Distinct Tissue Distribution in Pigs of Tenascin‐X and Tenascin‐C Transcripts

Abstract

-EJB 95 0444/2Tenascin-X and tenascin-C glycoproteins are phylogenetically conserved components of the extracellular matrix, although their specific roles remain to be determined. cDNA probes were produced from pig tenascin-X and tenascin-C genes and were used to examine the tissue distribution of the transcripts in 28 tissues from Large-White pigs, 4.5-42-months old (called adults) and 17 tissues from 87-day-old fetuses. The hybridization of Northern blots with tenascin-X probes revealed, in most tissues, a complex pattern of bands including a major band of about 13 kb, assumed to correspond to the main tenascin-X transcript. Hybridization with the tenascin-C probe showed two transcripts of 6.8 kb and 8.2 kb. The data from the ribonuclease-protection technique showed that both genes displayed large variations in the transcription levels among the tissues analysed. Overall, the tenascin-X gene was significantly expressed in two thirds of the tissues, and the tenascin-C gene in about 50% of them. The highest tenascin-X signals were observed in tendons, ligaments and, unexpectedly, in peripheral nerves. Other tissues, including colon, dermis, skin, heart, uterus, stomach, jejunum, placentae, aorta, lung, mammary and adrenal glands also exhibited significant signal intensities. In fetuses, mainly testes and skeletal muscle showed higher transcription levels than the adult counterparts. The tenascin-C gene was predominantly transcribed in the ligament, tendon, adrenal gland and colon, and more weakly in the stomach, jejunum, lung and spinal cord. In fetuses, the tenascin-C signal in the brain was higher than the signal in the brain of adult, whereas the reverse was true for the adrenal gland and the colon. Within a given tissue, the level of tenascin-X and tenascin-C transcripts varied greatly, indicating independent tenascin-X and tenascin-C transcription regulation mechanisms; this was particularly obvious in adult and fetal nerves but also in the dermis, skin, heart, uterus, placentae and aorta, where tenascin-X RNA molecules were much more abundant than those of tenascin-C. In addition, similar differences were observed in the skeletal muscle and adrenal gland of fetuses. In contrast, the amount of tenascin-C transcripts in the fetal brain and adult spinal cord was higher than those for tenascin-X. Our results draw attention to a possible specific role of tenascin-X in the peripheral nerve physiology.

Joint hypermobility syndromes: The pathophysiologic role of tenascin‐X gene defects

“…In developing rats, tenascin-X is expressed in tendon sheaths, ligaments, synovium, muscle, epicardium, and blood vessel adventitia (48), and a similar distribution has also been shown for pigs (49). In mice, tenascin-C and tenascin-X are coexpressed in muscle, gut, skin, and vasculature (50).…”

Identification of a significant association of a single nucleotide polymorphism in TNXB with systemic lupus erythematosus in a Japanese population

“…The TNXB gene is reported to encode a member of the tenascin family of extracellular matrix proteins that was highly expressed in skin, muscle, tendon sheath, peripheral nerve, and vasculature (Matsumoto et al 1994;Geffrotin et al 1995). Molecular pathogenesis of SLE was considered as the exaggerated B cell response caused by activated T cells or dendritic cells, or soluble mediators such as cytokines (Kyttaris et al 2005).…”

Distribution of Tenascin-C and -X, and Soft X-ray Analysis of the Mandibular Symphysis during Mandible Formation in the Human Fetus

“…Tenascin-X mRNA was highly expressed in some organs (skeletal muscle, lamina propria of the esophagus, extracellular matrices around blood vessels of the kidney and liver) in contrast to that of tenascin-C (smooth muscle, epithelial-mesenchymal interaction) (Matsumoto et al, 1994). The tenascin-C and -X mRNAs also showed different expressions in the embryonic and adult pig organs (Geffrotin et al, 1995). The changes in extracellular matrices were found in the formation of human fibrocartilage (Graham et al, 1996) in which the existence of chondrogenic cell affect the concentration of tenascin (Mackie et al, 1987).…”

“…Burch et al (1997) reported observing a 21-hydroylase deficiency, a connective tissue disorder in the skin and joint hyperextensibility associated with the contiguous-gene syndrome involving tenascin-X. Tenascin-X was also mainly observed in tendon, ligaments in adult and testes and skeletal muscle in fetal pigs (Geffrotin et al, 1995). These distributions between tenascin-C and -X play an important role in the formation of mandible between bone matrix and muscle fiber during development.…”