Background: Hypertrophy, myogenic differentiation, and mass gain of porcine skeletal muscle are key factors in meat production efficiency, regulated by miRNAs through post-transcriptional mechanisms. This study aims to identify miRNA-mRNA pairs linked to growth and muscle development in Jiangquan Black pigs with differing average daily gains (ADGs), providing a foundation for molecular breeding in this breed. Methods: This study divided eight pigs into two groups and analyzed the skeletal muscle characteristics of Jiangquan Black pigs with different average daily weight gains using HE staining. RNA-Seq was conducted to identify differentially expressed miRNAs and mRNAs, Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed, and an integrated miRNA-mRNA regulatory network was subsequently constructed. Results: RNA sequencing analysis identified 255 differentially expressed genes (DEmRNAs, |FC| > 1.5) and 27 differentially expressed miRNAs (DE miRNAs, |FC| > 2). Bioinformatics analysis revealed 330 significantly negatively correlated miRNA-mRNA regulatory pairs, with key pathways, including the MAPK, mTOR, insulin, FoxO, Wnt, and TGF-β signaling pathways, being implicated in muscular development. Quantitative real-time PCR (qRT-PCR) validation confirmed the reliability of the sequencing data. Conclusions: Different ADGs among half-sibling Jiangquan Black pigs with the same diet may be due to the DE miRNAs and DEmRNAs related to skeletal muscle growth and development. These findings reveal the potential regulatory mechanisms of DE miRNAs and DEmRNAs in porcine skeletal muscle growth, providing valuable insights for the next steps in molecular breeding strategies for Jiangquan Black pigs.

Porcine circoviruses (PCVs), encompassing porcine circovirus type 1 (PCV1), porcine circovirus type 2 (PCV2), porcine circovirus type 3 (PCV3), and porcine circovirus type 4 (PCV4), have been documented in China and represent a significant threat to the swine industry. Nevertheless, there is a paucity of data regarding the infection characteristics of PCVs across different age groups within intensive pig farming operations. In this investigation, a systematic cross-sectional methodology was employed to collect 415 testicular processing fluid samples and 1583 serum samples from 30 breeding farms and 27 fattening farms in China. All samples underwent analysis using real-time quantitative polymerase chain reaction (qPCR). Among the testicular fluid samples from suckling pigs, the detection rates for PCV1, PCV2, PCV3, and PCV4 were 56.9%, 31.1%, 75.4%, and 2.2%, respectively. The lowest mean cycle threshold (Ct) values for PCV1 and PCV3 were observed in testicular fluid as opposed to serum samples. At the individual level, the detection rate of PCV1 was significantly higher in fattening pigs (28.7%) and sows (28.7%) compared to nursery pigs (8.5%). The detection rate of PCV2 was highest in fattening pigs (43.1%) and lowest in sows (19.2%). The infection profile of PCV3 contrasted markedly with that of PCV2, exhibiting the lowest prevalence in fattening pigs (8.1%) and the highest in sows (46.1%). PCV4 was infrequently detected across all age groups, with prevalence rates ranging from 0% to 1.7%. Furthermore, the incidence of mixed infections involving the four PCV types was observed to be 12.7% in nursery pigs, 16.8% in fattening pigs, and 22.4% in sows. Notably, no strong correlation was identified between any two co-detected PCV types across all pig age categories. The findings of this study contribute valuable insights into the infection dynamics of PCVs across different pig age groups. Additionally, this research offers critical reference information for devising strategies to prevent PCV infections in intensive pig farming operations in China.

DNA methylation plays a pivotal role in the epigenetic regulation of gene expression and holds promise for enhancing livestock meat production. In this study, we analyzed the DNA methylome and transcriptome of the longissimus dorsi muscle (LDM) in Duroc pigs with varying growth rates. Our results reveal that DNA methylation suppressed the expression of key muscle development markers (MYOD, MYOG, MHC1) and proliferation markers (PI67, PCNA), as well as the protein expression and phosphorylation of PI3K and AKT (p < 0.05). Dual-luciferase reporter assays and EMSA showed that SP1 overexpression enhanced the luciferase activity of the wild-type LPAR1 promoter, an effect amplified by the demethylating agent 5-AZA (p < 0.05). The EMSA further demonstrates the relationship between SP1 and the LPAR1 promoter region. Overexpression of SP1 upregulated LPAR1 expression at both the mRNA and protein levels (p < 0.05). Knockdown of LPAR1 reduced muscle marker gene expression and delayed myotube formation, while silencing SP1 disrupted the expression of LPAR1, MEF2C, and MHC1 (p < 0.05), and the demethylation induced by 5-AZA partially reversed these effects. These findings suggest that the DNA methylation/SP1/LPAR1 axis is critical for skeletal muscle growth and development, underscoring the regulatory role of DNA methylation in muscle formation.

Background/Objectives: This study systematically investigated the expression characteristics of the ALDOA gene in skeletal muscle cells and its effects on cell proliferation, apoptosis, and differentiation. Methods: We constructed an ALDOA overexpression vector and transfected it into C2C12 cells and porcine skeletal muscle satellite cells. Results: We found that ALDOA exhibited the highest expression in the longissimus dorsi muscle and was primarily localized in the cell nucleus. Overexpression of ALDOA significantly inhibited cell proliferation, induced G0/G1 phase arrest, and downregulated the expression of proliferation-related genes such as CDK2 and Cyclin D1. Concurrently, ALDOA overexpression markedly promoted apoptosis. Regarding differentiation, although ALDOA expression was upregulated during differentiation, its overexpression significantly suppressed the expression of myogenic differentiation-related genes (such as MYOD, MYOG, MEF2C), suggesting a negative regulatory role in differentiation control. Conclusions: This study reveals the multifaceted regulatory functions of ALDOA in skeletal muscle cells, providing experimental evidence for deepening the understanding of its mechanisms in muscle development and regeneration. This study provides the first functional evidence that ALDOA acts as a multifunctional regulator in skeletal muscle cells, negatively governing cell growth and fate decisions by inhibiting proliferation, promoting apoptosis, and impeding myogenic differentiation, thereby extending its role beyond glycolysis to direct governance of cellular processes. This study reveals for the first time that ALDOA possesses dual functions in muscle cells, regulating both metabolism and transcription.

The TULP family was first identified in progressively obese mice, and TULP3, as a member of its family, has been much studied in tumor cells, but studies on its role in adipocytes have not yet been reported. This study found that the expression of TULP3 showed an increasing trend in the differentiation of 3T3-L1 cells, and overexpression of TULP3 enhanced the proliferation and differentiation capacity of the cells, while inhibition caused the opposite result. TULP3 is a negative regulator of the Hedgehog signaling pathway, which can control lipid metabolism in adipose tissues, but whether TULP3 can play a role in adipose tissues through the Hedgehog signaling pathway is not yet known. It was experimentally found that TULP3 could promote adipogenic differentiation of precursor adipocytes by inhibiting the activity of the Hedgehog signaling pathway. Our results elucidate the role of TULP3 in the generation of precursor adipocytes and provide useful information for a deeper understanding of the molecular mechanisms of adipocytogenesis, which will contribute to the improvement of the treatment of adipose tissue dysfunction or uncontrolled adipogenesis-related diseases.

Background: Thromboxane B2 Synthase 1 (THBS1), also known as TSP-1, is a multifunctional glycoprotein involved in various cellular processes that plays a crucial role in skeletal muscle development and repair. It acts as a key physiological activator of transforming growth factor-β1 (TGF-β1), both in vivo and in vitro. Methods: This study aimed to investigate the effects of THBS1 on myoblast proliferation and differentiation using the mouse skeletal muscle satellite cell line C2C12 and to reveal its regulatory relationship with the TGF-β signaling pathway through a series of cellular and molecular experiments. Results: Overexpression or knockout of THBS1 in C2C12 cells regulates and upregulates the activity of the TGF-β signaling pathway, thereby inhibiting the proliferation and differentiation of C2C12 cells. Conclusions: These results provide a theoretical foundation for future research aimed at enhancing skeletal muscle quality in livestock and poultry and lay the groundwork for developing therapeutic strategies for skeletal muscle disorders.