting after myocardial infarction in mice

Cited by 68 publications

References 27 publications

Glial cell line-derived neurotrophic factor (GDNF) enhances sympathetic neurite growth in rat hearts at early developmental stages

Glial cell line-derived neurotrophic factor (GDNF) enhances sympathetic neurite growth in rat hearts at early developmental stages

Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

Transplantation of iPSc Ameliorates Neural Remodeling and Reduces Ventricular Arrhythmias in a Post‐Infarcted Swine Model

Contact Info

Product

Resources

About