Støle Thea Parsberg, Romaine Andreas, Kleiberg Thea, Høst Vibeke, Lunde Marianne, Hasic Almira, Lintvedt Tiril Aurora, Sanden Karen Wahlstrøm, Kolset Svein O, Wold Jens Petter, Pisconti Addolorata, Rønning Sissel Beate, Carlson Cathrine Rein, Pedersen Mona Elisabeth
Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
Raw Materials and Optimalization, Nofima As, Ås, Norway.
Front Physiol. 2025 Mar 5;16:1547661. doi: 10.3389/fphys.2025.1547661. eCollection 2025.
Wooden breast disease is a myopathy of the skeletal muscle in chickens of commercial breeding. Although the underlying pathophysiology remains unknown, we and others have previously shown that affected broilers display varying degrees of fibrosis, extracellular matrix (ECM) remodeling, inflammation, and alterations in various molecular signaling pathways. Other myopathy conditions, such as Duchenne muscular dystrophy, also affect the cardiac muscle and are associated with fibrosis and reduced cardiac function. To determine potential cardiac implications of wooden breast disease and identify whether molecular and fibrotic changes were similar to what we have previously found in the breast, we have investigated the hearts of commercial Ross 308 broilers.
Hearts from male Ross 308 broiler chickens from mildly and severely wooden breast-affected chickens categorized in previous studies were analyzed. Ventricles from the hearts were analyzed by immunoblotting, real-time qPCR, near-infrared spectroscopy, Raman spectroscopy, and Masson`s trichrome histology. RNA sequencing was also conducted to identify the molecular footprint of the mildly and severely wooden breast-affected chickens.
Compared to mildly affected chickens, the severely wooden breast-affected chickens did not show an increase in heart weight, water-binding capacity, or macronutrient composition. The hearts did also not display any differences in fibrosis development, extracellular matrix gene expression, or typical cardiac and inflammatory markers. The severely affected chickens did, however, show a reduction in protein levels of biglycan and fibromodulin, as well as alterations in matrix metalloproteinase 2, Wnt ligands, mTOR signaling, heat shock protein 70, and muscle LIM protein. Functional enrichment analysis of RNA sequencing also suggested a different molecular footprint of biological processes and pathways between the two groups.
Hearts from wooden breast-affected chickens did not display the same fibrotic alterations as those previously found in the breast. Despite few alterations detected in the markers and signaling molecules tested, RNA sequencing indicated a different molecular footprint in the hearts of severely compared to mildly wooden breast-affected chickens.
木胸病是商业养殖鸡的骨骼肌肌病。尽管其潜在的病理生理学机制尚不清楚，但我们和其他人此前已表明，受影响的肉鸡表现出不同程度的纤维化、细胞外基质（ECM）重塑、炎症以及各种分子信号通路的改变。其他肌病情况，如杜氏肌营养不良症，也会影响心肌，并与纤维化和心脏功能降低有关。为了确定木胸病对心脏的潜在影响，并确定分子和纤维化变化是否与我们之前在鸡胸中发现的相似，我们对商业罗斯308肉鸡的心脏进行了研究。
分析了来自先前研究中分类为轻度和重度木胸病影响的雄性罗斯308肉鸡的心脏。通过免疫印迹、实时定量PCR、近红外光谱、拉曼光谱和Masson三色组织学分析心脏的心室。还进行了RNA测序，以确定轻度和重度木胸病影响的鸡的分子特征。
与轻度受影响的鸡相比，重度木胸病影响的鸡的心脏重量、水结合能力或常量营养素组成没有增加。心脏在纤维化发展、细胞外基质基因表达或典型的心脏和炎症标志物方面也没有显示出任何差异。然而，重度受影响的鸡确实显示出双糖链蛋白聚糖和纤调蛋白的蛋白质水平降低，以及基质金属蛋白酶2、Wnt配体、mTOR信号、热休克蛋白70和肌肉LIM蛋白的改变。RNA测序的功能富集分析也表明两组之间生物过程和通路的分子特征不同。
木胸病影响的鸡的心脏没有表现出与之前在鸡胸中发现的相同的纤维化改变。尽管在所测试的标志物和信号分子中检测到的变化很少，但RNA测序表明，与轻度木胸病影响的鸡相比，重度木胸病影响的鸡的心脏分子特征不同。
