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Laminin Chains (laminin + chain)
Selected AbstractsStromal laminin chain distribution in normal, hyperplastic and malignant oral mucosa: relation to myofibroblast occurrence and vessel formationJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 4 2010Marcus Franz J Oral Pathol Med (2010) 39: 290,298 Background:, The contribution of stromal laminin chain expression to malignant potential, tumour stroma reorganization and vessel formation in oral squamous cell carcinoma (OSCC) is not fully understood. Therefore, the expression of the laminin chains ,2, ,3, ,4, ,5 and ,2 in the stromal compartment/vascular structures in OSCC was analysed. Methods:, Frozen tissue of OSCC (9× G1, 24× G2, 8× G3) and normal (2×)/hyperplastic (11×) oral mucosa was subjected to laminin chain and ,-smooth muscle actin (ASMA) immunohistochemistry. Results were correlated to tumour grade. The relation of laminin chain positive vessels to total vessel number was assessed by immunofluorescence double labelling with CD31. Results:, Stromal laminin ,2 chain significantly decreases and ,3, ,4, ,5 and ,2 chains and also ASMA significantly increase with rising grade. The amount of stromal ,3, ,4 and ,2 chains significantly increased with rising ASMA positivity. There is a significant decrease in ,3 chain positive vessels with neoplastic transformation. Conclusions:, Mediated by myofibroblasts, OSCC development is associated with a stromal up-regulation of laminin isoforms possibly contributing to a migration promoting microenvironment. A vascular basement membrane reorganization concerning ,3 and ,2 chain laminins during tumour angioneogenesis is suggested. [source] Remodeling of extracellular matrix at ovulation of the bovine ovarian follicleMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 10 2006H.F. Irving-Rodgers Abstract Using immunohistochemistry and RNA analyses we examined the fate of components of a newly identified matrix that develops between granulosa cells (focimatrix, abbreviated from focal intraepithelial matrix) and of the follicular basal lamina in ovulating bovine ovarian follicles. Pre- and postovulatory follicles were generated by treatment with estradiol (Day 1), progesterone (Days 1,10), and prostaglandin analogue (Day 9) with either no further treatment (Group 1, n,=,6) and or with 25 mg porcine LH (Day 11, Group 2, n,=,8 or Day 10, Group 3, n,=,8) and ovariectomy on Day 12 (12,14 hr post LH in Group 2, 38,40.5 hr in Group 3). In the time frame examined no loss of follicular basal lamina laminin chains ,2 and ,1 or nidogen 1 was observed. In the follicular basal lamina collagen type IV ,1 and perlecan were present prior to ovulation; after ovulation collagen type IV ,1 was discontinuously distributed and perlecan was absent. Versican in the theca interna adjacent to the follicular basal lamina in preovulatory follicles was not observed post ovulation, however, the granulosa cells then showed strong cytoplasmic staining for versican. Expression of versican isoforms V0, V1, and V3 was detected at all stages. Focimatrix was observed in preovulatory follicles. It contained collagen type IV ,1, laminins ,2 and ,1, nidogen 1 and perlecan and underwent changes in composition similar to that of the follicular basal lamina. In conclusion focimatrix and the follicular basal lamina are degraded at ovulation. Individual components are lost at different times. Mol. Reprod. Dev. © 2006 Wiley-Liss, Inc. [source] The neuromuscular junction microenvironment in extraocular and limb musclesACTA OPHTHALMOLOGICA, Issue 2009F PEDROSA DOMELLOF Purpose To characterise the components of the neuromuscular junction (NMJ) in normal and pathological extraocular muscles (EOMs) and to assess the dynamics of progressive denervation. Methods Limb and EOM samples from 11 controls,8 ALS patients and from transgenic mice with SOD1 mutations (D90A, G93A) paralleling familiar ALS were processed for immunocytochemistry with antibodies against Schwann cell markers (S-100, p75, GFAP), gangliosides GD1b and GQ1b/GT1a, neurotrophic factors (BDNF, GDNF, NT-3, NT-4) and their receptors, parvalbulmin, nestin, desmin and laminin chains. Results The NMJs of normal EOMs had a different cytoskeleton composition. Differences in the expression of gangliosides GD1b and GQ1b/GT1a, Schwann cell marker S-100, agrin and nestin at the NMJs were noted in the human ALS EOMs. Parvalbumin was absent or scarce in EOM nerve trunks of ALS patients. The analysis of the time aspects of denervation in the animal models is ongoing. Conclusion The human EOMs in late stages of ALS and the EOMs of the transgenic mice show signs of denervation, although these muscles appear remarkably well preserved. High levels of parvalbumin, proposed to be protective for oculomotor neurons in ALS, are not apparent in advanced stages of the disease. The identification of similar endpoints in the EOMs of patients with D90A mutation and the ALS transgenic mice carrying the same mutation indicates that this is a useful model to study the temporal aspects of progressive denervation in the EOMs, to explore aspects of muscle-nerve interplay that protect the EOMs in motoneuron disease and to gain further knowledge useful for the development of selective tools to modulate eye muscle function in the treatment of strabismus. [source] | ||||||||||