Histology and histopathology Vol.34,nº12 (2019)
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- PublicationOpen AccessCytochrome c1 as a favorable prognostic marker in estrogen receptor-positive breast carcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Sato, Ai; Miki, Yasuhiro; Takagi, Kiyoshi; Yoshimura, Ayano; Hara, Mizuki; Ishida, Takanori; Sasano, Hironobu; Suzuki, TakashiBackground. Cytochrome c1 (CYC1) is a heme-containing subunit of mitochondria complex III and is mainly involved in cellular energy production. A recent study has demonstrated that CYC1 was overexpressed in breast carcinoma tissues and induced proliferation, migration and invasion of estrogen receptor (ER)-negative breast carcinoma cells. However, the clinical significance of CYC1 protein remains largely unclear in invasive breast carcinoma, and biological functions of CYC1 have not been reported in ER- positive breast carcinoma cells. Materials and methods. We immunolocalized CYC1 in 172 invasive breast carcinomas and evaluated its clinical significance according to the ER-status. Subsequently, we examined the effects of CYC1 on proliferation, glycolysis and chemosensitivity to paclitaxel, which is one of the most common chemotherapeutic agents in breast cancer, in ER-positive breast carcinoma cells (MCF7 and T47D). Results. CYC1 immunoreactivity was detected in 47% of ER-positive cases and 30% of ER-negative cases. Immunohistochemical CYC1 status was inversely associated with Ki67 in ER-positive cases, and it was a significantly favorable prognostic factor for both disease-free and breast cancer-specific survival of the patients. On the other hand, no significant association was detected between CYC1 status and clinico- pathological factors in ER-negative cases. In in vitro experiments, MCF7 and T47D cells transfected specific siRNA for CYC1 significantly increased cell proliferation activity, L-lactate production and cell viability after paclitaxel treatment. Conclusion. These results suggest that CYC1 inhibits cell proliferation, glycolytic activity and increases chemosensitivity to paclitaxel in ER-positive breast carcinoma cells and that CYC1 status is a potent favorable prognostic factor in ER-positive breast cancer patients
- PublicationOpen AccessHGSNAT enzyme deficiency results in accumulation of heparan sulfate in podocytes and basement membranes(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Nagel, Lauren; Oliveira, Regiana; Pshezhetsky, Alexey V.; Morales, Carlos R.ucopolysaccharidosis III type C is a lysosomal storage disorder caused by the accumulation of heparan sulfate in lysosomes. The disorder occurs due to Heparan Acetyl-CoA: α-glucosaminide N- acetyltransferase (HGSNAT) deficiency, an enzyme which typically catalyzes the transmembrane acetylation of heparan sulfate, a basement membrane component. When the gene encoding this enzyme is mutated, it cannot perform the processing of heparan sulfate, leading to un-acetylated heparan sulfate build-up in the lysosomes of cells, causing a storage disorder. This defect has been studied primarily in brain and liver cells, but its effect on the structural integrity of the glomerulus is poorly known. The present study focuses on the effect of Hgsnat gene inactivation and heparan sulfate toxicity on the integrity of the renal corpuscle. This cortical structure was chosen because of its abundance of basement membranes and heparan sulfate as well as the renal corpuscle’s physiological importance in glomerular filtration. Light microscopy, electron microscopy, and immunocytochemistry of genetically modified mice revealed a buildup of lysosomes in the podocytes, suggesting that these cells are responsible for the processing of glomerular basement membranes
- PublicationOpen AccessPotential therapeutic effect of SO2 on fibrosis.(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Wang, Xin Bao; Cui, Hong; Du, Jun BaoFibrosis is a pathological feature of most chronic diseases and leads to the dysfunction of various organs. However, there is currently no effective method for treating fibrosis. In recent years, a small gas, sulfur dioxide (SO2), which can be generated endogenously in mammals, has been found to have vasorelaxation activity, improve cardiac function and decrease myocardial injury. Endogenous SO 2 also mediates the process of fibrosis. Inhibition of endogenous SO 2 can aggravate small pulmonary artery remodeling and abnormal collagen accumulation. SO 2 treatment significantly improves pulmonary fibrosis and pulmonary arterial remodeling. Overexpression of the key enzymes associated with endogenous SO 2 generation, aspartate aminotransferase (AAT) 1 and AAT2, mimics the effect of SO 2 on the down-regulation of collagen synthesis, while AAT1 or AAT2 knockdown aggravates abnormal collagen accumulation in vascular smooth muscle cells (VSMCs). SO 2 also improves myocardial fibrosis induced by myocardial infarction or diabetes in rats, and inhibits myocardial fibroblast proliferation and migration by the extracellular signal- regulated protein kinase pathway. The mechanisms underlying the inhibition of fibrosis by SO 2 are related to its antioxidant effect, anti-inflammation effect, improvement in cardiac function, and cell proliferation inhibition. Therefore, SO 2 has a potential therapeutic effect on fibrosis.
- PublicationOpen AccessAbnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Wei, Ting; Shalin, Sara; Draper, Elizabeth; Miller, Emily; Zhang, Haihong; Sun, Ravi; Lee, Madison; Albert, Gregory; Richter, Gresham T.Background. Vascular malformations are characterized by anomalous vascular channels with fragile walls and a propensity to bleed. Arteriovenous malformations (AVMs) in particular have disorganized vascular spaces with intervening fibrosis. Characterization of the structural abnormalities of these vessels has not been comprehensively evaluated. We hypothesize that AVMs are likely to demonstrate altered elastic and collagen fiber organization and distribution, reflecting their fragility, vascular instability, and abnormal development. Methods. Fifteen AVMs were histologically evaluated by H&E, elastin and trichrome staining. To identify potential differences between extracranial and intracranial AVMs, 5 AVMs were harvested from the brain (n=5) and 10 from extracranial sites involving the skin and deep soft tissue (n=10). Results. The elastin staining demonstrated reduplication, fragmentation and disruption of internal elastic lamina as well as irregular thickness, and inconsistent vascular density of all AVM specimens. Trichrome staining revealed thickening of the intimal layers of AVM arteries and demonstrated an irregular thickness of venous walls within the malformation and some areas of medial degeneration. Intracranial AVMs are characterized by more intramural inflammation with predominant neutrophil and lymphocyte infiltration. In contrast, extracranial AVMs display more extravascular inflammation with mast cell and neutrophil infiltration. Microvascular proliferations intervening between larger blood vessels were also noted in both types of AVMs, but more obvious in extracranial AVMs. Conclusion. These observed histologic anomalies of AVMs demonstrate disorganized deposition of elastin and collagen that point to the clinically observed vascular instability and fragility of these lesions
- PublicationOpen AccessMolecular evidence of tissue remodeling in an animal model of heart failure(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Silva Nascimento, Lais; Martins Tedesco, Larissa; Silva Araujo, Natiele; Marinho Priviero, Fernanda Bruschi; Claudino, Mario Angelo; Gonçalves Priolli, Denise; Rocha, ThalitaHeart failure (HF) is the final common pathway of many cardiovascular diseases. Metalloproteinases and their inhibitors, such as MMP9 and TIMP-1, assist in maintaining the extracellular matrix, leading to tissue remodeling observed after HF. Previous studies have shown that L-Arginine (LA) appears to have beneficial effects for the treatment of HF, contributing to vasodilation, the reestablishment of the endothelial function and an increase in muscle contractile force. This study analyzed heart tissue remodeling in an animal model of HF induced by aortocaval fistula (ACF) and submitted to LA treatment. After 4 weeks of ACF, animals were treated with LA for 4 weeks (SHAM-LA, HF-LA) or for 8-12 weeks with saline (SHAM, HF8, HF12). Rats were euthanized and the hearts removed for histological processing. The samples were stained with Hematoxylin-Eosin (HE), Masson’s Thichome (MT), or submitted to immunohistochemistry (IHC) for MMP9 and TIMP-1. Light microscopy analysis showed cardiac striated muscle without fibrosis in all experimental groups. Immunostaining of MMP9 and TIMP-1 were positive for all experimental groups. LA administration significatively reduced MMP9 content after HF. These data indicate molecular changes in metalloproteinases expression prior to tissue remodeling and point out LA as an adjuvant therapy to pharmacological treatment of patients with HF.
- PublicationOpen AccessThe combined effect of honey and olive oil against methotrexate mediated hepatotoxicity in rats: A biochemical, histological and immunohistological study(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Alturkistani, Hani A.; Abuzinadah, Osama A.H.; Kelany, Abdelhakeem M.; Aziz, Gamal S. Abd El; Alrafiah, Aziza R.Background. Honey and olive oil are natural products that have high nutritional values, and therapeutic properties. Cytotoxic drugs, like methotrexate (MTX) are used to treat malignancies in tumour cells; however, these drugs also have serious side effects that could threaten the patient's life. Aim. To evaluate the potential protective effects of honey and olive oil, administered alone or together, against MTX-induced hepatotoxicity in rats. Methods. Adult male albino rats were divided: Group I: negative control (n=8); II: honey (daily by oral 1.2 g/kg bwt (n=8), III: olive oil (1 ml/day) (n=8), IV: single intraperitoneal injection of MTX (20 mg/kg bwt) (n=8), V: diluted honey for 3 days before injection of MTX (n=8), Group VI: olive oil for 3 days before injection of MTX (n=8), Group VII: both honey and olive oil for 3 days before injection of MTX (n=8). After treatment, rats were sacrified and blood samples were collected to determine liver function parameters, liver tissue used to measure the oxidative (malondialdehyde), antioxidative parameters (superoxide dismutase, catalase and glutathione peroxidase), histological and immunohistochemical techniques. Results. The administration of honey and olive oil exerted a protective effect against MTX-induced hepatotoxicity, as demonstrated by the normalization of the liver enzymes, proteins and total bilirubin and by the histopathological and immunohistological changes observed in the livers. Both agents also reversed the oxidative damage in the liver by decreasing level of MDA levels and increasing the antioxidant related by enzymes in the liver homogenates compared to the control rats. These effects were more evident when the two agents were administered together. Conclusion. The combined intake of honey and olive oil could be hepatoprotective. Co-administration of these agents might form an effective adjuvant therapy and minimize side effects of chemoherapy in cancerous patients.
- PublicationOpen AccessPreliminary analysis of the association of TRPV1 to the formation of Marfan syndrome aneurysms(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Soto, María Elena; Soria Castro, Elizabeth; Guarner Lans, Verónica; Martínez Guzmán, Andrés; Morales Marín, Cesar Amilcar; Martínez Zavala, Karla Susana; Pérez Torres, IsraelMarfan syndrome (MS) is an autosomal dominant disorder of connective tissue that is caused by mutations in the fibrillin-1 (FBN-1) gene that cause degeneration of the artery. It is accompanied by endothelial dysfunction. The potential transient receptor of the vanilloid subfamily 1 (TRPV1) ion channel plays an important role in endothelial vascular functioning. Here we determine the association of the presence TRPV1 in aortic aneurysm with dilation and dissection of the artery in MS patients. Histological sections of aortic aneurysm tissue obtained by the surgical procedure of Bentall and De Bono or David, were processed by immunohistochemistry with antibodies against ICAM, VCAM, iNOS, eNOS, TRPV1 and TNF- α and the immunolabelling area was determined. We also measured the NO 3- /NO 2- ratio in the aortic tissue. C-reactive protein and HDL in plasma were quantified. A significant increase in iNOS, TRPV1, VCAM (p≤0.05), NO 3- /NO 2- ratio (p=0.002) and a significant decrease in eNOS (p=0.04) and HDL in plasma (p=0.02) in the MS vs. the C group were found. Conclusion: TRPV1 is over-expressed in aortic tissue from MS patients and can be associated with increases in iNOS, VCAM and a decrease in eNOS. These changes might contribute to the progression and rupture of the thoracic aneurysm.