title: Transition of myosin heavy chain isoforms in human laryngeal abductors following denervation.
abstract: The objective of this study was to investigate the myofiber subtype transition of human posterior cricoarytenoid (PCA) muscle after the injury to recurrent laryngeal nerve (RLN). PCA muscle specimens were obtained from 38 bilateral vocal fold paralysis patients underwent arytenoidectomy. According to the duration of RLN injury, all the cases were divided into five denervation groups: 6-12 months, 1-2, 2-3, 3-6, and >6 years. The normal PCA muscles from total laryngectomy patients were chosen as controls. Immunofluorescence was adopted to detect the expression level of myosin heavy chain (MHC)-I and MHC-II in PCA muscle. Quantitative real-time PCR was also used to assess the transcriptional level of MHC subtypes (MHC-I, MHC-IIa, MHC-IIb, MHC-IIx, embryonic-MHC, and peri-natal-MHC). Immunofluorescence showed that MHC-I-positive myofibers in denervation groups were much lower than control group, respectively, while MHC-II-positive myofibers were significantly higher than control group (P < 0.05). With the extension of denervation, the number of MHC-I-positive myofibers gradually decreased, while MHC-II gradually increased and peaked in 1- to 2-year group. Transcriptional level of MHC-I, MHC-IIa, and MHC-IIb in denervation groups significantly down-regulated compared with the control (P < 0.05), respectively. However, MHC-IIx, embryonic-MHC, and peri-natal-MHC significantly up-regulated in all denervation groups, and the highest level was in 1- to 2-year denervation group. Data from the present study demonstrated that the maximum transition of MHC subtypes in human PCA muscles occurred in 1-2 years after denervation, suggesting that laryngeal reinnervation before the occurrence of irreversible transition of MHC subtypes could maintain the structural integrity of laryngeal PCA muscles.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China.
authors.forename: Xiaoxia
authors.initials: X
authors.lastname: Qiu
authors.forename: Donghui
authors.initials: D
authors.lastname: Chen
authors.forename: Meng
authors.initials: M
authors.lastname: Li
authors.forename: Yingna
authors.initials: Y
authors.lastname: Gao
authors.forename: Fei
authors.initials: F
authors.lastname: Liu
authors.forename: Hongliang
authors.initials: H
authors.lastname: Zheng
authors.forename: Shicai
authors.initials: S
authors.lastname: Chen
mesh_terms: D024722:Cardiac Myosins / Q000235:genetics / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007821:Laryngeal Muscles / Q000378:metabolism* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D020409:Molecular Motor Proteins / Q000235:genetics / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000235:genetics / Q000378:metabolism*; D024501:Nonmuscle Myosin Type IIB / Q000235:genetics / Q000378:metabolism*; D020033:Protein Isoforms; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D061226:Recurrent Laryngeal Nerve Injuries / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D013997:Time Factors; D014826:Vocal Cord Paralysis / Q000209:etiology / Q000378:metabolism / Q000601:surgery
chemical_list: C501641:MYH7 protein, human; C103814:MYH9 protein, human; D020409:Molecular Motor Proteins; D020033:Protein Isoforms; D012333:RNA, Messenger; D024722:Cardiac Myosins; D024501:Nonmuscle Myosin Type IIB; C103815:nonmuscle myosin type IIB heavy chain; D018995:Myosin Heavy Chains