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Association of myostatin deficiency with collagen related disease-umbilical hernia and tippy toe standing in pigs
Transgenic Research ( IF 3 ) Pub Date : 2021-07-25 , DOI: 10.1007/s11248-021-00275-6
Hyo-Jin Paek 1 , Zhao-Bo Luo 1 , Hak-Myong Choe 1 , Biao-Hu Quan 1 , Kai Gao 1 , Sheng-Zhong Han 1 , Zhou-Yan Li 1 , Jin-Dan Kang 1 , Xi-Jun Yin 1
Affiliation  

Herein, we investigate the high incidence of umbilical hernia and tippy-toe standing and their underlying changes in gene expression and proliferation in myostatin knockout (MSTN−/−) pigs. Thirty-six male MSTN−/− pigs were generated by somatic cell nuclear transfer (SCNT). These pigs presented a considerably high incidence of tippy-toe standing and umbilical hernia (69.4% and 61.1%, respectively). The tendon to body weight ratio was significantly lower than wild-type pigs (0.202 ± 0.017 vs 0.250 ± 0.004, respectively). The crimp length of the MSTN−/− tendon was significantly longer than that of wild-type pigs. The expression of MSTN and the activin type IIB (ACVR2B) was detected in the tendon and linea alba of MSTN−/− pigs. MSTN treatment significantly increased the phosphorylation of Smad2/3 in both tendon and linea alba fibroblasts. Type I collagen (Col1A) and Scleraxis (Scx) expression levels in the tendon and linea alba of MSTN−/− pigs were significantly lower than those in wild-type in vivo, whereas and cyclin-dependent kinase inhibitor 1 (p21) expression levels were higher. Treatment of tendon and linea alba fibroblasts with recombinant MSTN increased Col1A and Scx and decreased p21 expression in vivo. Moreover, there was a significant increase in fibroblast proliferation after treatment. The results indicated that MSTN regulates collagen expression and proliferation in tendon and linea alba fibroblasts; thus, MSTN deficiency causes collagen-related pathological features in MSTN−/− pigs. Hence, MSTN could be used as a therapeutic target for treating UH and tendon abnormalities.



中文翻译:

肌肉生长抑制素缺乏与胶原相关疾病——猪脐疝和踮脚站立的关系

在此,我们调查了在肌肉抑制素敲除 ( MSTN -/- ) 猪中脐疝和踮起脚尖站立的高发病率及其基因表达和增殖的潜在变化。通过体细胞核移植 (SCNT) 产生了36 头雄性MSTN -/-猪。这些猪的踮起脚尖站立和脐疝的发生率相当高(分别为 69.4% 和 61.1%)。肌腱与体重的比值显着低于野生型猪(分别为 0.202 ± 0.017 vs 0.250 ± 0.004)。MSTN -/-肌腱的卷曲长度明显长于野生型猪。MSTN的表达和激活素IIB型(ACVR2B) 在MSTN -/-猪的肌腱和白线中检测到。MSTN 治疗显着增加了肌腱和白线成纤维细胞中 Smad2/3 的磷酸化。MSTN -/-猪的腱和白线中I 型胶原蛋白 ( Col1A ) 和 Scleraxis ( Scx ) 的表达水平显着低于体内野生型,而细胞周期蛋白依赖性激酶抑制剂 1 ( p21 ) 的表达水平更高。用重组 MSTN 治疗腱和白线成纤维细胞增加Col1AScx并减少p21体内表达。此外,治疗后成纤维细胞增殖显着增加。结果表明,MSTN调节肌腱和白线成纤维细胞中胶原蛋白的表达和增殖;因此,MSTN缺乏会导致MSTN -/-猪出现胶原相关的病理特征。因此,MSTN 可用作治疗 UH 和肌腱异常的治疗靶点。

更新日期:2021-07-25
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