Histology and histopathology Vol.14, nº 2 (1999)
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- PublicationOpen AccessT-2 toxin-induced acute skin lesions in 3 Wistar-derived hypotrichotic WBNIILA-Ht rats(Murcia : F. Hernández, 1999) Albarenque, S.M.; Shinozuka, J.; Iwamoto, S.; Nakayama, Hiroyuki; Doi, K.Acute lesions in the dorsal skin topically applied with T-2 toxin (10 p1 of 0.5 mg/ml-solution to lcm2) were examined in Wistar-derived hypotrichotic WBNIILA-Ht rats up to 24 hours after treatment (24HAT). In the epidermis, depression of basal cell proliferating activity was detected at 3HAT by immunostaining for proliferating cell nuclear antigen (PCNA), and the percentage of PCNA-positive basal cells decreased thereafter. At 12HAT, in addition to intracytoplasmic edema of spinous cells, acidophilic degeneration of basal cells characterized by shrinkage of cell body with acidophilic cytoplasm and pyknotic or karyorrhectic nuclei became prominent. Most of these nuclei were positive for TUNEL which is a widely used immunostaining for the in situ detection of fragmented DNA, i.e. apoptosis, and the percentage of TUNELpositive basal cells increased thereafter. The nuclei of these basal cells also showed ultrastructural changes characteristic for apoptosis. On the other hand, in the dermis, infiltration of inflammatory cells including mast cells started at 3HAT and increased thereafter. In addition, capillary and small vessel endothelial degeneration developed at 6HAT and progressed thereafter. These results suggest that T-2 toxin directly affects the epidermis and produces apoptosis in basal cells.
- PublicationOpen AccessRegulation of tumor cell invasion by extracellular matrix(Murcia : F. Hernández, 1999) Crowe, D.L.; Shuler, C.F.The ability of malignant tumor cells to invade normal surrounding tissue contributes in large part to the significant morbidity and mortality of these cancers. The process of invasion involves adherence of the tumor cells to the extracellular matrix (ECM), degradation of matrix components, and movement of the cell body. Attachment to ECM molecules is mediated by the integrin family of extracellular matrix receptors. Integrins are a large family of heterodimeric proteins which transduce a variety of signals from the ECM. Ligand occupancy is critical for activation of integrin signaling. This signaling may occur via several different pathways. One of the best characterized of these pathways is the mitogen activated protein kinase (MAPK) cascade. This serial phosphorylation of substrate proteins terminates in activation of transcription factors which regulate expression of target genes. Many of these genes are critical for extracellular matrix degradation or cell migration. Among these are the matrix metalloproteinases (MMPs), a large family of ECM-degrading enzymes. Regulatory elements in the promoters of MMPs have been characterized, providing insight into how MMP expression is controlled. This review focuses on mechanisms by which the ECM regulates tumor cell invasion through integrin signaling via the MAPK pathway using MMP expression as the model.
- PublicationOpen Accesslmmunohistochemical analysis for cell proliferation-related protein expression in small cell carcinoma of the esophagus a comparative(Murcia : F. Hernández, 1999) Okudela, K.; Ito, T.; Kameda, Y.; Nakamura, N.; Kitamura, H.Small cell carcinoma is a rare neoplasm in the esophagus. To evaluate cell proliferation activity and its underlying mechanisms in this tumor, we examined immunohistochemically 5 cases of small cell carcinoma of the esophagus (SCCE) for expressions of tumor suppressor proteins, oncoproteins and cell proliferation markers including p53, p21WAF1/C1P1r,e tinoblastoma (Rb) protein, bcl-2, Ki-67 and PCNA, and compared the results with those of 5 cases of small cell carcinoma of the lung (SCCL) and 10 cases of squamous cell carcinoma of the esophagus (SQCE). The prevalence and labeling index of p53-immunoreactivity tended to be higher in SCCE (415; 56.6%) and SCCL (415; 79.9%) than in SQCE (6110; 48.8%). Expression of p21wAFl/C1P1w as observed in 2 of 10 cases of SQCE. In contrast, its expression could not be detected in any cases of SCCE and SCCL examined. Expression of Rb protein was observed in 9 out of 10 cases of SQCE, but not in any cases of SCCE and SCCL. SCCE and SCCL showed more frequent and intense immunoreactivity for bcl-2 than SQCE. In expression of cell proliferation markers (Ki-67 and PCNA), no remarkable difference was observed among SCCE, SCCL and SQCE. These results suggest that SCCE and SCCL could share some genetic alternations including mutation of p53, loss of Rb gene and overexpression of bcl-2, and these may be related to the similar biological potentials between the two. Futhermore, SCCE was different from SQCE in expression of Rb protein and bcl-2, and these two types of esophageal carcinoma could arise through different molecular mechanisms.
- PublicationOpen AccessPersistence of Cajal-Retzius cells in the adult human cerebral cortex. An immunohistochemical study(Murcia : F. Hernández, 1999) Martí, R.; Gutierrez, A. ,; Peñafiel, A.; Marin-Padilla, M.; De la Calle, A.The presence of Cajal-Retzius cells in the adult human prefrontal and visual cortices has been demonstrated with calcium binding protein immunocytochemistry and NADPH-diaphorase histochemistry. These cells expressed parvalbumin, calbindin and calretinin calcium binding proteins and displayed NADPH-diaphorase enzyme activity. The three basic morphological profiles-horizontal, pyriform and multipolar-were observed. The morphologies of labelled cells resembled those of neurons observed in Golgi studies of the human cerebral cortex. The presence of calcium binding proteins and NADPH-diaphorase in these cells suggests a possible inhibitory role as GABAergic neurons. The persistence of Cajal-Retzius cells in the adult cerebral cortex supports the idea that they undergo developmental dilution rather than postnatal degeneration.
- PublicationOpen AccessInduction of NADPH diaphoraselnitric oxide synthase in the spinal cord motor neurons of rats following a single and multiple non-penetrative blasts(Murcia : F. Hernández, 1999) Kaur, C.; Singh, J.; Moochhala, S.; Lim, M.K.; Lu, J.; Ling, E. A.The present study has demonstrated the induction of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity and nitric oxide synthase-like immunoreactivity (NOS-LI) in the ventral horn motoneurons of the spinal cord in rats subjected to a single or multiple underground, or a single surface blast. Both enzyme activities were first detected in some motoneurons in laminae V111 and IX of Rexed, 3 hours after the blast. Some NADPH-d and NOS-L1 positive neurons were also distributed in laminae V1 and V11. The number and intensity of the labelled cells appeared to increase progressively, peaking at 2-3 days after the blast but were drastically reduced thereafter, so that at 7 days after the blast only a few positive neurons were observed. In rats killed at 2 weeks and in longer surviving intervals, i.e. up to 1 month, NADPH-d/NOS reactivity in the ventral horn motor neurons had diminished. The functional significance of the transient expression of neuronal NADPH-d/NOS after the blasts remains uncertain, although from a speculative point of view, the induction of these enzymes probably would reflect an increased production of nitric oxide (NO). In view of the lack of atrophic changes in most, if not all, of motor neurons, it is suggested that the increased levels of NO production after the blast injury may be involved in a neuroprotective function.