BACKGROUND: Defective adhesion and migration of melanocyte may be involved in pathogenesis of vitiligo. Tenascin, a glycoprotein of the extracellular matrix, has a role in cell adhesion and migration. It has been reported that abundant expression of tenascin in vitiligo lesion may inhibit melanocyte adhesion and migration. OBJECTIVE: To investigate the tenascin expression in vitiligo skin lesions and to compare with clinical findings. METHODS: We studied 9 patients with vitiligo. The expressions of tenascin were studied by immunahistochemieal techniques.
Cell Adhesion ; Extracellular Matrix ; Glycoproteins ; Humans ; Melanocytes ; Skin ; Tenascin* ; Vitiligo*

OBJECTIVE: Growth of cerebral gliomas depends on their neovascularization and invasion into the adjacent neural tissue. There are several extracellular and intracellular factors affecting its growth. Tenascin(TN) is a type of extracellular matrix(ECM) protein which may be responsible for the migration of neoplastic cells and tumor angiogenesis, but its exact role has not been established. We studied the relation between the expression of TN and the histological grade of the glial cell tumors as well as to determine the expression of TN-C in tumor vessel. PATIENTS AND METHODS:In the fifty-six patients with glial cell tumors, we characterized the expression of tenascin-C(TN-C) in the neoplastic vessel, intercellular network, and tumor cell by immunohistochemistry using monoclonal antibody. The relationship between the histological malignancy and TN-C expression was evaluated. In addition, TN-C expression of the tumor vessels was also examined. RESULTS: The tumors included 32 glioblastomas, 13 astrocytomas, 4 pilocytic astrocytoma, 3 anaplastic astrocytoma, 1 pleomorphic xanthoastrocytoma, 1 oligodendroglioma, 1 anaplastic oligodendroglioma, and 1 mixed oligoastrocytoma. TN-C expression in intercellular network of glioblastoma, anaplastic astrocytoma, and astrocytoma was 87. 5%, 66.7%, and 61.5%, respectively. There was a close relationship between the TN-C expression and histological grade of the glial cell tumors. In 28(87.5%) of 32 glioblastomas, TN-C was significantly expressed in the tumor vessels(p<0.05). CONCLUSION: Present results demonstrate that TN-C in the glial cell tumors may be identified as a one of the related factors contributing to malignant progression. And also, enhanced expression of TN-C in the tumor vessels of glioblastoma indicate the possibility that TN-C could be involved in neoplastic angiogenesis.
Astrocytoma ; Glioblastoma ; Glioma* ; Humans ; Immunohistochemistry ; Neuroglia* ; Oligodendroglioma ; Tenascin*

Tenascin is suggested the one of cause of vitiligo by interfering melanocyte adhesion and migration. The distribution and expression levels of tenascin were examined by semiquantitative immunohistochemistry on skin biopsies from vitiligo patients with varying area of photodamage. The level of tenascin on adult skin is severely restricted but we had observed the increase on vitiligo skin lesions. Although it is uncertain that the increased tenascin expression is the cause or the result of disease, vitiligo and increased tenascin expression is thought to be related each other. This study has shown that tenascin increased on photodamaged vitiligo skin lesions. So we shoud consider choosing phototherapy to vitiligo.
Adult ; Biopsy ; Humans ; Immunohistochemistry ; Melanocytes ; Phototherapy ; Skin* ; Tenascin* ; Vitiligo*

OBJECTIVETo investigate the expression of tenascin-C (Tn-C) in keloid and hyperplastic scar (HS).

METHODSTissue samples were harvested from 10 patients with keloid and 10 with HS (6 - 10 months) and from the skin of 5 adult healthy volunteers. The expression of Tn-C in these samples was determined with immunohistochemistry method.

RESULTSThere was scarce expression of Tn-C in the skin tissue in adult healthy volunteers, and it was only present in the dermal papillae at the dermis epidermis conjunctions and partly in the blood vessels and skin appendages adjacent to the basement membrane. There was enhanced expression of Tn-C in the dermal scar tissue and skin appendages in both keloid and HS, especially in keloid, which exhibited a diffused pattern in the tissue. When compared with that in normal skin, the Tn-C expression in the normal skin adjacent to the keloid was enhanced markedly, but not in the normal skin near HS tissue.

CONCLUSIONThere was increased Tn-C expression in keloid and HS (6 - 10 months).

Cicatrix, Hypertrophic ; metabolism ; Female ; Humans ; Immunohistochemistry ; Keloid ; metabolism ; Male ; Skin ; chemistry ; Tenascin ; analysis

Glomerulosclerosis is a common outcome in various progressive glomerular diseases, and results from accumulation of extracellular matrices. Depending on the disease progression the extracellular matrices show quantitative and qualitative alterations. Tenascin is a significant extracellular matrix glycoprotein that expresses in normal and pathologic tissue of varying organs including kidney. We performed immunohistochemical staining for tenascin using 30 cases of renal biopsy specimens diagnosed as IgA nephropathy to study the alteration of tenascin expression in IgA nephropathy according to the histologic grading. The results were as follows; 1. The more high histologic grade, the more increase of tenascin was found in the glomerulus. 2. Tenascin was increased in proportion to the mesangial matrix. 3. The staining of tenascin was more intense in glomerular sclerotic area and was increased in proportion to the progression of sclerosis. 4. Cellular crescents showed strong positivity for tenascin. 5. Tenascin was increased in proportion to the degree of interstitial fibrosis in renal cortex. In conclusion, tenascin is an important extracellular matrix component which is significantly increased in both glomerulus and cortical interstitium according to the progress of the disease in IgA nephropathy.
Biopsy ; Disease Progression ; Extracellular Matrix ; Fibrosis ; Glomerulonephritis, IGA* ; Glycoproteins ; Immunoglobulin A* ; Kidney ; Sclerosis ; Tenascin*

OBJECTIVE: Uterine leiomyomas are the most common tumor of the uterus. But the molecular causes of uterine leiomyoma remain unclear. We conducted the current investigation in order to elucidate the molecular mechanisms in the development of uterine leiomyoma. METHODS: We employed a new and accurate reverse transcription-polymerase chain reaction (RT-PCR) method that involved annealing control primers (ACPs) to identify the genes that are differently expressed in uterine leiomyoma. RESULTS: Using 120 ACPs, we identified and sequenced 14 differently expressed genes (DEGs) in uterine leiomyoma compared with normal myometrium. Basic Local Alignment Search Tool (BLAST) searches were performed to examine the known functions of these genes associated with uterine leiomyoma. We confirmed differently expressed patterns in more cases using the RT-PCR method. We also detected two novel genes, Tenascin-X and Leukemia Inhibitory Factor Receptor (LIFR), which had not yet been reported to have any functions associated with uterine leiomyoma. RT-PCR confirmation shows that both of these two genes are down-regulated in uterine leiomyoma. CONCLUSION: Our results suggest that Tenascin-X and LIFR may play a role in the development of uterine leiomyoma. Although further studies are required to establish the precise mechanisms with which these genes are involved in the genesis of uterine leiomyoma, the present research is significant in that it is the first study which detects down-regulated novel genes in uterine leiomyoma using the ACP system.
Animals ; Female ; Leiomyoma ; Leukemia ; Leukemia Inhibitory Factor ; Mice ; Myometrium ; Receptors, OSM-LIF ; Tenascin ; Uterus

OBJECTIVETo investigate the expression of Tenascin-C mRNA in keloids and hypertrophic Total RNA was isolated from normal adult skin. A cDNA fragment (base 5941-6481bp) of the scars.

METHODSfull-length human Tenascin-C cDNA was synthesized by polymerase chain reaction and subcloned in pGEM-T-easy. Dioxygen-labeled anti-sense and sense probes were synthesized by using a Sp6/T7 RNA synthesis kit in the present of Dig-UTP in vitro. The samples were taken from keloids in 10, hypertrophic scars in 10 and normal adult skin in 5. The hybridization was performed with 4% paraformaldehyde-fixed and wax-embedded sections to detect the Tenascin-C mRNA.

RESULTSThe Tenascin-C mRNA was negative in the normal adult epidermis and weakly located in the fibroblasts of the papillary dermis and the epidermal adnexa. In all of the 10 keloid specimens, the Tenascin-C mRNA was positive throughout the epidermis and widely distributed in the dermis included in the fibroblasts, endothelial cells and epidermal adnexa. In the specimens of the 3 hypertrophic scars,the Tenascin-C mRNA was also positive in the epidermis, but in the other 7 cases, it became negative. In the dermis of the hypertrophic scar,the Tenascin-C mRNA was weaker than that in the keloid, but stronger than that in the normal skin.

CONCLUSIONSThe expression of Tenascin-C mRNA is markedly enhanced in the keloids.

Cicatrix, Hypertrophic ; genetics ; metabolism ; pathology ; Female ; Humans ; Keloid ; genetics ; metabolism ; pathology ; Male ; RNA, Messenger ; metabolism ; Tenascin ; genetics ; metabolism

Tenascin-C (TNC) is an extracellular matrix glycoprotein, which is usually highly expressed in embryonic tissues and tumor tissues, but is not expressed or just lowly expressed in mature tissues. TNC is involved in various complex signaling pathways during tumor metastasis, especially through modulating FAK, RhoA, Wnt and Notch pathways by interacting with syndecan-4, integrin α5β1, matrix metalloproteinases (MMPs) and vascular endothelial growth factor (VEGF). As a result, TNC affects epithelial mesenchymal transition, tumor cell adhesion, proliferation and angiogenesis, which eventually enhances the invasion and metastasis ability of many tumors. Further studies have demonstrated that TNC could be used as prognosis or metastasis marker of patients with malignant tumor.
Cell Adhesion ; Humans ; Integrins ; Matrix Metalloproteinases ; Neoplasm Metastasis ; Neoplasms ; Neovascularization, Pathologic ; Signal Transduction ; Tenascin ; physiology ; Vascular Endothelial Growth Factor A

BACKGROUNDBioprosthetic heart valves derived from glutaraldehyde (Glut)-fixed xenografts have been widely used to replace diseased cardiac valves. However, calcification and degeneration are common following their implantation. Inflammation is closely associated with calcification of Glut-fixed xenografts via macrophage infiltration. Tannic acid (TA) possesses anti-inflammatory effects. This study was designed to investigate the anti-calcification of TA treatment on the Glut-fixed bovine pericardium (BP) in a rat subdermal model.

METHODSFresh BP was divided into two groups (10 in each group) and separately subjected to different fixation procedures as follows: (1) Glut group: fixation with 0.6% Glut alone; (2) Glut/TA group: fixation with 0.6% Glut and subsequent 0.3% TA. Then the BP samples were subdermally implanted in juvenile male Sprague-Dawley rats and explanted 21 days after implantation. Each explanted BP sample was divided into three parts for calcium content analysis, von Kossa's staining and immunohistochemical staining, and reverse transcription-polymerase chain reaction study.

RESULTSThe data from quantitative calcium analysis and von Kossa's staining showed that Glut-fixed BP developed significantly more calcification than Glut/TA-fixed BP ((90.3 +/- 32.5) mg/g dry weight vs (6.4 +/- 1.3) mg/g dry tissue, P < 0.01). Immunostaining demonstrated lower matrix metalloproteinase-9 and tenascin-C expression as well as macrophage infiltration into Glut/TA-fixed BP than in its Glut-fixed counterpart (P < 0.01 for all). Additionally, the reverse transcription-polymerase chain reaction study showed that higher levels of expression of matrix metalloproteinase-9 and tenascin-C mRNA occurred within Glut-fixed BP than within the Glut/TA-fixed ones (P < 0.01 for all).

CONCLUSIONTA exerts excellent anti-calcification effects on Glut-fixed BP via inhibiting macrophage infiltration and expression of matrix metalloproteinase-9 and tenascin-C.

Animals ; Calcinosis ; prevention & control ; Cattle ; Glutaral ; pharmacology ; Male ; Matrix Metalloproteinase 9 ; analysis ; Pericardium ; pathology ; Rats ; Rats, Sprague-Dawley ; Tannins ; pharmacology ; Tenascin ; analysis ; Tissue Fixation

OBJECTIVETo understand the mechanism by which tenascin-C regulates osteoblast differentiation and the role of tenascin-C in osteoporosis.

METHODSTenascin-C protein expression in femoral spongy bone of mice with or without osteoporosis was analyzed using Western blotting. In MC3T3-E1 osteoblasts with or without tenascin-C depletion by a specific siRNA targeting tenascin-C, alkaline phosphatase activity and Dickkopf-1 (DKK-1) expression were determined using quantitative RT-PCR and Western blotting, and the transcriptional activity of Wnt signaling pathway was analyzed using a luciferase reporter assay. The possible interaction of tenascin-C with DKK-1 predicted by STRING software was verified by immunoprecipitation.

RESULTSs Tenascin-C was markedly down-regulated in hemoral spongy bone of mice with osteoporosis as compared with the control mice. Osteoblastic differentiation was markedly suppressed in MC3T3-E1 osteoblast after tenascin-C depletion, and was significantly reversed by simultaneous β-catenin over-expression. siRNA-mediated knockdown of tenascin-C, which bound DKK-1, up-regulated the expression of DKK-1 and consequently lowered the transcriptional activity of Wnt pathway.

CONCLUSIONTenascin-C knockdown attenuates its negative control on DKK-1 to suppress the transcriptional activity of Wnt pathway, which in turn suppresses osteoblastic differentiation and promotes osteoporosis.

Animals ; Cell Differentiation ; Gene Knockdown Techniques ; Mice ; Osteoblasts ; cytology ; Osteogenesis ; Osteoporosis ; physiopathology ; RNA, Small Interfering ; genetics ; Tenascin ; genetics ; metabolism ; Up-Regulation ; Wnt Signaling Pathway ; beta Catenin ; metabolism