Histology and histopathology Vol.12, nº 2 (1997)
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- PublicationOpen AccessGastric mucosal injury and repair, effect of aging(Murcia : F. Hernández, 1997) Majumdar, A.P.N.; Fligiel, S.E.G.; Jaszewski, R.Although the gastric mucosa of healthy adult animals possesses the inherent capacity to promptly repair (often within 24 h) after a minor to moderate injury, aging appears to diminish its reparative capacity. At least two different repair mechanisms are thought to participate in full repair of the damaged gastric mucosa: the initial rapid process of mucosal restitution begins by migration of viable epithelial cells from gastric pits and glands; the subsequent slower process is replacement of lost cells by cell division. Intracellular events that regulate these processes are poorly understood, nor do we know how they may be affected by aging. However, evidence is accumulating which suggests that a number of gastrointestinal hormones/growth factors, most notably EGF and TGF-a may play a critica1 role in regulating gastric mucosal reparative processes. Since EGF and TGF-a exert their physiological actions by activating the intrinsic tyrosine kinase (Tyr-k) activity of their common receptor, the EGF-R, studies have been performed to assess the role of EGF-R Tyr-k in regulating mucosal reparative processes during aging. Recent data suggest that the age-related decline in mucosal repair after acute injury could in part be due to decreased activation of EGF-R Tyr-k. In addition, polyamines and prostaglandins are also thought to be involved in gastric mucosal reparative processes. Although the involvement of polyamines in gastric mucosal reparative processes during aging has not yet been studied, decreased mucosal prostaglandin levels in the aged are thought to be a causative factor for the increased susceptibility of the mucosa to injury. These and other relevant matters are discussed in the current review.
- PublicationOpen AccessGrowth factors and remyelination in the CNS(Murcia : F. Hernández, 1997) Woodruff, R.H.; Franklin, R.J.M.It is now well established that there is an inherent capacity within the central nervous system (CNS) to remyelinate areas of white matter that have undergone demyelination. However this repair process is not universally consistent or sustained, and persistent demyelination occurs in a number of situations, most notably in the chronic multiple sclerosis (MS) plaque. Thus there is a need to investigate ways in which myelin deficits within the CNS rnay be restored. One approach to this problem is to investigate ways in which the inherent remyelinating capacity of the CNS rnay be stimulated to remyelinate areas of long-term demyelination. The expression of growth factors, which are known to be involved in developmental myelinogenesis, in areas of demyelination strongly suggests that they are involved in spontaneous remyelination. Therefore delivery of exogenous growth factors into areas of persistent demyelination is a potential therapeutic strategy for stimulating remyelination. This review will discuss the evidence that growth factors rnay have a role in promoting CNS remyelination by enhancing the survival and stimulating the proliferation and recruitment of remyelinating oligodendrocytes.
- PublicationOpen AccessThe microanatomy of calcium stores in human neutrophils, Relationship of structure to function(Murcia : F. Hernández, 1997) Pettit, E.J.; Davies, E.V.; Hallett, M.B.As changes in cytosoiic free ca2+ play key roles in coupling responses in neutrophils, it is important to locate and identify ca2+ storage sites within these cells. Here, recent data is presented which highlights the functional link between rnicroanatomical structure and cell signailing function. Fluorescent opticai probes for cytosolic free ca2+ have been used, together with organelle specific markers. We present evidence from conventional fluorescence microscopy, together with ratiometric and confocal laser scanning fluorescence microscopy, which pin-points two celiular locations for ca2+ within the neutrophil; one within the nuclear lobes, and the other towards the ceii periphery. Knowledge of these two locations provides a clear insight into how signailing in this cell type is regulated and provides a framework for explaining how specific stimuli act to produce specific responses.
- PublicationOpen AccessThe alveolar type II cell is a pluripotential stem cell in the genesis of human adenocarcinomas and squamous cell carcinomas(Murcia : F. Hernández, 1997) Ten Have-pbroek, A.A.W.; Benfield, J.R.; Van Krieken, J.H.J.M.; Dijkman, J.H.Studies in a canine bronchogenic carcinoma model indicate that alveolar type 11 cells may differentiate from carcinogen-exposed epithelium of larger bronchi and generate adenocarcinomas with bronchioloalveolar and other growth patterns. In this study, we investigated whether type 11 cells are one of the major proliferating cells (=stem cells) in the genesis of two major subsets of bronchogenic carcinoma in humans. Adenocarcinomas (17 bronchioloalveolar; 3 papillary; and 10 other) and squamous cell carcinomas (n=27) as well as (pre)neoplastic lesions in adjacent bronchi and bronchioles were examined for the presence of type 11 cell markers and cellular proliferation markers (PCNA; Ki-67) using light and electron microscopy and immunohistochemistry. Distinctive features of type 11 cells, which do not depend upon the degree of cell maturity, are the approximately cuboid shape, large and roundish nucleus, cytoplasmic staining for surfactant protein A (SP-A), and presence of multilamellar bodies or their precursory forms. Cells with this phenotype were found in early progressive (i.e., dysplastic, in situ, microinvasive) lesions in conducting airways and in al1 the carcinomas investigated, although with a much greater abundance among glandular lesions compared to squamous lesions. The most consistent sites of type 11 cells were the basal and adjacent epithelial layers. Nuclear PCNA (Ki-67) expression usually predominated in the same region. None of the lesions displayed specific Clara cell features. Our findings strongly suggest that the type 11 cell is a pluripotential stem cell in human lung carcinogenesis. Based on our findings in humans and dogs, we postulate that type 11 tumor stem cells may originate from one of two sources: (1) normal bronchial epithelium (by an oncofetal mechanism of differentiation); and (2) normal alveolar type 11 cells.
- PublicationOpen AccessUltrastructural changes in the synthetic and secretory patterns of pulmonary surfactant following pilocarpine in vivo(Murcia : F. Hernández, 1997) Smith, Dennis M.; Sommers Smith, Sally K.Previous studies have demonstrated that the muscarinic agonist pilocarpine stimulates the secretion of pulmonary surfactant from mammalian alveolar type 11 cells. The results of the present study quantify, via ultrastructural stereologic analysis, this response through 24 hours. The cytoplasmic volume density of lamellar bodies decreases significantly at 0.5 and 4 hours postinjection. This value is increased significantly at 12 hours post-injection. Elements of the secretory apparatus increase significantly at many of the post-injection times. At 12 hours post-injection many of the type 11 cells are quite laden with lamellar bodies, with some appearing surprisingly large. This may be a useful model for continued study of the relationship between synthesis and secretion of pulmonary surfactant.