Expression of cationic amino acid transporters in pig skeletal muscles during postnatal development

Abstract

The cationic amino acid transporter (CAT) protein family transports lysine and arginine in cellular amino acid pools. We hypothesized that CAT expression changes in pig skeletal muscles during rapid pig postnatal development. We aimed to investigate the tissue distribution and changes in the ontogenic expression of CATs in pig skeletal muscles during postnatal development. Six piglets at 1, 12, 26, 45, and 75 days old were selected from six litters, and their longissimus dorsi (LD), biceps femoris (BF), and rhomboideus (RH) muscles, and their stomach, duodenum, jejunum, ileum, colon, liver, kidney, heart, and cerebrum were collected. CAT-1 was expressed in all the 12 tissues investigated. CAT-2 (CAT-2A isoform) expression was highest in the skeletal muscle and liver and lowest in the jejunum, ileum, kidney, and heart. CAT-3 was expressed mainly in the colon and detected in the jejunum, ileum, and cerebrum. The CAT-1 expression was higher in the skeletal muscle of day 1 pigs than in that of older pigs (P < 0.05). The CAT-2 mRNA level was lowest at day 1, but increased with postnatal development (P < 0.05). There was no significant change in CAT-1 expression among the LD, BF, and RH during postnatal development (P > 0.05); however, there was a change in CAT-2 expression. The CAT-2 expression was highest in the LD of 12-, 26-, 45-, and 75-day-old pigs, followed by the BF and RH (P < 0.05). These results suggest that CAT-1 and CAT-2 play different roles in pig skeletal muscles during postnatal development.

Effects of low-protein diet and feed restriction on mRNA expression of cationic amino acid transporters in porcine skeletal muscles

“…In a previous study, we found a difference in the postnatal expression pattern of CAT-1 and CAT-2A, as well as differences in CAT-2A expression levels among LD, BF, and RH muscles (Ishida et al 2017). Here, we compared the effects of a low-protein diet and feed restriction on the expression of CAT-1 and CAT-2A among three skeletal muscles of growing piglets.…”

“…The protocols we used for total RNA extraction and quantitative real-time PCR analysis have been described previously (Ishida et al 2017). The CATs data of pigs were normalized using the geometric means of the ribosomal protein L4 (RPL4) and the TATA box-binding protein (TBP) as reference genes for skeletal muscles (Vandesompele et al 2002).…”

“…We have previously reported on the tissue distribution and changes in CATs mRNA expression in pig skeletal muscles during postnatal development, i.e., from day 1 to day 75 (Ishida et al 2017). CAT-1 and CAT-2A mRNA are expressed in porcine skeletal muscles, whereas CAT-3 is not.…”

Identification of stable reference genes for quantitative gene expression analysis in the duodenum of meat-type ducks

“…Another study on chickens found that the most suitable reference gene in the liver is ribosomal protein L13 ( RPL13 ); in the jejunum it is glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ), while hydroxymethylbilane synthase ( HMBS ) is compatible in all tissues ( 9 ). In pigs, HPRT1 and HMBS are reference genes for skeletal muscles and affect their postnatal growth ( 10 ). In goats, beta-actin (β -actin ) was the most stable in the stomach, small intestine, and ovary; 18S ribosomal RNA ( 18S rRNA ) in the heart and spleen; HMBS in the uterus and lungs; TATA box binding protein ( TBP ) in the liver; HPRT1 in the kidney; and GAPDH in the muscles ( 11 ).…”

Glucocorticoid Regulates the Synthesis of Porcine Muscle Protein through m6A Modified Amino Acid Transporter SLC7A7

“…y+L+ amino acid transporter-1 (y+LAT1) is encoded by the SLC7A7 gene, and the substrates of this system are arginine, lysine, leucine, glutamine and methionine [ 8 ]. The expression level of SLC7A7 is high in intestine and kidney but low in skeletal muscle, and the mutation of SLC7A7 gene usually induces many complications, such as persistent hypotonia, birth retardation, osteoporosis, coma and mental development disorder [ 9 , 10 ]. It has been demonstrated that SLC7A7 −/− mice exhibit intrauterine growth restriction and persistent growth retardation that generates fetal growth retardation through downregulation of IGF1, thus resulting in mouse death [ 11 ].…”