Musci Robert V, Walsh Maureen A, Konopka Adam R, Wolff Christopher A, Peelor Frederick F, Reiser Raoul F, Santangelo Kelly S, Hamilton Karyn L
Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, United States.
Department of Medicine, University of Wisconsin-Madison, Madison, WI, United States.
Front Physiol. 2020 Oct 29;11:571372. doi: 10.3389/fphys.2020.571372. eCollection 2020.
Skeletal muscle dysfunction, articular cartilage degeneration, and bone loss occur essentially in parallel during aging. Mechanisms contributing to this systemic musculoskeletal decline remain incompletely understood, limiting progress toward developing effective therapeutics. Because the progression of human musculoskeletal aging is slow, researchers rely on rodent models to identify mechanisms and test interventions. The Dunkin Hartley guinea pig is an outbred strain that begins developing primary osteoarthritis by 4 months of age with a progression and pathology similar to aging humans. The purpose of this study was to determine if skeletal muscle remodeling during the progression of osteoarthritis in these guinea pigs resembles musculoskeletal aging in humans. We compared Dunkin Hartley guinea pigs to Strain 13 guinea pigs, which develop osteoarthritis much later in the lifespan. We measured myofiber type and size, muscle density, and long-term fractional protein synthesis rates of the gastrocnemius and soleus muscles in 5, 9, and 15-month-old guinea pigs. There was an age-related decline in skeletal muscle density, a greater proportion of smaller myofibers, and a decline in type II concomitant with a rise in type I myofibers in the gastrocnemius muscles from Dunkin Hartley guinea pigs only. These changes were accompanied by age-related declines in myofibrillar and mitochondrial protein synthesis in the gastrocnemius and soleus. Collectively, these findings suggest Dunkin Hartley guinea pigs experience myofiber remodeling alongside the progression of osteoarthritis, consistent with human musculoskeletal aging. Thus, Dunkin Hartley guinea pigs may be a model to advance discovery and therapeutic development for human musculoskeletal aging.
骨骼肌功能障碍、关节软骨退变和骨质流失在衰老过程中基本同时发生。导致这种全身性肌肉骨骼衰退的机制仍未完全明了,限制了有效治疗方法开发的进展。由于人类肌肉骨骼衰老进程缓慢,研究人员依靠啮齿动物模型来确定机制并测试干预措施。Dunkin Hartley豚鼠是一种远交系,4月龄时开始出现原发性骨关节炎,其进展和病理与衰老的人类相似。本研究的目的是确定这些豚鼠骨关节炎进展过程中的骨骼肌重塑是否类似于人类的肌肉骨骼衰老。我们将Dunkin Hartley豚鼠与13号品系豚鼠进行比较,后者在寿命后期才会出现骨关节炎。我们测量了5、9和15月龄豚鼠腓肠肌和比目鱼肌的肌纤维类型和大小、肌肉密度以及长期蛋白质合成率。仅在Dunkin Hartley豚鼠的腓肠肌中,骨骼肌密度出现与年龄相关的下降,较小肌纤维的比例增加,II型肌纤维减少,同时I型肌纤维增加。这些变化伴随着腓肠肌和比目鱼肌中肌原纤维和线粒体蛋白质合成与年龄相关的下降。总体而言,这些发现表明Dunkin Hartley豚鼠在骨关节炎进展过程中经历了肌纤维重塑,这与人类肌肉骨骼衰老一致。因此,Dunkin Hartley豚鼠可能是推进人类肌肉骨骼衰老发现和治疗开发的一种模型。