Hong Kong catfish (Clarias fuscus) exhibit sexual dimorphism, particularly in body size. Due to the fast growth rate of males, the sexual size dimorphism of Hong Kong catfish has become an economically important trait. However, limited knowledge is known about the molecular mechanisms of sex determination and sex differentiation in this species. In this study, a first de novo transcriptome sequencing analysis of testes and ovaries was performed to identify sex-biased genes in Hong Kong catfish. The results showed that a total of 290,291 circular consensus sequences (CCSs) were obtained, from which 248,408 full-length non-chimeric (FLNC) reads were generated. After non-redundant analysis, a total of 37,305 unigenes were predicted, in which 34,342 unigenes were annotated with multiple public databases. Comparative transcriptomic analysis identified 5750 testis-biased differentially expressed genes (DEGs) and 6991 ovary-biased DEGs. The enrichment analysis showed that DEGs were classified into 783 Gene Ontology (GO) terms and 16 Kyoto Encyclopedia of Gene and Genome (KEGG) pathways. Many DEGs were involved with sex-related GO terms and KEGG pathways, such as oocyte maturation, androgen secretion, gonadal development and steroid biosynthesis pathways. In addition, the expression levels of 23 unigenes were confirmed to validate the transcriptomic data by quantitative real-time polymerase chain reaction (qRT-PCR). This is the first investigation into the transcriptome of Hong Kong catfish testes and ovaries. This study provides an important molecular basis for the sex determination and sex control breeding of Hong Kong catfish.
Store-operated channels (SOCs) are highly selective Ca2+ channels that mediate Ca2+ influx in non-excitable and excitable (i.e., skeletal and cardiac muscle) cells. These channels are triggered by Ca2+ depletion of the endoplasmic reticulum and sarcoplasmic reticulum, independently of inositol 1,4,5-trisphosphate (InsP3), which is involved in cell growth, differentiation, and gene transcription. When the Ca2+ store is depleted, stromal interaction molecule1 (STIM1) as Ca2+ sensor redistributes into discrete puncta near the plasma membrane and activates the protein Ca2+ release activated Ca2+ channel protein 1 (Orai1). Accumulating evidence suggests that SOC is associated with several physiological roles in endothelial dysfunction and vascular smooth muscle proliferation that contribute to the progression of cardiovascular disease. This review mainly elaborates on the contribution of SOC in the vasculature (endothelial cells and vascular smooth muscle cells). We will further retrospect the literature implicating a critical role for these proteins in cardiovascular disease.
Graphical Abstract
Abstract. The aim of the present study was to investigate the effect of hydroxy safflower yellow A (HSYA) on coronary heart disease through assessing the expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-like protein 4 (Bax) and peroxisome proliferator-activated receptor (PPAR)-γ. Coronary heart disease was induced in male Bama miniature swines via thoracoscope to serve as an animal model. Coronary heart disease swine were lavaged with 20 or 40 mg/kg HSYA. The mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were detected using reverse transcription-quantitative polymerase chain reaction. The protein expression of Bcl-2, Bax, PPAR-γ, phosphorylation of Janus kinase (JAK)2 and phosphorylation of signal transducer and activator of transcription (STAT)3 were detected using western blot analysis. Treatment with HSYA significantly suppressed the mRNA levels of IL-1β (P<0.01), IL-6 (P<0.01), TNF-α (P<0.01), COX-2 (P<0.01) and iNOS (P<0.01), and significantly increased IL-10 mRNA level in the coronary heart disease model (P<0.01). Furthermore, HSYA treatment significantly decreased the Bcl-2/Bax ratio (P<0.01) in the coronary heart disease model group, and enhanced the phosphorylation of JAK2/STAT3 pathway (P<0.01). However, HSYA had no significant effect on the expression of PPAR-γ protein. The results of the present study suggest that HSYA is able to weaken coronary heart disease via inflammation, Bcl-2/Bax and the PPAR-γ signaling pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.