雜志名稱：Cell Proliferation
影響因子：5.9
文章題目：Single-nucleus transcriptomics reveals subsets of degenerative myonuclei after rotator cuff tear-induced muscle atrophy
DOI：https://doi.org/10.1111/cpr.13763
第一作者：Ziying Sun, Xi Cheng, Zheng Wang, Chenfeng Qiao, Hong Qian, Tao Yuan, Zhongyang Lv, Wenshuang Sun, Hanwen Zhang, Yuan Liu, Zhihao Lu, Jintao Lin, Chengteng Lai, Yang Wang, Xiaojiang Yang, Xingyun Wang, Jia Meng, Nirong Bao
作者單位：
南京大學(xué)醫(yī)學(xué)院附屬醫(yī)院南京金陵醫(yī)院
市南京大學(xué)醫(yī)學(xué)院附屬醫(yī)院南京鼓樓醫(yī)院
南京大學(xué)藥物生物技術(shù)國(guó)家重點(diǎn)實(shí)驗(yàn)室
南京中醫(yī)藥大學(xué)金陵臨床醫(yī)學(xué)院
上海交通大學(xué)醫(yī)學(xué)院附屬同仁醫(yī)院虹橋國(guó)際醫(yī)學(xué)研究所
引用YOBIBIO產(chǎn)品：
YB007 四標(biāo)多重免疫熒光試劑盒
UBI5010 40，6-二脒基-2-苯基吲哚(DAPI ）
文章摘要：
Rotator cuff tear (RCT) is the primary cause of shoulder pain and disability and frequently trigger muscle degeneration characterised by muscle atrophy, fatty infiltration and fibrosis. Single-nucleus RNA sequencing (snRNA-seq) was used to reveal the transcriptional changes in the supraspinatus muscle after RCT. Supraspinatus muscles were obtained from patients with habitual shoulder dislocation (n = 3) and RCT (n = 3). In response to the RCT, trajectory analysis showed progression from normal myonuclei to ANKRD1+ myonuclei, which captured atrophy-and fatty infiltration-related regulons (KLF5, KLF10, FOSL1 and BHLHE40). Transcriptomic alterations in fibro/adipogenic progenitors (FAPs) and muscle satellite cells (MuSCs) have also been studied. By predicting cell–cell interactions, we observed communication alterations between myofibers and muscle-resident cells following RCT. Our findings reveal the plasticity of muscle cells in response to RCT and offer valuable insights into the molecular mechanisms and potential therapeutic targets of RCT.
肩袖撕裂 （RCT） 是肩部疼痛和殘疾的主要原因，經(jīng)常引發(fā)以肌肉萎縮、脂肪浸潤(rùn)和纖維化為特征的肌肉退化。單核 RNA 測(cè)序 （snRNA-seq） 用于揭示 RCT 后岡上肌的轉(zhuǎn)錄變化。岡上肌來(lái)自習(xí)慣性肩脫位 （n = 3） 和 RCT （n = 3） 患者。作為對(duì) RCT 的反應(yīng)，軌跡分析顯示從正常肌核進(jìn)展到 ANKRD1+ 肌核，后者捕獲了萎縮和脂肪浸潤(rùn)相關(guān)的調(diào)節(jié)子 （KLF5 、 KLF10 、 FOSL1 和 BHLHE40）。還研究了纖維/成脂祖細(xì)胞 （FAP） 和肌肉衛(wèi)星細(xì)胞 （MuSC） 的轉(zhuǎn)錄組改變。通過(guò)預(yù)測(cè)細(xì)胞間相互作用，我們觀察到 RCT 后肌纖維和肌肉駐留細(xì)胞之間的通訊改變。我們的研究結(jié)果揭示了肌肉細(xì)胞響應(yīng) RCT 的可塑性，并為 RCT 的分子機(jī)制和潛在治療靶點(diǎn)提供了有價(jià)值的見(jiàn)解。
