a Department of Biopharmacy Faculty of Pharmacy , Srinakharinwirot University , Nakhon Nayok , Thailand.
b Department of Physiology Faculty of Science , Mahidol University , Bangkok , Thailand.
Int J Hyperthermia. 2018 Jun;34(4):432-441. doi: 10.1080/02656736.2017.1350758. Epub 2017 Jul 18.
Capillary regression is commonly observed in response to disuse muscle atrophy. Heat stress is known to alleviate muscle atrophy, while effect of heat exposure on capillary adaptation following disuse atrophy is not defined. Here, we examined the effect of heat treatment on capillarisation and the associated signalling in slow-oxidative soleus and fast-glycolytic plantaris muscles following Achilles tendon ablation (tenotomy).
Male Wistar rats were assigned into control (CON), control with heat stress (CON + HEAT), tenotomy (TEN) and tenotomy with heat stress (TEN + HEAT) groups. Tenotomy was induced for 8 days in TEN and TEN + HEAT groups. Heat stress was maintained at 40.5-41.5 °C, 30 min for 7 days.
Tenotomy resulted in reduction of capillary-to-fibre ratio, decreased VEGFR-2 and increased TSP-1 in soleus muscle, whereas VEGF protein expression remained unaffected. Tenotomy had no effect on capillary distribution and angiogenic signalling in plantaris muscle. These results were concomitant with larger reduction of cross-sectional area (CSA) in MHC type I and II myofibres of soleus compared to plantaris muscles. Interestingly, heat stress increased VEGFR-2 and attenuated TSP-1 protein expression in tenotomised soleus, but not plantaris muscles. Additionally, CSA of both type I and type II myofibres was greater in tenotomised soleus than plantaris muscles after heat treatment.
Heat stress mitigated effect of tenotomy-induced capillary regression in a fibre-type-specific response, in part, by shifting the balance between angiogenic and angiostatic regulators. These results suggest beneficial effect of heat treatment for maintaining microcirculation in disuse muscle atrophy.
毛细血管回缩是肌肉废用性萎缩的常见反应。热应激可缓解肌肉萎缩,而热暴露对废用性萎缩后毛细血管适应性的影响尚不清楚。在这里,我们研究了热处理对跟腱切断(肌腱切断术)后慢氧化比目鱼肌和快糖酵解跖肌的毛细血管化及其相关信号的影响。
雄性 Wistar 大鼠被分为对照组(CON)、对照组加热应激(CON+HEAT)、肌腱切断组(TEN)和肌腱切断加热应激组(TEN+HEAT)。TEN 和 TEN+HEAT 组在 8 天内进行肌腱切断术。热应激保持在 40.5-41.5°C,每天 30 分钟,持续 7 天。
肌腱切断术导致比目鱼肌毛细血管与纤维比降低,VEGFR-2 减少,TSP-1 增加,而 VEGF 蛋白表达不受影响。肌腱切断术对跖肌的毛细血管分布和血管生成信号没有影响。这些结果与比目鱼肌 MHC 型 I 和 II 肌纤维横截面积(CSA)的减少幅度大于跖肌相一致。有趣的是,热应激增加了肌腱切断比目鱼肌中的 VEGFR-2 并减弱了 TSP-1 蛋白表达,但对跖肌没有影响。此外,热处理后,肌腱切断比目鱼肌的 I 型和 II 型肌纤维 CSA 均大于跖肌。
热应激以纤维类型特异性反应的方式减轻了肌腱切断引起的毛细血管回缩效应,部分原因是通过改变血管生成和血管生成抑制剂之间的平衡。这些结果表明热治疗对维持废用性肌肉萎缩中的微循环有益。