Litter size is an important indicator to measure the reproductive performance of goats, which is affected by the reproductive function of animals. The hypothalamus, as the regulatory center of the endocrine system, plays an important role in the reproduction of female animals. Here, we performed high-throughput RNA sequencing using hypothalamic tissue from high-fecundity and low-fecundity Leizhou goats to explore critical functional genes associated with litter size. Differentially expressed mRNA, lncRNA, and circRNAs were screened using DESeq and were enriched, and then analyzed by Gene Ontology and Kyoto Encyclopedia of Gene and Genome. Results showed that some of these differentially expressed mRNAs could be enriched in reproductive processes, jak-STAT, prolactin signaling pathway, and other signaling pathways related to reproduction, such as SOCS3. Furthermore, the central proteins POSTN, MFAP5, and DCN from protein–protein interaction may regulate animal reproductive activity by affecting cell proliferation and apoptosis. lncRNA MSTRG.33887.2 as well as circRNAs chicirc_098002, chicirc_072583, and chicirc_053531 may be able to influence animal reproduction by participating in folate metabolism and energy metabolism homeostasis through their respective target genes. Our results expand the molecular mechanism of hypothalamic regulation on animal reproduction.
Doxorubicin-induced cardiomyopathy (DCM) is a life-threatening event. The long noncoding RNAs (lncRNAs) have been reported with close associations with DCM, which may provide novel insight into pathophysiological mechanisms of DCM. DCM rat model and cell models were established using doxorubicin. Echocardiography analyses were performed to assess cardiac function. We found that testis developmental-related gene 1 (TDRG1) expression was upregulated in DCM rats and in doxorubicin-treated human umbilical vein endothelial cells (HUVECs). TDRG1 knockdown enhanced cell viability, promoted tube formation, and inhibited apoptosis of doxorubicin-treated HUVECs. Additionally, knockdown of TDRG1 alleviated cardiac injury in DCM rats. Mechanistically, miR-873-5p was identified to bind with TDRG1. In addition, protein kinase cAMP-dependent type II regulatory subunit alpha (PRKAR2) was confirmed to bind with miR-873-5p as a target mRNA. MiR-873-5p negatively regulated PRKAR2 mRNA and protein levels. At last, rescue assays indicated that the overexpression of PRKAR2 restored the effect of TDRG1 knockdown on doxorubicin-treated HUVEC angiogenesis and apoptosis. To conclude, TDRG1 aggravates DCM progression by binding with miR-873-5p to upregulate PRKAR2. This work suggested the potential of TDRG1 as a target for DCM treatment.
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