The aim of this study was to evaluate prognostic and/or diagnostic factors of canine mammary tumors by immunohistochemically analyzing the expression of alpha basic crystallin (alphaB-c). For this, formalin-fixed, paraffin-embedded blocks of 51 naturally-occurring canine mammary tumors (11 benign and 40 malignant) were used. Tissue from eight normal canine mammary glands were served as a control. Immunohistochemically, in the control mammary tissues, a few luminal epithelial cells were alphaB-c positive but myoepithelial cells were negative. In benign or simple type malignant tumors, alphaB-c expression was observed in luminal epithelial cells while the myoepithelial basal cells were negative. In benign or complex type malign tumors, positive staining was predominantly found in the cytoplasm of epithelial cells. Immunoreactivity of alphaB-c was also observed in neoplastic myoepithelial cells. Statistically, the number of cells immunolabeled with alphaB-c was found to be significantly different among tissues from normal canine mammary glands, benign lesions, and malignant tumors (p < 0.05). alphaB-c immunoreactivity was higher in malignant tumors than the control mammary tissues (p < 0.001). Data obtained in the current study revealed a strong association between high expression levels of alphaB-c and primary mammary gland tumors in canines.
Animals ; Dog Diseases/*metabolism ; Dogs ; Female ; Immunohistochemistry/veterinary ; Logistic Models ; Mammary Neoplasms, Animal/*metabolism ; alpha-Crystallins/*biosynthesis

alphaB-crystallin is the structural protein of vertebrate lens, which is widely expressed in non-lens tissue. As one of the heat shock protein family members, alphaB-crystallin possesses biological properties of molecular chaperones and anti-apoptotic effects. Multi-factor injuries, such as retinopathy, inflammation and nervous system diseases, have a closely relationship with alphaB-crystallin. This paper reviews the research progress of the expression and mechanism of alphaB-crystallin in retina and extraocular tissues and organs.
Crystallins ; Gene Expression Regulation, Developmental ; Heat-Shock Proteins/metabolism* ; Humans ; Lens, Crystalline ; Retina ; alpha-Crystallin B Chain/metabolism*

Bietti's crystalline retinopathy is a rare form of tapetoretinal degeneration characterized by yellow, polygonal, glistening intraretinal crystals in the posterior pole and in the superficial paralimbal cornea, which may be due to a systemic abnormality of lipid metabolism, and has been to have a autosomal recessive pattern.Also lots of the reports described similar cases without any corneal changes. 56 years-old female with complaint of progressive visual decrease had corrected visual acuity of 0.1 in her right eye and 1.0 in her left eye.Yellow intraretinal crystals with retinal pigment epithelial (RPE)dystrophy and choroidal sclerosis were noticed without any corneal changes.During follow-up for thirty months, visual acuity gradually decreased to counting fingers in her right eye and 0.7 in her left eye, and RPE degeneration and choroidal sclerosis worsened with no change in intraretinal crystals.
Choroid ; Cornea ; Crystallins* ; Female ; Fingers ; Follow-Up Studies ; Humans ; Lipid Metabolism ; Middle Aged ; Retinaldehyde ; Retinitis Pigmentosa ; Sclerosis ; Visual Acuity

A 62-year-old female visited our clinic with progressively decreased vision in both eyes beginning 12 years prior. Idiopathic corneal opacity in all layers of the cornea was found in both eyes. One year later, we performed penetrating keratoplasty on the undiagnosed right eye. During post-surgical follow-up, corneal edema and stromal opacity recurred, and penetrating keratoplasty was performed two more times. The patient's total serum protein level, which had previously been normal, was elevated prior to the final surgery. She was diagnosed with monoclonal gammopathy of undetermined significance. We made a final diagnosis of monoclonal gammopathy-associated crystalline keratopathy after corneal biopsy. Monoclonal gammopathy-associated crystalline keratopathy is difficult to diagnose and may lead to severe visual loss. A systemic work-up, including serologic tests like serum protein or cholesterol levels, is needed in patients with unexplainable corneal opacity.
Corneal Edema/etiology/*metabolism/physiopathology/surgery ; Corneal Neovascularization/etiology/*metabolism/physiopathology/surgery ; Corneal Opacity/etiology/*metabolism/physiopathology/surgery ; Crystallins/*metabolism ; Female ; Humans ; Keratoplasty, Penetrating ; Microscopy, Electron ; Middle Aged ; Monoclonal Gammopathy of Undetermined Significance/*complications/pathology ; Reoperation ; Visual Acuity

PURPOSE: Ischemia-reperfusion injury (I/R injury) is known not only to induce hypoxic and oxidative stress, but also to cause retinal degeneration in rats. Crystallins, known to inhibit the formation of reactive oxygen species, reduce apoptotic cell death. Our goal was to clarify not only the role of I/R injury-mediated crystallins, but also to evaluate the correlation of these compounds to anti-inflammation in the vitreous body. METHODS: Twenty-four Sprague-Dawley rats were used in this study. We induced I/R injury by clamping the optic nerve for 30 minutes and then releasing it. The vitreous bodies were obtained from the experimental and control subjects 24, 48, and 72 hours after I/R injury. Two-dimensional electrophoresis was performed, and the targeted spots were further investigated using matrix-assisted laser desorption-ionization time-of-flight mass spectrometry, spectrophotometry, Western blotting, and histological examination. RESULTS: After I/R injury, 23 spots were identified as crystallins. The betaB2 crystallins were transcriptionally and post-translationally regulated, whereas the alphaB crystallins were controlled by post-translational modifications in the vitreous bodies of the rats. The total amounts of alphaA and beta crystallins (including isotypes of beta crystalline) had increased 48 hours after injury. The phosphorylation of alphaB crystallin (at serine residues 19, 45, and 59) was significantly increased 48 hours later, whereas phosphorylation of ERK1/2 showed the greatest decrease. CONCLUSIONS: During hypoxic and oxidation stress, our results suggest that phosphorylated alphaB crystalline inhibits RAS, resulting in the inactivation of ERK1/2. The phosphorylation of alphaB crystallin may be associated with the inflammatory suppression in the vitreous body via the I/R injury model system.
Animals ; Blotting, Western ; Oxidative Stress ; Phosphorylation ; Protein Processing, Post-Translational ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/*metabolism/pathology ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Vitreous Body/*metabolism/pathology ; beta-Crystallins/*metabolism