Distribution Of Tenascin Research Articles

Infrared LED light therapy influences the expression of fibronectin and tenascin in skin wounds of malnourished rats—A preliminary study

The aim of this investigation was to evaluate the effect of infrared (λ 846±20nm) LED irradiation on the expression profile of the extracellular matrix protein components, tenascin and fibronectin on skin wounds induced in well nourished and malnourished rats. Eighteen albino rats (21 days old) were randomly divided into a well-nourished group (standard diet) and a malnourished group (regional basic diet). After receiving the diet for 70 days, skin wounds were created and the animals were subdivided into three groups: well-nourished control (n=6), malnourished control (n=6), and malnourished+LED irradiated (λ 846±20nm, 100mW, 4J/cm2) (n=6). The animals were sacrificed 3 and 7 days after injury and histological sections were immunostained for both proteins. They were examined for the presence, intensity, distribution and pattern of immunolabeling. At 3 days, the distribution of tenascin was shown to be greater in the wound bed of malnourished animals compared to the well-nourished group. The intensity and distribution of tenascin was shown to be lower in the malnourished LED irradiated group compared to the malnourished control. There was a significant difference regarding the presence of fibronectin in the malnourished and well-nourished groups after 7 days (p=0.03). The intensity of fibronectin was slight (100%) in the irradiated group and moderate to intense in the malnourished control group. The results of the present study indicate that infrared LED irradiation modulates positively the expression of tenascin and particularly fibronectin.

Differential elastin and tenascin immunolabeling in the uterosacral ligaments in postmenopausal women with and without pelvic organ prolapse

Connective tissue, consisting mainly of collagen and structural glycoproteins, is an important part of the supportive structures of the genitourinary region. Relatively few data have been published with respect to the role of elastin and glycoproteins in pelvic organ prolapse (POP). Connective tissue of the uterosacral ligament in postmenopausal women with and without genital prolapse was compared. Fifty-nine consecutive women referred for hysterectomy were included in the study. The patients had POP or benign gynecological disease (e.g. myoma of the uterus). Tissue samples from the uterosacral ligament were investigated for localization and distribution of tenascin and elastin using immunofluorescence microscopy. Tissue samples of women with prolapse showed a significantly (p<0.001) weaker immunofluorescent labeling of tenascin compared to samples taken from women without prolapse. Tenascin was detectable in tissues of all women with POP, whereas its immunolabeling was decreased in the uterosacral ligament in women without POP. Intact elastin fibers were observed in tissues of all women without POP, whereas elastin was undetectable or sometimes fragmented in the uterosacral ligament in women with POP. Greater amounts of tenascin and lesser amounts of elastin were therefore found in patients with POP. These results suggest that an altered turnover of connective tissue in the uterosacral ligament might be responsible for the presence of pelvic floor relaxation in postmenopausal women. These data indicate a complex architecture of the extracellular matrix in the uterosacral ligaments, with marked differences in tenascin and elastin expression between postmenopausal women with or without POP.

Changes in the Distribution of Tenascin and Fibronectin in the Mouse Ovary During Folliculogenesis, Atresia, Corpus Luteum Formation and Luteolysis

Tenascin and fibronectin are components of the extracellular matrices that oppose and promote adhesion, respectively. Using immunohistochemical techniques, we studied the distribution of tenascin and fibronectin in the mouse ovary, in which dynamic reconstruction and degeneration occur during folliculogenesis, atresia, ovulation, corpus luteum formation and luteolysis. In growing follicles, tenascin was only detected in the theca externa layer, while fibronectin was detected in the theca externa layer, theca interna layer and basement membrane. During follicular atresia, granulosa cells, which are surrounded by the basement membrane, began to die through apoptosis. In atretic follicles, tenascin was detected in the basement membrane and theca externa layer. Distribution of fibronectin in atretic follicles was similar to that in healthy growing follicles, except that granulosa cells were slightly immunopositive for fibronectin. In young corpus luteum, luteal cells exhibit high 3 beta -hydroxysteroid dehydrogenase (3 beta -HSD) activity, an enzyme indispensable for progesterone production. Tenascin was barely detected in young luteal cells. 3 beta -HSD activity in luteal cells declines with corpus luteum age, and in older corpus luteum there is an increase in apoptotic death of luteal cells. Tenascin was intensely immunopositive in old luteal cells.In contrast, fibronectin immunostaining in luteal cells was relatively constant during corpus luteum formation and luteolysis. Our observations suggest that tenascin is critical in controlling the degenerative changes of tissues in mouse ovaries. Moreover, in all circumstances observed in this study, tenascin always co-localized with fibronectin, suggesting fibronectin is indispensable for the function of tenascin.

Immunohistochemical assessment of extracellular matrix components in syndrome and non-syndrome odontogenic keratocysts.

Investigate the immunohistochemical distribution of fibronectin, tenascin, laminin and collagen IV in syndrome (SOKC) and non-syndrome odontogenic keratocysts (NSOKC). Ten cases of SOKC and five of NSOKC were selected and streptoavidin-biotin technique was applied. The specimens were analyzed taking into account the following evaluation parameters: presence, continuity and thickness in the basement membrane and intensity, distribution and association with inflammatory cells in the cyst wall. Differences could be detected regarding tenascin, fibronectin and collagen IV between the SOKC and NSOKC. Tenascin was present in all cases along the basement membrane in SOKC and in five cases of NSOKC predominated negative areas. Furthermore, tenascin distribution was focal in the cyst wall in SOKC whereas in NSOKC it was diffuse. Concerning fibronectin, it was detected as a discontinuous band when present in SOCK and as a continuous band in NSOKC. Collagen IV was not present in the majority of the cases in SOKC. Negative areas for laminin predominated in the basement membrane in both groups. These findings show differences between the immunohistochemical expression of tenascin, fibronectin and collagen IV which might indicate a more aggressive biological behavior of SOKC as compared with NSOKC.

MICROARRAY ANALYSIS REVEALS PHENOTYPIC DIFFERENCES BETWEEN VALVULAR AND VASCULAR ENDOTHELIAL CELLS IN STATIC AND FLUID FLOW ENVIRONMENTS

Oxidative stress may be involved in monocrotaline (MCT)-induced endothelial cell injury and upregulation of extracellular matrix proteins in the pulmonary vasculature. To test this hypothesis, cytotoxicity, expression and distribution of tenascin (TN) as well as cellular oxidation were determined in porcine pulmonary artery endothelial cells (PAECs) exposed to MCT and/or to an oxygen radical scavenger, dimethylthiourea (DMTU). Relative to controls, treatment with 2.5 mM MCT for 24 hr produced cytotoxicity as evidenced by changes in cellular morphology, cell detachment, hypertrophy, reduction in cellular proliferation and severe cytoplasmic vacuolization. Parallel studies showed that MCT markedly altered the expression and distribution of TN in PAEC as determined by immunocytochemistry. Western analysis showed that MCT increased cellular TN content and promoted the appearance of an additional, smaller TN isoform. Northern analysis demonstrated an increase in the steady-state level of TN-specific mRNA in response to MCT treatment. Exposure to MCT also increased the synthesis of cell-associated and media-associated TN as determined by immunoprecipitation. In addition, MCT increased the intensity of cellular oxidative stress as measured by 2,7-dichlorofluorescein fluorescence. Co-treatment with DMTU prevented MCT-induced cytotoxicity, alterations in TN distribution and content, and reduced the increase in DCF fluorescence. These results suggest that MCT-induced cytotoxicity and upregulation of TN are mediated, at least in part, by induction of cellular oxidative stress.

Tenascin Expression at the Invasive Front Is Associated with Poor Prognosis in Intrahepatic Cholangiocarcinoma

Tenascin and decorin are components of the extracellular matrix (ECM) that are implicated in cell proliferation in tumors. Here, we propose that abnormal expression of stromal ECM may play an important role in the progression of intrahepatic cholangiocarcinoma, which is characterized by desmoplastic reaction. To explore this hypothesis, we performed immunohistochemical analysis in order to examine the expression and distribution of tenascin and decorin in 75 cases of intrahepatic cholangiocarcinoma. In the intratumoral stroma, positive staining for tenascin was observed in 51 (68%) cases, and positive staining for decorin was observed in 61 (81%) cases. However, at the invasive front, positive staining for tenascin was found in 23 (31%) cases, and positive staining for decorin was found in 6 (8%) cases. Decorin staining was not correlated with aggressive behavior of intrahepatic cholangiocarcinoma, whereas intratumoral tenascin staining was correlated with lymphatic permeation and proliferative activity measured by Ki67. Tenascin staining at the invasive front was associated with tumor size, lymphatic permeation, lymph node metastasis, and proliferative activity and appeared to be a useful prognostic factor by univariate analysis, although it was not an independent prognostic factor. These results indicate that tenascin plays a role in tumor progression in cases of intrahepatic cholangiocarcinoma and that tenascin expression, especially at the invasive front, may be a useful marker in evaluating an unfavorable prognosis in patients with intrahepatic cholangiocarcinoma.

Immuno-histochemical evaluation of conjunctival remodelling in vernal keratoconjunctivitis

To study the expression of the extracellular matrix (ECM) proteins, tenascin, laminin, and fibronectin in the conjunctiva of patients with active vernal keratoconjunctivitis (VKC). Conjunctival biopsy specimens were obtained from nine patients with active VKC and 6 normal control subjects. The presence and distribution of tenascin, laminin, and fibronectin were assessed microscopically with immunohistochemical techniques and a panel of monoclonal and polyclonal antibodies directed against tenascin, laminin, and fibronectin. In normal conjunctiva, weak immunoreactivity for tenascin was localized to the walls of blood vessels in the upper substantia propria. Weak immunoreactivity for laminin was located at the epithelial-stromal junction and in the walls of blood vessels. Staining for fibronectin was absent. In VKC specimens, intense immunoreactivity for tenascin was noted in the substantia propria associated with the inflammatory infiltrate and in the perivascular stroma. Intense immunoreactivity for laminin around all stromal vessels and fibrillar immunoreactivity among basal epithelial cells were noted. There was no immunoreactivity for fibronectin. Our data indicate increased deposition of tenascin and laminin in the conjunctiva from patients with active VKC. Our findings suggest that tenascin and laminin might play distinct roles in chronic inflammation seen in VKC.

The role of large extracellular matrix glycoproteins in regenerating laser-treated tissue

The distribution of large extracellular matrix glycoproteins tenascin, cellular fibronectin and laminin was studied in healing CO 2 laser, scalpel incision and excision wounds of rat tongue dorsal mucosa in 153 rats over a period of 42 days by indirect immunofluorescence microscopy using mono- and polyclonal antibodies. A local increase in tenascin distribution in the basement membrane zone indicated that this protein was important to epithelial cell proliferation and movement. The increased amount of cellular fibronectin in the provisional stromal matrix showed that this protein was a crucial component in healing wounds. An increased expression of laminin in the basement membranes of the wound borders, blood vessel walls and nerve structures suggested that this protein could guide and stimulate the regenerating epithelial cells. In laser wounds, re-epithelialization seemed to progress upon the laminin-containing structures, although the formation and subsidation of laminin back to normal seemed to be somewhat slower. The results show that long observation times are needed when studying laser wound healing.

Topographic and zonal distribution of tenascin in human articular cartilage from femoral heads: normal versus mild and severe osteoarthritis

Objective: The extracellular matrix glycoprotein tenascin (TN) is upregulated in articular cartilage with severe osteoarthritis (OA). This study gives a detailed description of TN expression in areas of articular cartilage from femoral heads with mild OA showing structural lesions and in structurally normal areas of the same femoral heads compared with normal cartilage and cartilage with severe OA. Methods: Immunohistochemical evaluation was performed on cryosections stained with antibodies against TN. Sections were selected as follows: from each macroscopically normal femoral head ( n=6) a normal central and peripheral biopsy; from each femoral head with macroscopically mild OA ( n=8) a central biopsy that showed structural lesions and a peripheral normal biopsy; from each femoral head with severe OA ( n=9) a central and a peripheral biopsy with structural lesions. Central biopsies represent load bearing areas, whereas peripheral biopsies are non-load bearing. Results: Central cartilage with mild OA contains significantly higher levels of TN in the superficial zone than structurally normal, peripheral cartilage from the same femoral heads. Normal cartilage and cartilage with severe OA do not display this topographic variation. Central cartilage with mild OA shows significantly higher levels of TN than normal, central cartilage. Peripheral, normal cartilage with mild OA shows significantly less TN than peripheral cartilage with severe OA. Conclusions: In femoral heads with mild OA, TN is accumulated in areas displaying structural damage. This proposes mild OA to be a localized disorder. Extreme caution is necessary for sampling of articular cartilage, especially from joints with mild OA.

Tenascins are associated with lipid rafts isolated from mouse brain

Lipid rafts are microdomains of the plasma membrane which are enriched in glycosphingolipids and specific proteins. The reported interactions of several raft-associated proteins (such as, e.g., F3) with tenascin C and tenascin R prompted us to consider that these oligomeric multidomain glycoproteins of the extracellular matrix (ECM) could associate with rafts. Here, we show punctate immunocytochemical distributions of tenascin C (TN-C) and tenascin R (TN-R) at the membrane surface of neural cells resembling the pattern reported for raft-associated proteins. Moreover, cholesterol depletion with methyl-β-cyclodextrin reduced the punctate surface staining of TN-C. Consistently, TN-C was associated with lipid rafts of neonatal mouse brain according to sucrose density gradient centrifugation experiments. Furthermore, TN-R was also found in rafts prepared from myelin of adult mice. Thus, brain-derived tenascins are able to associate with lipid rafts.

Tenascin in the human intervertebral disc: alterations with aging and disc degeneration

Our objective for this study was to determine the presence and distribution of tenascin in the human intervertebral disc. The tenascins are a family of extracellular matrix proteins with repeated structural domains homologous to epidermal growth factor, fibronectin type III and the fibrinogens. Little is known about the presence of this protein in the disc. Ten normal human discs donated from subjects newborn to 15 years old, 10 control discs from adult donors aged 24-41 years, and 11 surgical disc specimens from patients aged 26-76 years were examined for immunolocalization of tenascin. In young discs, tenascin was localized throughout the annulus; in the nucleus, localization was confined to pericellular matrix. In adult control and degenerating disc specimens, tenascin in the annulus was localized primarily in pericellular matrix regions encircling either single cells or clusters of disc cells; in rare instances localization was more diffuse in the intraterritorial matrix. In young, healthy disc, tenascin was abundant throughout the annulus. In contrast, degenerating discs in adults showed a localization restricted to the pericellular, and rarely, more restricted intraterritorial matrix. These observations indicate that changes in the amount and distribution of tenascin may have a role in disc aging and degeneration, possibly by modulating fibronectin-disc-cell interactions, and causing alterations in the shape of disc cells.

Quantitative analysis of tenascin in chordae tendineae of human left ventricular papillary muscle with aging

A computer image analysis was done to investigate the distribution of tenascin and collagenous matrix components (collagen types I and III) in the chordae tendineae of the anterior cusp of the left ventricular papillary muscle, using confocal laser scanning microscopy in both a 20s age group and an 80s-90s age group. Tenascin and the collagenous matrix components showed marked accumulation in the 80s-90s age group with elastic fiber concentration being increased in the same region as that in the 20s age group. The highest content of intersurface layer staining with an anti-tenascin antibody and with anti-collagen type III in the inner layer was found in the 80s-90s age group. These content levels were low in each region in the 20s age group. The distribution and content of these extracellular matrix changes are related to the changes in mechanical performance of the cardiac muscle with age.

Tenascin—A Marker for the Malignant Potential of Preinvasive Breast Cancers

Objective. Up to now, the mechanisms responsible for progression from noninvasive to invasive breast cancer have remained obscure. Tenascin is an extracellular matrix glycoprotein, present in embryonal and fetal tissues, which is also found in the stroma of various benign and malignant pathologies. We studied the expression and immunohistochemical behavior of tenascin in specimens of invasive and preinvasive breast cancer in order to assess its potential role as a marker for tumor invasion.Materials and methods. Sixty-eight specimens including 29 noninvasive ductal cancers, 12 invasive ductal cancers, 5 adenoses, 7 fibroadenomas, and 15 samples of normal human breast tissue were evaluated. An immunofluorescent microscopic technique was used for analysis of the localization and distribution of tenascin. Paraffin-embedded biopsies were incubated with primary monoclonal anti-tenascin antibodies (1:25, Dako-tenascin, TN2). Subsequently, trimethylrhodamine-isothiocyanate-conjugated secondary antibodies (rabbit anti-mouse immunglobulins (Dakopatts, Denmark) were added to visualize the protein.Results. A significant tenascin expression was observed around the ducts in all samples of patients with preinvasive breast cancers. Intensive staining was also found in the periductal stroma of all specimens of patients with invasive breast cancers. Benign breast lesions showed weaker reactivity. No tenascin expression was detectable in normal human breasts, while tissue samples of in situ cancers presented variable staining intensities positively correlating with the degree of differentiation.Conclusion. Tenascin immunofluorescence may prove a suitable and helpful adjunct for diagnosing malignant disease and for predicting the invasive potential of premalignant breast lesions.

Immunohistochemical Localization of Tenascin, Fibronectin, and Type III Collagen in Human Dental Pulp

The distribution of tenascin (TN), fibronectin (FN), and type III collagen (col III) in the extracellular matrix of the connective tissue of normal, inflamed, and hyalinized human dental pulp was studied by immunohistochemical staining with monoclonal antibodies against these molecules. TN, FN, and col III were present in all normal tissues studied. In areas of hyalinization only col III was observed. None of the molecules studied were seen in areas of inflammatory exudate. Strong staining for TN and FN was found in the periphery of all specimens analyzed next to the odontoblastic layer. We therefore conclude that TN, FN, and col III are present in the extracellular matrix of normal human dental pulp. TN, FN, and col III distribution in inflammatory and degenerative processes is different from that observed in normal human dental pulp.

Alterations in Distribution of Tenascin, Fibronectin and Fibrinogen in Vulval Lichen sclerosus

Background: The pathophysiology of lichen sclerosus remains uncertain. The clinical features, including increased fragility and scarring, and the histology suggest that significant reorganisation of the extracellular matrix is occurring. Tenascin, fibrinogen and fibronectin are extracellular matrix components that play a significant role in tissue remodelling, for example during wound repair. Aim: To examine the distribution of tenascin, fibrinogen and fibronectin in vulval lichen sclerosus. Materials and Methods: Immunohistochemical staining was performed to study the distribution of tenascin, fibronectin and fibrinogen in 16 specimens of untreated vulval lichen sclerosus and 1 specimen of extragenital lichen sclerosus. Haematoxylin and eosin staining of the specimens was also performed to identify the position of the pale staining homogenous zone/zone of sclerosis and the inflammatory infiltrate below this. The control tissues studied included biopsies taken from the uninvolved thigh of 13 of the lichen sclerosus patients and 6 samples of normal vulva tissue obtained during gynaecological procedures from women of similar age to the lichen sclerosus women. Results: All the lichen sclerosus specimens demonstrated increased immunostaining of tenascin in the upper dermis and comparing this with the haematoxylin and eosin staining this corresponded to the zone of sclerosis with relatively little tenascin staining associated with the inflammatory band. In 14 out of the 16 vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen fibrinogen immunostaining was increased in the upper dermis which corresponded – in haematoxylin and eosin staining – to the zone of sclerosis. There was also slightly increased fibrinogen staining in the mid dermis which corresponded to the inflammatory band. Fibronectin staining was reduced in the upper dermis of 12 of the vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen which corresponded to the zone of sclerosis. However, in 14 of the vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen, fibronectin was slightly increased in the mid and deeper dermis which corresponded to the zone of inflammatory cells and the area below this. There was also increased fibronectin staining around blood vessel walls both in the mid dermis and within the zone of sclerosis. Conclusion: The distribution of tenascin, fibrinogen and fibronectin is altered in lichen sclerosus and the alteration in these extracellular matrix components may be relevant to the initiation of scarring in lichen sclerosus and the associated increased skin fragility.

Epimorphin expression during human foetal hair follicle development.

Epimorphin is a mesenchymal protein expressed in several organs and known to have an essential role in epithelial tissue organization, including hair follicle morphogenesis, in mice. Although about 90% homology has been reported between human and mouse epimorphin exon sequences, there is no information about expression and function of epimorphin in hair follicle development in humans. In order to elucidate the expression pattern of epimorphin in human hair follicle morphogenesis and to compare it with the distribution of tenascin and neural cell adhesion molecule (NCAM), skin samples from human foetuses of a series of estimated gestational ages (EGAs) (46-168 days EGA) were studied using monoclonal anti-epimorphin antibody MC-1, anti-tenascin antibody and anti-human NCAM antibody. Epimorphin was detected in the mesenchymal cell condensation at the pregerm stage (< 75 days EGA), and there was strong expression of epimorphin in the perifollicular mesenchymal cells around the hair germ (75-84 days EGA). At the hair peg stage (85-104 days EGA), epimorphin was around the hair peg with the strongest staining in the neck portion. This sequence of staining patterns was similar to that of tenascin. In the bulbous hair peg (105-134 days EGA), the perifollicular dermal mesenchymal cells were evenly positive for epimorphin. Mesenchymal cells underneath the follicle bulb prior to formation of the dermal papilla were also positive for epimorphin. In the lanugo hair follicle (> 134 days EGA), dermal papilla cells expressed epimorphin as well as tenascin and NCAM. These results indicate that epimorphin expression is closely linked to developing hair follicles in human foetuses. This suggests that epimorphin may have an important part in induction of morphogenesis during human foetal hair follicle development.

Epithelial involution and basement membrane loss during early rhombencephalic tectoria lamina development.

Extracellular material molecules play a key role in the regulation of morphogenesis and differentiation of a large number of organs including the central nervous system. However, the role of the neural basement membrane in the growth of different parts of the neural tube has yet to been delineated. Here, the structural and compositional modifications of the basement membrane (BM) of rhombencephalic tectoria lamina anlage (RTLA) have been examined during the process of RTLA epithelial attenuation. Between stages 10 to 11-the presumptive RTLA epithelium showed a structure, thickness and cell-proliferating capacity similar to those observed in other zones of the rhombencephalic walls. Moreover, the rhombencephalic vesicles were surrounded by a continuous BM that was heterogeneous both ultrastructurally and with regard to ruthenium red, laminin and tenascin distribution. After stage 11, the RTLA epithelium underwent a rapid process of attenuation and change to a stratified flattened epithelium. During this remodelling process, apoptosis and inhibition of both PCNA expression and 3H-thymidine uptake occurred in the RTLA epithelium. The BM of the RTLA underwent a process of degration at the beginning of the remodelling, and apoptosis and cell proliferation inhibition of RTLA epithelium were also observed. The loss of the biochemical signals encoded within the BM could lead to cell shape changes, cell proliferation inhibition and to the anoikis type of cell death. Our findings support the idea that the BM surrounding the neural tube plays a key role in controlling both the structure and growth of the CNS during the early developmental stages.

Immunolocalization of tenascin in the chinchilla inner ear

Tenascin was immunolocalized in the chinchilla cochlea and vestibular system to better understand the functional morphology of the inner ear. Inner ear tissues were fixed with acetone, decalcified and cryosectioned. Indirect immunofluorescence, using antibodies directed against human tenascin epitopes, were used to detect tenascin. As a positive control, tenascin immunoreactivity was found in kidney, cortical mesangial cells and the extracellular matrix of glomeruli and medullary tubule interstitial spaces, concurring with previously reported results. In the cochlea, tenascin immunoreactivity was present in osteocytes, the mesothelial cells underlying the basilar membrane (BM) and within the fibrous matrix of the BM. Greater reactivity was observed in the mesothelial cells than in the fibrous matrix of the BM. In the vestibular system, tenascin immunoreactivity formed a diffuse band directly beneath the basal lamina of the ampullary and otoconial organs. Tenascin immunoreactivity was also observed in cup-shaped regions between the type I vestibular hair cells and their surrounding VIII nerve calyces in the ampullary and otoconial organs. This is the first report of the anatomical distribution of tenascin in the adult, mammalian inner ear, other than our previously published abstract P.A. Santi and D. Swartz, Soc. Neurosci. Abstr. 23 (1997) 731.

Tenascin Expression and Angiogenesis in Breast Cancers

The expression and the distribution of tenascin as well as the extent of blood vessel formation (angiogenesis) were investigated in 70 invasive human breast carcinomas. Formalin-fixed, paraffin-embedded specimens were stained with monoclonal antibody against tenascin-C (DAKO and Biogenex). Anti-CD31 antibody (Biogenex), an acknowledged marker of stromal angiogenesis, was used to detect endothelial cells. Tenascin immunostaining was positive in the tumours around the persisting normal ducts, around tumour-cell nests, in the neostroma, in some tumour cells, and it was found in or around vascular channels. Tumour vascularity was assessed by quantitative vascular grading (Chalkley point count) and was related to the localization and intensity of tenascin immunoreactivity. 19 tumours (27.1%) were scored as low, 35 (50%) as medium, and 16 (22.9%) as having a high vascular grade. The positive correlation between the vascular grade and the tenascin immunopositivity in tumour stroma was observed. Our results suggest that tenascin expression may be associated with endothelial cell activation and may play an important role in tumour angiogenesis.

Expression of tenascin, fibronectin, and laminin in rat liver fibrogenesis — a comparative immunohistochemical study with two models of liver injury

The aim of this study was to follow semiquantitatively by immunohistochemical means the alterations of the expression of the hepatic glycoproteins tenascin, fibronectin, and laminin in two different models of chronic liver injury, i.e. thioacetamide-induced liver cirrhosis and fibrosis after bile duct ligation. The tenascin distribution pattern observed during cholostasis-induced liver fibrosis showed some similarities, but also some differences in comparison with the results obtained after TAA intoxication. Most importantly, the data show that tenascin staining was detectable in almost all areas of the chronically injured livers up to 3 and 6 months in bile duct-ligated and chemically-injured livers, respectively. Thus, tenascin does not seem to play only a transient role in the fibrogenetic process as previously suggested. Laminin was strongly stained in proliferating ductules, whereas only a weak continuous distribution was observed along the sinusoidal wall. Furthermore, our findings confirm the role of fibronectin as a pacemaker of fibrosis. Regional differences in the kinetics of the expression of the glycoproteins may reflect local differences in their production by parenchymal or non parenchymal cells or regional patterns of proteolytic activity.