Testosterone Promotes the Proliferation of Chicken Embryonic Myoblasts Via Androgen Receptor Mediated PI3K/Akt Signaling Pathway

Abstract

Testosterone (T) is essential for muscle fiber formation and growth. However, the specific mechanism by which T regulates skeletal muscle development in chicken embryos remains unclear. In this study, the role of T in myoblast proliferation both in vivo and in vitro was investigated. Results showed that the T administration significantly increased the ratio of breast muscle and leg muscle. T induced a significant increase in the cross-sectional area (CSA) and density of myofiber and the ratio of PAX7-positive cells in the skeletal muscle. Exogenous T also induced the upregulation of myogenic regulatory factors (MRFs) and cyclin-dependent kinases (CDK2)/Cyclin D1 (CCND1) and protein levels of androgen receptor (AR), p-Akt and PAX7. Furthermore, T treatment significantly promoted myoblasts cultured in vitro entering a new cell cycle and increased PAX7-positive cells. The mRNA and protein expression of AR and PAX7 were upregulated when treated with T compared to that of the control. The addition of T induced proliferation accompanied by increasing AR level as well as PI3K (Phosphoinositide 3-kinase)/Akt activation. However, T-induced proliferation was attenuated by AR, PI3K, and Akt-specific inhibitors. These data indicated that the pro-proliferative effect of T was regulated though AR in response to the activation of PI3K/Akt signalling pathway.

Analysis of mRNA and lncRNA Expression Profiles of Breast Muscle during Pigeon (Columba livia) Development

“…Interestingly, most of these common DE-mRNAs were also down-regulated during muscle development and were enriched in various cell division and cell cycle-related terms. This was consistent with the studies on skeletal muscle development: during embryonic stages, it relies on myoblast proliferation and the number of myofibers; during postnatal phases, it depends on fiber hypertrophy and the accumulation of new myonuclei inside preexisting myofibers [ 10 , 17 , 18 ]. Hence, cell division-related genes such as BUB1 [ 50 ], CDCA8 [ 51 ], CDK1 [ 52 ], CKAP2 [ 53 ], and FOXM1 [ 54 ] could regulate cell proliferation and be downregulated during breast muscle development in postnatal phases.…”

“…There are embryonic and postnatal periods in the development of skeletal muscles [ 16 ]. Throughout the embryonic stages, skeletal muscle development is influenced by myoblast proliferation and the number of myofibers [ 10 , 17 , 18 ]. The primary causes of postnatal skeletal muscle development are fiber hypertrophy and the formation of new myonuclei inside preexisting myofibers [ 10 ].…”

Identification of biomarkers associated with the feed efficiency by metabolomics profiling: results from the broiler lines divergent for high or low abdominal fat content

“…Testosterone is an anabolic steroid from the androstane class of steroids [ 45 ]. It is the most important androgen, stimulating muscle growth and inhibiting lipid synthesis [ 46 , 47 ]. In humans, testosterone replacement therapy reduces the body fat mass, particularly in truncal adiposity, cholesterol, and triglycerides [ 48 ].…”

Integrating Genetic and Genomic Analyses of Combined Health Data Across Ecotypes to Improve Disease Resistance in Indigenous African Chickens

“…Live body weight was unsurprisingly associated with androgen signaling, which has long been known to affect body growth (Li et al, 2020). In addition, two missense variants were identified in the adipose triglyceride lipase (ATPL/PNPLA2) gene that has been previously associated with chicken growth and fat deposition traits (Fennell and Scanes, 1992;Fennell et al, 1996;Nie et al, 2010).…”