Disease relevance of DES

• Clomiphene citrate decreased the adverse effects of DES on appetite and body weight, and sharply decreased the gains in the pituitary and uterine weights from 243 to 80% and 59 to 14%, respectively [1].
• Once daily, 7 bitches were given diethylstilbestrol (DES; 5 mg, PO) until sanguineous vaginal discharge and vulvar edema were observed (designated as day 1 of proestrus) and for 2 days thereafter [2].
• This is especially unfortunate in view of the potential toxicity of DES to small animals [3].
• Myofibrillar myopathy with desmin accumulation in a young Australian Shepherd dog [4].
• Among muscle actin- and vimentin-positive CHP, one case could be reclassified as leiomyosarcoma because it was desmin-positive, two cases expressed lysozyme, and nine cases expressed S-100 protein [5].

High impact information on DES

• Germinal matrix sections were also stained for antibodies to alpha-smooth muscle actin, collagen IV, collagen V, desmin, factor VIII-related antigen, fibronectin, glial fibrillary acidic protein, laminin, transferrin, and vimentin [6].
• During the proliferative phase of healing (3-7 days) alpha-smooth muscle actin (alpha-SMAc) expression was markedly increased in the fibrotic areas. alpha-SMAc predominantly localized in myofibroblasts which were vimentin positive, smooth muscle myosin, calponin and desmin negative [7].
• From the canine DES gene BAC clones, a polymorphic microsatellite marker was isolated [8].
• Using data deposited in the NCBI trace archive and GenBank, the canine DES gene DNA sequence was assembled and seven single nucleotide polymorphisms (SNPs) were identified [8].
• A missense mutation in the desmin gene (DES) causes DCM in a human family [8].

Chemical compound and disease context of DES

• Sections of formalin-fixed, paraffin-embedded canine leiomyomas, leiomyosarcomas, or fibrosarcomas were examined by immunohistochemical methods for the presence of desmin [9].

Biological context of DES

• Availability of the microsatellite marker, SNPs and DNA sequence reported in this study enable fast evaluation of the DES gene as a DCM candidate gene in other dog breeds with DCM occurrence [8].
• We have isolated bacterial artificial chromosome clones (BACs) containing the canine DES gene and determined the chromosomal location by fluorescence in situ hybridization (FISH) [8].
• The microsatellite marker and four informative desmin SNPs were typed in a Dobermann family with frequent DCM occurrence, but the disease phenotype did not associate with a desmin haplotype [8].
• Our findings indicate that induction of Cx37 and reduction of desmin precede the phenotypic changes of SMCs, which are characterized by down-regulation of alpha-SM actin, calponin and vinculin, and the formation of a neointima [10].
• The 7 bitches treated with DES had a mean proestrus period of 7.7 days and a mean estrus period of 5.7 days up to the day of mating [2].

Anatomical context of DES

• Presence of Cx37 and lack of desmin in smooth muscle cells are early markers for arteriogenesis [10].
• There were no significant differences in the amount of cytoskeletal intermediate filament proteins, desmin and vimentin between sensitized and control TSM [11].
• Actin, myosin, desmin, filamin, talin, vinculin, and alpha-actinin in the basilar artery were studied by immunoblotting [12].
• Vascular mural cells in healing infarcts undergo phenotypic changes, showing minimal expression of desmin during the proliferative phase (1 hr occlusion/7 days reperfusion) but in the mature scar (8 weeks reperfusion) acquire a phenotype similar to that of vascular smooth muscle cells in control areas [13].
• In this study, the stromal cell type was determined by immunohistochemical labelling with antibodies to desmin, vimentin and alpha-smooth muscle actin (alpha-SMA) during the progressive and regressive stages of spontaneous CTVT [14].

Associations of DES with chemical compounds

• A further group of ten animals received clomiphene citrate (2 mg/kg/day) and DES (6 mg/kg/day), while two groups, each of ten animals, acted as controls [1].
• Two groups, each of ten female rats, were orally dosed with the synthetic oestrogens diethylstilboestrol (DES; 6 mg/kg day) and hexoestrol (60 mg/kg/day) for 6 wk [1].
• Serum estradiol-17 beta and progesterone concentrations remained at base line during the period of DES treatment [2].
• In the KCI and serotonin groups, slight degradation was usually observed in filamin, often in alpha-actinin, and occasionally in actin, whereas desmin, vinculin, and metavinculin were not degraded [12].
• Formalin-fixed histologic and acetone-fixed cytologic preparations from 87 surgically removed subcutaneous and soft tissue canine tumors were examined for immunoreactivity to cytokeratin, desmin, and vimentin [15].

Other interactions of DES

• Low flow samples exhibited enhanced expression of GAPDH (+89%) and phosphoglycerate kinase (+100%), whereas hydroxyacyl-CoA dehydrogenase, electron transfer flavoprotein, myoglobin, and desmin were decreased [16].
• Consistent with their osteoblastic lineage and malignant phenotype, all cell lines were immunoreactive to vimentin, osteopontin, PCNA, p53, MMP-2 and MMP-9, while they were negative for cytokeratin, desmin, SMA, Factor VIII, NSE, GFAP, Rb and p21 protein [17].
• The panel included vimentin, desmin, Myo D1, smooth muscle actin, cytokeratin, S100, von Willebrand factor (factor VIII), Mac 387, CD3, major histocompatibility complex (MHC) class II, and CD79a [18].
• Cell identity was established by immunohistochemistry with factor VIII antibody, Ulex europaes, leukocyte common antigen, and antibodies to alpha-actin, desmin, vimentin, and basic fibroblast growth factor [19].

Analytical, diagnostic and therapeutic context of DES

• We used confocal microscopy with antibodies against connexin37 (Cx37), alpha-smooth muscle actin (alpha-SM actin), calponin, desmin and vinculin [10].
• Muscle biopsies evaluated by light and electron microscopy, and immunohistochemistry revealed the presence of a myofibrillar myopathy with accumulation of desmin and other proteins [4].
• BMSCs also expressed alpha-smooth muscle actin by immunohistochemical staining and Western blotting, but did not express desmin or myosin [20].
• Our results support the hypothesis of a pericytic origin of CHP, and suggest that muscle actin, desmin, vimentin, and lysozyme could be useful for the differential diagnosis of canine spindle cell tumors, but not all these neoplasms can be identified with these tumor tissue markers [5].
• Spindle cell tumours were stained by Masson trichrome, Orcein-Van Gieson and labelled immunohistochemically (vimentin, desmin, smooth muscle actin, protein S100, glial fibrillar acid protein, CD117 and MIB-1) and the histological grade, mitotic index, nuclear size and cellular density were also assessed [21].

References