Blockade of glial-derived neurotrophic factor in laryngeal muscles promotes appropriate reinnervation

Hernández-Morato, Ignacio; Tewari, I.; Sharma, S. C.; Pitman, Michael J.

doi:10.1002/lary.25953

Cited by 20 publications

(29 citation statements)

References 35 publications

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“…Vocal fold movement was recorded and evaluated after nerve injury and before sacrifice using a camera attached to the endoscope with a digital recording system (Richard Wolf Solid State Color Video Camera, Melville, NY). The videos were reviewed for blinded grading of motion of the right vocal fold: 0 for immobile, 1 for slight nonpurposeful motion, 2 for purposeful but paretic motion, and 3 for normal motion …”

Section: Methodsmentioning

confidence: 99%

“…Similarly, an injection of an anti‐Netrin‐1 antibody into the PCA also led to reinnervation of TA before the PCA. However, nonselective reinnervation was still observed . To better understand the critical role that trophic factors play during RLN regeneration, one also needs to investigate the trophic factors receptors, which are produced in the nucleus ambiguus following RLN injury.…”

Section: Introductionmentioning

confidence: 99%

“…To better understand the critical role that trophic factors play during RLN regeneration, one also needs to investigate the trophic factors receptors, which are produced in the nucleus ambiguus following RLN injury. Expressions of both trophic factors and receptors are synchronized in specific patterns during nerve regeneration …”

Section: Introductionmentioning

confidence: 99%

“…Supernumerary axons are then removed, and the neuromuscular junction matures when GNDF expression decreases . In the rat model of RLN injury, GDNF overexpression reaches its peak within PCA and TA as newly formed axons reach denervated muscles . GDNF has three glycosylphosphatidylinositol‐linked cell surface receptors (GFRα1, 2, 3) and a required tyrosine kinase, called rearranged during transfection (Ret), which triggers intracellular signaling pathways for neural survival and axonal outgrowth .…”

Section: Introductionmentioning

confidence: 99%

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Expression of trophic factors receptors during reinnervation after recurrent laryngeal nerve injury

et al. 2019

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Objective: An injury of the recurrent laryngeal nerve (RLN) triggers axonal regeneration but results in a poor functional recovery. Netrin-1 and glial cell-derived neurotrophic factor (GDNF) expression are up-regulated in laryngeal muscles during RLN regeneration, but the role of their receptors produced in the nucleus ambiguus is unknown. The aim of this work was to determine the timing of the production of Netrin-1 and GDNF receptors during RLN regeneration and correlate this with the previously identified timing of up-regulation of their trophic factors in the laryngeal muscles.Study Design: Laboratory experiment with rat model. Methods: The right RLN was transected and dextran amine tracer applied. At 7, 14, and 21 days postinjury (DPI), brainstems were removed and harvested. Immunostaining was performed for Netrin-1 (deleted in colorectal carcinoma [DCC], UNC5A) and GDNF receptors (rearranged during transfection [Ret], glycosylphosphatidylinositol-linked cell surface receptors [GFRα1, GFRα2, GFRα3]). The timing and type of receptor production relative to injury as well as their position in the nucleus ambiguus was analyzed.Results: Netrin-1 UNC5A receptors were minimal in the nucleus ambiguus during RLN regeneration. DCC, the receptor that plays an attract role, was immunopositive from 7 to 21 DPI. All GDNF receptors, except GFRα2, were clearly positive from 7 to 14 DPI. No differences of production were observed according to the position of the motor neurons in the nucleus ambiguus.Conclusion: An injury of the RLN leads to a higher production of Netrin-1 DCC and GDNF receptors in the nucleus ambiguus. The timing of receptor production is similar to up-regulation of their trophic factors in the laryngeal muscles.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression of trophic factors receptors during reinnervation after recurrent laryngeal nerve injury

et al. 2019

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“…Selectively promoting desired reinnervation sources and targets and/or preventing undesired ones using growth factors or neurotoxins is an important current arena of investigation, and elegant work is being done in the laboratories of Halum, Paniello, Pitman, and others. A thorough characterization of spontaneous reinnervation sources and mechanisms is a necessary prerequisite to achieving the goals of physiologic reinnervation and improved outcomes for patients with laryngeal paralysis.…”

Section: Discussionmentioning

confidence: 99%

Immunohistologic analysis of spontaneous recurrent laryngeal nerve reinnervation in a rat model

Rosko

Kupfer

et al. 2017

The Laryngoscope

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Characteristics of Early Internal Laryngeal Muscle Atrophy After Recurrent Laryngeal Nerve Injuries in Rats

Wang

et al. 2020

The Laryngoscope

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Objectives/Hypothesis: The present study investigated the characteristics of early internal laryngeal muscle atrophy in recurrent laryngeal nerve injury (RLNI) rats. Study Design: To observe the characteristics of early internal laryngeal muscle atrophy post RLNI. Methods: Rats were divided into three groups: sham-operated control group (n = 20), recurrent laryngeal nerve transverse injury group (RLNTI, n = 50), and recurrent laryngeal nerve blunt contusion group (RLNBC, n = 50). Five weeks after RLNI, certain rats were sacrificed weekly, and their laryngeal tissues were harvested. The atrophic features of internal laryngeal muscles were detected using hematoxylin and eosin. NF-κB and MuRF-1 levels were tested using IHC. Results: The atrophic degree and fibrosis of thyroarytenoid, posterior cricoarytenoid, and lateral cricoarytenoid muscles were related to the type of RLNI. The average myofiber cross-sectional areas increased before an obvious decrease in the RLNTI and RLNBC groups. Muscle recovery occurred in the RLNBC group starting 4 weeks after RLNI, but only a weak trend was observed in the RLNTI group in the 5th week. During the muscle atrophy process, MuRF-1 and NF-κB were upregulated early and were maintained at a high level, which showed a trend similar to muscle atrophy. However, NF-κB expression was opposite to MuRF-1 expression and muscle atrophy when the muscles recovered. Conclusion: The atrophy degree of internal laryngeal muscles was associated with the type of RLNI. The NF-κB/MuRF-1 signaling pathway was involved in internal laryngeal muscle atrophy after RLNI, which is different from skeletal muscle after denervation.

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Blockade of glial-derived neurotrophic factor in laryngeal muscles promotes appropriate reinnervation

Abstract: NA Laryngoscope, 126:E337-E342, 2016.

Cited by 20 publications

References 35 publications

Expression of trophic factors receptors during reinnervation after recurrent laryngeal nerve injury

Expression of trophic factors receptors during reinnervation after recurrent laryngeal nerve injury

Immunohistologic analysis of spontaneous recurrent laryngeal nerve reinnervation in a rat model

Characteristics of Early Internal Laryngeal Muscle Atrophy After Recurrent Laryngeal Nerve Injuries in Rats

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