Histology and histopathology Vol.27, nº12 (2012)

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http://hdl.handle.net/10201/178869

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Open Access
Expression and localization of VEGF receptors in human fetal skeletal tissues
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Marini, Mirca; Sarchielli, Erica; Toce, Mariateresa; Acocella, Alessandro; Bertolai, Roberto; Ciulli, Carlotta; Orlando, Claudio; Sgambati, Eleonora; Vannelli, Gabriella Barbara
During development the vertebrate skeleton is the product of deriving cells from distinct embryonic lineages. The craniofacial skeleton is formed by migrating cranial neural crest cells, whereas the axial and limb skeletons are derived from mesodermal cells. The Vascular Endothelial Growth Factors (VEGFs) / receptors (VEGFRs) system plays an important role in angiogenesis, as well as osteogenesis, during bone development, growth, and remodeling, attracting endothelial cells and osteoclasts and stimulating osteoblast differentiation. Recent evidence has shown that during development VEGFR-3 is also expressed in neural and glial precursors of forebrain and cerebellum, as well as in the eye. In this study, we found that VEGFR-1, VEGFR-2 and VEGFR-3 are expressed in human bone both in fetal and adult life. The gene expression levels were significantly higher in fetal samples especially in mandibles. In addition, higher levels of VEGFR-3 in orofacial district were confirmed by western blotting analysis. We also observed that in fetal mandibular samples VEGFRs colocalized in several osteoblasts, osteoclasts and osteoprogenitor cells. Furthermore, some cells coexpressed VEGFR-3 and ET-1, a marker of neural crest cells. The results demonstrated different expression of VEGFRs in human mandibular and femoral bones which could be correlated to their different structure, function and development during organogenesis. VEGFR-3 might represent a specific signal for ectomesenchymal lineage differentiation during early human development.
Open Access
Proposed mechanism in the change of cellular composition in the outer medullary collecting duct during potassium homeostasis
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Park, Eun-Young; Kim, Wan-Young; Kim, Yu-Mi; Lee, Jeong-Hwa; Han, Ki-Hwan; Weiner, I. David; Kim, Jin
Potassium depletion (K+-D) induces hypertrophy and hyperplasia of collecting duct cells, and potassium repletion (K+-R) induces regression of these changes. The purpose of this study was to examine the time courses of the changes in cellular composition, the origin of intercalated cells (ICs) and the mechanism responsible for these changes. SD rats received K+-depleted diets for 1, 7, or 14 days. After K+-D for 14 days some of the rats received normal diets for 1, 3, 5, or 7 days. In the inner stripe of the outer medulla, K+-D increased significantly the number and proportion of H+-ATPase-positive ICs, but decreased the proportion of H+-ATPase-negative principal cells (PCs). However, proliferation was limited to H+-ATPase-negative PCs. During K+-R, the cellular composition was recovered to control level. Apoptosis increased during K+-R and exclusively limited in H+-ATPase-negative PCs. Double immunolabeling with antibodies to PC and IC markers identified both cells negative or positive for all markers during both K+-D and K+-R. Electron microscopic observation showed that ultrastructure of AE1-positive some cells were similar to AE1-negative some cells during K+-R. LC3 protein expression increased significantly and autophagic vacuoles appeared particularly in PCs on days 14 of K+-D and in ICs on days 3 of K+-R. These results suggest that PCs and ICs may interconvert in response to changes in dietary K+ availability and that autophagic pathways may be involved in the interconversion.
Open Access
Fluorescence in situ hybridization for ambiguous melanocytic tumors
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Gammon, Bryan; Gerami, Pedram
The large majority of melanocytic lesions can be reliably classified as either benign or malignant based upon morphology alone, but a minority of lesions remains difficult to classify by traditional histologic methods. Recently, a panel of fluorescence in situ hybridization (FISH) probes targeting loci on chromosomes 6 and 11 has emerged as a powerful tool to discriminate melanoma from nevi. This has been validated in numerous difficult diagnostic scenarios. In addition, this same FISH panel has been shown to provide independent prognostic information in traditional melanomas. There is accumulating evidence that FISH targeting these loci as well as several other key chromosomal loci such as 9p21 and 8q24 can provide valuable prognostic information in histologically ambiguous melanocytic tumors. However, since the vast majority of atypical spitz tumors have an indolent course, larger studies including adequate numbers of cases with adverse events is necessary to provide sufficient proof of its role in clinically relevant cases. In this review, we discuss the current literature and studies to date on this topic.
Open Access
Role of extracellular matrix remodelling in adipose tissue pathophysiology. Relevance in the development of obesity
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Catalán, Victoria; Gómez-Ambrosi, Javier; Rodríguez, Amaia; Frühbeck, Gema
Adipose tissue responds dynamically to alterations in nutrient excess through adipocyte hypertrophy and hyperplasia, followed by increased angiogenesis, immune cell infiltration, extracellular matrix (ECM) overproduction, and thus, increased production of proinflammatory adipokines during the progression of chronic inflammation. Adipose tissue remodelling is an ongoing process that is pathologically accelerated in the obese state in large part mediated by ECM proteins and proteases. The ECM is subject to major modifications by adipocytes and other cell types that are infiltrated in the adipose tissue, such as macrophages and vascular cells. In obesity, unusual expression of ECM components and fragments derived from tissue-remodelling processes can influence immune cell recruitment and activation, actively contributing to inflammation. ECM turnover requires a tightly regulated balance between the synthesis of the components and their proteolysis, mainly by fibrinolytic systems and matrix metalloproteases (MMPs). In this review, we discuss the key cellular steps that lead to adipose tissue remodelling and the main molecular mechanisms and mediators in this process. We highlight the importance of hypoxia and angiogenesis in the adipose remodelling process, as well as the cross-talk between adipocytes, macrophages and ECM components
Open Access
Fluoxetine may worsen hyperoxia-induced lung damage in neonatal rats
(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Porzionato, Andrea; Zaramella, Patrizia; Macchi, Verónica; Grisafi, Davide; Salmaso, Roberto; Baraldi, Maura; Fornaro, Enrica; Tassone, Evelyn; Masola, Valentina; Onisto, Maurizio; Chiandetti, Lino; De Caro, Raffaele
Fluoxetine shows controversial lung effects as it prevents pulmonary hypertension in adult rats but exposure during gestation causes pulmonary hypertension in neonatal rats. In the present study, we tested the null hypothesis that the antidepressant drug fluoxetine does not modify the development of bronchopulmonary dysplasia (BPD) in neonatal rats. Experimental categories included I: room air (controls) with daily injection of saline; II: room air with daily injection of 10 mg/kg fluoxetine, i.p., during two weeks; III: 60% oxygen with daily injection of saline; and IV: 60% oxygen with daily injection of 10 mg/kg fluoxetine, i.p., during two weeks. Hyperoxia resulted in significant reduction in alveolar density and an increase in pulmonary endocrine cells, as well as increases in muscle layer areas of bronchi and arteries. Fluoxetine treatment generated a further increase in muscularisation and did not significantly modify the hyperoxia-induced reductions in alveolar density and increases in the endocrine cells. In hyperoxia, Real-Time PCR showed a lower pulmonary expression of vascular endothelial growth factor (VEGF) with no significant changes in the expression of matrix metalloproteinases (MMP) 2 and 12. Fluoxetine did not affect VEGF or MMP-2 expression but it significantly increased MMP-12 mRNA in both normoxic and hyperoxic groups. Zymographic analysis of MMP-2 activity in bronchoalveolar fluid showed a significantly reduced MMP-2 activity in hyperoxia, while fluoxetine treatment restored MMP-2 activity to levels comparable with the normoxic group. In conclusion, our data show that fluoxetine may worsen bronchial and arterial muscularisation during development of BPD and may up-regulate MMP expression or activity.

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