{"title":"Developmental Expression of Calcium Activated Chloride Ion Channels Anoctamin 5 in Mouse Skeletal Muscle","authors":"Hai-yan Song, Yi-Min Zhang, Hui Lian, Li Zhou, Yue-Min Tian, Jin-Xia Zhu","doi":"10.4172/2167-1052.1000179","DOIUrl":null,"url":null,"abstract":"Anoctamin 5 (Ano5), also named TMEM16E, belongs to the Anoctamin gene family. The mutations in the \nAno5 gene cause Limb-girdle muscular dystrophy (LGMD) 2L type and Miyoshi muscular dystrophy (MMD3). Both patients showed sarcolemmal lesions. The studies showed that TMEM16E mRNA expressed in the somites during embryogenesis, particularly in the myotomal cells, and also in the muscle myotome-derived progenitor cells. However, no report has been done to examine Ano5 expression during mouse skeletal muscle development. In the present study, we investigated the distribution and quantification of Ano5 in the skeletal muscles of mice during their development, with the methods of immunofluorescence, Reverse transcription-polymerase chain reaction (RT-PCR) \nand Western blot analyses. The results indicated that Ano5 mRNA and protein are expressed in skeletal muscle of the mouse from 1 day to 6 months, but with development and aging, the expression of Ano5 reduced gradually. Taken together, our results demonstrate that Ano5 expression level decreased throughout development and aging, and this may explain why the musculardystrophy syndrome of Ano5 mutant patients only starts during the later stage of their lives.","PeriodicalId":7385,"journal":{"name":"Advances in Pharmacoepidemiology and Drug Safety","volume":"33 1","pages":"136-140"},"PeriodicalIF":0.0000,"publicationDate":"2015-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in Pharmacoepidemiology and Drug Safety","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2167-1052.1000179","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Anoctamin 5 (Ano5), also named TMEM16E, belongs to the Anoctamin gene family. The mutations in the
Ano5 gene cause Limb-girdle muscular dystrophy (LGMD) 2L type and Miyoshi muscular dystrophy (MMD3). Both patients showed sarcolemmal lesions. The studies showed that TMEM16E mRNA expressed in the somites during embryogenesis, particularly in the myotomal cells, and also in the muscle myotome-derived progenitor cells. However, no report has been done to examine Ano5 expression during mouse skeletal muscle development. In the present study, we investigated the distribution and quantification of Ano5 in the skeletal muscles of mice during their development, with the methods of immunofluorescence, Reverse transcription-polymerase chain reaction (RT-PCR)
and Western blot analyses. The results indicated that Ano5 mRNA and protein are expressed in skeletal muscle of the mouse from 1 day to 6 months, but with development and aging, the expression of Ano5 reduced gradually. Taken together, our results demonstrate that Ano5 expression level decreased throughout development and aging, and this may explain why the musculardystrophy syndrome of Ano5 mutant patients only starts during the later stage of their lives.