Disease relevance of TNC

• Because pulmonary vascular disease in children with congenital heart defects is commonly associated with changes in pulmonary hemodynamics, we hypothesized that changes in pulmonary blood flow regulate TN-C and MMPs [1].
• Unlike tenascin-X, tenascin-C is highly up-regulated in pig cutaneous and underlying muscle tissue developing fibrosis after necrosis induced by very high-dose gamma radiation [2].
• Using semiquantitative RT-PCR, we observed a 3.6-fold mean increase of TN-C RNAs in melanoma compared to normal skin [3].

High impact information on TNC

• Tenascin-C binds heparin by its fibronectin type III domain five [4].
• SMCs cultivated on native collagen supplemented with tenascin-C (TN-C), a protein recognized by alpha(v)beta(3) integrins, showed a 33-fold increase in transfection compared to control (P<0.001); this effect was also blocked with anti-alpha(v)beta(3) antibody [5].
• We also found that SOD significantly lowered the levels of the myofibroblast marker alpha-sm actin, of beta-actin, and of the extracellular matrix components alpha1(I) collagen and tenascin-C [6].
• Altered hemodynamics controls matrix metalloproteinase activity and tenascin-C expression in neonatal pig lung [1].
• Tenascin-C (TN-C) expression and matrix metalloproteinase (MMP) activity are induced within remodeling pulmonary arteries (PAs), where they promote cell growth [1].

Biological context of TNC

• Localization of the tenascin-C gene to pig chromosome 1 [7].
• The mechanism for this effect was shown to be an increase in the Ca affinity of the regulatory binding sites of troponin C (TNC) [8].
• Distinct tissue distribution in pigs of tenascin-X and tenascin-C transcripts [9].

Anatomical context of TNC

• 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 [9].
• In contrast, the amount of tenascin-C transcripts in the fetal brain and adult spinal cord was higher than those for tenascin-X [9].
• We found that, in the healed fibrotic dermis and underlying muscle fibrosis, the amount of TN-C mRNA was increased up to 18- and 39-fold, respectively, compared to normal dermis, whereas the level of TN-X mRNA remained almost unchanged [2].
• The immunohistochemical study revealed a significantly decreased number of neointimal macrophages and neovascularizations (p < 0.05, p < 0.01, respectively), and a stronger expression of tenascin-C in the radius [10].
• Whereas pig normal skin displayed a discrete TN-C signal at the dermo-epidermal junction, around blood vessels and hair bulbs, the swine tumour showed enhanced expression of TN-C in these areas and around stromal and tumour cells [3].

Associations of TNC with chemical compounds

• Optical intensity and color analyses showed significantly higher tenascin R and tenascin C expression in the MSC and BM groups than in the MI-only or Control group (P < 0.01) [11].

Other interactions of TNC

• Overall, the tenascin-X gene was significantly expressed in two thirds of the tissues, and the tenascin-C gene in about 50% of them [9].

Analytical, diagnostic and therapeutic context of TNC

• In analyses by Western blotting, the two main TN-C isoforms of 235-240 and 190-200 kDa increased up to 45- and 105-fold in fibrotic tissues, respectively [2].
• CONCLUSIONS: Increased production of ECM, especially tenascin-C, played a greater role in the neointimal formation in the radius stent than inflammation [10].
• This opposite regulation of TN-C and TN-X RNAs was confirmed at the protein level by indirect immunofluorescence [3].

References