Nerve Growth Factor Facilitates Regeneration across Nerve Gaps: Morphological and Behavioral Studies in Rat Sciatic Nerve

Derby, A; Engleman, V. Wayne; Frierdich, Gregory E.; Neises, Gabrielle R.; Rapp, Steve; Roufa, Dikla G.

doi:10.1006/exnr.1993.1019

Cited by 134 publications

(63 citation statements)

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“…To evaluate the recovery of the sensory nerve function in the 6 months group, we used the withdrawal reflex elicited by a hot water stimulus (Derby et al, 1993;Young et al, 2001) before and 1, 4, 8, and 12 weeks after implantation, respectively. For testing, the respective rat was held above a hot water bath (50-C).…”

Section: Sensory Recovery-withdrawal Testmentioning

confidence: 99%

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

Haastert

Lipokatic

Fischer

et al. 2006

Neurobiology of Disease

111

118

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Section: Sensory Recovery-withdrawal Testmentioning

confidence: 99%

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

Haastert

Lipokatic

Fischer

et al. 2006

Neurobiology of Disease

111

118

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“…NGF has been shown to stimulate neurite outgrowth and promote the survival of sensory ganglia, including those which give rise to spinal sensory nerves and sciatic nerves [23][24][25]. Due to their potent functions, LN-1 (an isoform of LN) and NGF have been used successfully for neurite extension in vitro and for nerve regeneration in vivo [26][27][28][29][30]. Hence, in this study we have used LN-1 and NGF to promote sciatic nerve regeneration across a 20 mm nerve gap in rats.…”

Section: Introductionmentioning

confidence: 99%

Differences between the effect of anisotropic and isotropic laminin and nerve growth factor presenting scaffolds on nerve regeneration across long peripheral nerve gaps

2008

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Anisotropic scaffolds of agarose hydrogels containing gradients of laminin-1 (LN-1) and nerve growth factor (NGF) molecules were used to promote sciatic nerve regeneration across a challenging 20 mm nerve gap in rats.Step and continuous gradient anisotropic scaffolds were fabricated and characterized and regeneration was compared to that in isotropic scaffolds with uniform concentrations of LN-1 and NGF and sciatic nerve grafts harvested from syngenic rats. Polysulfone tubular guidance channels were used to present the agarose based scaffolds to the nerve stumps. Fourmonths after implantation, regenerating axons were observed in animals implanted with anisotropic scaffolds with gradients of both LN-1 and NGF molecules and nerve grafts, but not in animals with isotropic scaffold implants. Also, the scaffolds with gradient of either LN-1 or NGF, with the other component being uniformly distributed in the scaffold, did not elicit axonal regeneration. The total number of myelinated axons was similar for the anisotropic scaffold and the nerve graft conditions, with the anisotropic scaffolds having a higher density of axons than the nerve grafts. Axonal diameter distribution was similar for the anisotropic scaffolds and the nerve grafts. The nerve grafts and anisotropic scaffolds resulted in better functional outcome compared to isotropic scaffolds as measured by the relative gastrocnemius muscle weight (RGMW). Additionally the state of neuromuscular junctions as assessed by pre-and post-synaptic staining revealed that both the anistropic scaffolds performed as well as nerve grafts.

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“…12 Peripheral nerve injury results in increased local NGF expression, which facilitates nerve regeneration. 13 It is possible that increased NGF expression also underlies the mechanisms of cardiac nerve sprouting after ischemic injury and MI. In the present study, we sampled blood and harvested tissues from the left ventricle and from the left stellate ganglion at different time points after experimental canine MI.…”

mentioning

confidence: 99%

Mechanisms of Cardiac Nerve Sprouting After Myocardial Infarction in Dogs

Zhou

Chen

Miyauchi

et al. 2004

Circulation Research

306

291

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Abstract-Cardiac nerve sprouting and sympathetic hyperinnervation after myocardial infarction (MI) both contribute to arrhythmogenesis and sudden death. However, the mechanisms responsible for nerve sprouting after MI are unclear. The expression of nerve growth factor (NGF), growth associated protein 43 (GAP43), and other nerve markers were studied at the infarcted site, the noninfarcted left ventricle free wall (LVFW), and the left stellate ganglion (LSG) at several time points (30 minutes to 1 month) after MI. Transcardiac (difference between coronary sinus and aorta) NGF levels were also assayed. Acute MI resulted in the immediate elevation of the transcardiac NGF concentration within 3.5 hours after MI, followed by the upregulation of cardiac NGF and GAP43 expression, which was earlier and more pronounced at the infarcted site than the noninfarcted LVFW. However, cardiac nerve sprouting and sympathetic hyperinnervation were more pronounced in the noninfarcted than the infarcted LVFW site and peaked at 1 week after MI. The NGF and GAP43 protein levels significantly increased in the LSG from 3 days (PϽ0.01 for all) after MI, without a concomitant increase in mRNA. There was persistent elevation of NGF levels in aorta and coronary sinus within 1 month after MI. We conclude MI results in immediate local NGF release, followed by upregulation of NGF and GAP43 expression at the infarcted site. NGF and GAP43 are transported retrogradely to LSG, which triggers nerve sprouting at the noninfarcted LVFW. A rapid and persistent upregulation of NGF and GAP43 expression at the infarcted site underlies the mechanisms of cardiac nerve sprouting after MI. Key Words: nerve growth factor Ⅲ nerve sprouting Ⅲ sympathetic nerve Ⅲ ventricular arrhythmia W e previously demonstrated that heterogeneous cardiac nerve sprouting and sympathetic hyperinnervation play important roles in arrhythmogenesis and sudden cardiac death in both human patients and animal models of myocardial infarction (MI). 1-6 However, the mechanisms and time course of nerve sprouting after MI are unclear. Nerve growth factor (NGF) is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. 7,8 NGF also regulates the synthesis of neurofilament and tubulin proteins, promotes Schwann cell migration, 9 modulates synaptic transmission between sympathetic neurons and cardiac myocytes, 10 and increases the half-life of growth associated protein-43 (GAP43). 11 Overexpression of NGF within the heart of transgenic mice causes hyperinnervation. 12 Peripheral nerve injury results in increased local NGF expression, which facilitates nerve regeneration. 13 It is possible that increased NGF expression also underlies the mechanisms of cardiac nerve sprouting after ischemic injury and MI. In the present study, we sampled blood and harvested tissues from the left ventricle and from the left stellate ganglion at different time points after experimental canine MI. NGF expression and the magnitude of cardiac nerve sprouting...

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Nerve Growth Factor Facilitates Regeneration across Nerve Gaps: Morphological and Behavioral Studies in Rat Sciatic Nerve

Cited by 134 publications

References 0 publications

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

Differentially promoted peripheral nerve regeneration by grafted Schwann cells over-expressing different FGF-2 isoforms

Differences between the effect of anisotropic and isotropic laminin and nerve growth factor presenting scaffolds on nerve regeneration across long peripheral nerve gaps

Mechanisms of Cardiac Nerve Sprouting After Myocardial Infarction in Dogs

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