Journal of Molecular Histology

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Alterations of epithelial layer after ischemic preconditioning of small intestine in rats
Journal of Molecular Histology - Tập 43 - Trang 171-178 - 2012
M. Maretta, Š. Tóth, M. Bujdoš, Z. Jonecová, J. Veselá
Ischemic-reperfusion (IR) injury of the small intestine makes a serious complications associated with various surgical procedures and is related to changes in motility, secretory activity and structural alterations. Preconditioning can reduce range of this damage. The aim of the experimental study was to determine the influence of ischemic preconditioning (IPC) on IR injury on jejunal epithelial layer. Wistar rats (n = 56) were divided in two experimental groups. IR group was subjected to 60 min ischemia of cranial mesenteric artery and followed by reperfusion periods: 1,4,8,24 h (IR1, IR4, IR8, IR24). Group with ischemic preconditioning (IPC+IR) was subjected to two subsequent ischemic attacks (12 min) with 10 min of reperfusion between them, and after 2nd attack ischemia was induced for 60 min followed by relevant reperfusion period. IPC showed the protective impact on the jejunal tissue architecture after 1 h reperfusion, when in IR1 group the highest and significant damage was observed (p < 0.001) in contrast to IPC+IR1 group. Histopathological damage of the intestine in pretreated groups was postponed to 4 h of reperfusion. Protective effect of IPC together with later accumulation of injury signs were confirmed by weaker impact on goblet cell (p < 0.001) and Paneth cell populations (p < 0.05).The increased cells proliferation in preconditioned groups came later, but stronger after 8 h of reperfusion (p < 0.001) and after 24 h of reperfusion still remained at the high activity level (p < 0.001). Our experimental results on the histopathological changes in the jejunum during ischemic preconditioning proved that IPC may have a positive effect on maintaining intestinal barrier function.
A human PBPK model for ethanol describing inhibition of gastric motility
Journal of Molecular Histology - Tập 35 - Trang 687-696 - 2004
George D. Loizou, Martin Spendiff
A physiologically based pharmacokinetic model for investigating inter-individual and inter-racial variability in ethanol pharmacokinetics is presented. The model is a substantial modification of an existing model which described some genetic polymorphisms in the hepatic alcohol dehydrogenase enzymes. The model was modified to incorporate a description of ethanol absorption from the stomach and gastro-intestinal tract and the retardation of gastric emptying due to a concentration-dependent inhibition of gastric peristalsis. In addition, intra-venous and intra-arterial routes of administration were added to investigate whether the biological structure of the model provided a core which may be easily adapted for any route of exposure. The model is proposed as suitable for the investigation of the effects of both acute and chronic ethanol exposure.
Monte Carlo simulations of receptor dynamics: Insights into cell signaling
Journal of Molecular Histology - Tập 35 - Trang 667-677 - 2004
Christopher J. Brinkerhoff, Peter J. Woolf, Jennifer J. Linderman
Many receptor-level processes involve the diffusion and reaction of receptors with other membrane-localized molecules. Monte Carlo simulation is a powerful technique that allows us to track the motions and discrete reactions of individual receptors, thus simulating receptor dynamics and the early events of signal transduction. In this paper, we discuss simulations of two receptor processes, receptor dimerization and G-protein activation. Our first set of simulations demonstrates how receptor dimerization can create clusters of receptors via partner switching and the relevance of this clustering for receptor cross-talk and integrin signaling. Our second set of simulations investigates the activation and desensitization of G-protein coupled receptors when either a single agonist or both an agonist and an antagonist are present. For G-protein coupled receptor systems in the presence of an agonist alone, the dissociation rate constant of agonist is predicted to affect the ratio of G-protein activation to receptor phosphorylation. Similarly, this ratio is affected by the antagonist dissociation rate constant when both agonist and antagonist are present. The relationship of simulation predictions to experimental findings and potential applications of our findings are also discussed.
Clusterin and DNA repair: a new function in cancer for a key player in apoptosis and cell cycle control
Journal of Molecular Histology - - 2006
Batool Shannan, Markus Seifert, David A. Boothman, Wolfgang Tilgen, Joerg Reichrath
Calenduloside E alleviates cerebral ischemia/reperfusion injury by preserving mitochondrial function
Journal of Molecular Histology - Tập 53 - Trang 713-727 - 2022
Jianxiong Li, Yujie Bu, Bin Li, Hailin Zhang, Jia Guo, Jianping Hu, Yanfang Zhang
Calenduloside E (CE) isolated from Aralia elata (Miq.) Seem. is a natural triterpenoid saponin that can reportedly ameliorate myocardial ischemia/reperfusion injury. However, its potential roles and mechanism in cerebral ischemia/reperfusion injury are barely understood. In this study, we established an oxygen-glucose deprivation/reoxygenation (OGD/R) model in HT22 cells. We found that CE significantly attenuated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Moreover, CE treatment significantly ameliorated OGD/R-induced mitochondrial fission by inhibiting mitochondrial dynamin-related protein 1 (Drp1) recruitment and increasing Drp1 phosphorylation at Ser637. CE treatment significantly ameliorated OGD/R-induced mitochondrial dysfunction by increasing the mitochondrial membrane potential and reducing the mitochondrial ROS and cellular calcium accumulation. Moreover, CE treatment significantly inhibited the OGD/R-induced release of mitochondrial Cytochrome C and increase in Bax, Cleaved-caspase3 and Cleaved-caspase9 protein levels, whereas CE treatment significantly reversed the OGD/R-induced decrease in Bcl-2 and full length of caspase3 and caspase9 protein levels. In vivo, we found that CE treatment significantly ameliorated ischemic/hypoxic-induced brain infarct volume, neurological deficits, and neuronal apoptosis in mice after middle cerebral artery occlusion and reperfusion. CE treatment also significantly ameliorated the mitochondrial transmembrane potential, decreased Cytochrome C release, and reversed the increase in Bax, Cleaved-caspase3 and Cleaved-caspase9 protein levels and the decrease in Bcl-2 and full length of caspase3 and caspase9 protein levels induced by cerebral ischemia/reperfusion (I/R). All these results indicated that CE treatment exerted a neuroprotective effect by ameliorating mitochondrial dysfunction during cerebral I/R injury.
STAT1-caspase 3 pathway in the apoptotic process associated with steroid-induced necrosis of the femoral head
Journal of Molecular Histology - Tập 45 - Trang 473-485 - 2014
Xinxian Xu, Hong Wen, Yuezheng Hu, Huachen Yu, Yu Zhang, Chengwang Chen, Xiaoyun Pan
Osteocyte apoptosis is the main manifestation of steroid-induced avascular necrosis of the femoral head (SANFH). STAT1 and caspase 3 participate in the process of apoptosis and STAT1 upregulates the expression of caspase 3. We examined the relationship between the STAT1-caspase 3 pathway and apoptosis in SANFH. All specimens were divided into four groups: the negative control group, Ficat I–II group, Ficat III group, and Ficat IV–V group, and examined histologically, with a TUNEL assay, immunohistochemically, with a caspase 3 activity assay, with ELISAs of STAT1 and phospo-STAT1 (p-STAT1), with a western blotting analysis of p-STAT1 and with real-time RT-PCR. The proportion of empty lacunae increased significantly with the development of SANFH. The proportion of TUNEL-positive cells and immunohistochemical analysis of caspase 3 also increased significantly, although the Ficat I–II group did not differ significantly from the negative control group. Immunohistochemical analysis of STAT1 and p-STAT1, caspase 3 activity all showed significant differences among the groups. An ELISA and a western blotting analysis of p-STAT1 showed significant differences among the groups. An ELISA of STAT1, real-time RT-PCR analysis of caspase 3 and STAT1 all showed significant differences among the groups except between the Ficat I–II and negative control groups. The correlation analysis showed strong positive relationships between the proportion of empty lacunae and the proportion of TUNEL-positive cells between caspase 3 activity and the proportion of TUNEL-positive cells and between the levels of p-STAT1 protein and caspase 3 mRNA. The apoptotic process in SANFH develops with the upregulated expression of caspase 3 via the expression and activation of STAT1. The STATI-caspase 3 pathway plays a critical role in the development of SANFH.
Expression of the proliferation-associated nuclear protein MIB-1 and its relationship with microvascular density in bone marrow biopsies of patients with myelodysplastic syndromes
Journal of Molecular Histology - Tập 35 Số 8-9 - Trang 857-863 - 2004
Michael G. Alexandrakis, Freda Passam, Despina Kyriakou, Constantina Dambaki, G Katrinakis, George Tsirakis, J Konsolas, Efstathios N. Stathopoulos
635 nm LED irradiation may prevent endoplasmic reticulum stress in MC3T3-E1 cells
Journal of Molecular Histology - - 2022
Hyejoung Cho, Ok-Su Kim, Byung-Gook Kim, Ying Yang, Jianan Song, Danyang Liu, Young Kim, Sangmi Jeon, Okjoon Kim
A simple method for the production of bacterial controls for immunohistochemistry and fluorescent in situ hybridization
Journal of Molecular Histology - Tập 39 - Trang 459-462 - 2008
Camilla Recordati, Enrico Radaelli, Kenneth W. Simpson, Eugenio Scanziani
Immunohistochemical and fluorescent in situ hybridization (FISH) assays are useful diagnostic methods for the identification of bacteria on formalin fixed paraffin embedded histological sections. To validate an anti-bacterial antibody or an oligonucleotide probe and to ensure fidelity during subsequent analyses, suitable positive and negative controls are necessary. Suspensions of fixed bacteria are often used, but ideally, these controls should be fixed, embedded and processed in the same way of tissue samples under analysis. Herein, we describe a simple method for the production of bacterial histological control samples: the sandwich. The sandwich is composed of two external layers of equine lung parenchyma and a central layer of the target bacterium. We prepared sandwiches containing Escherichia coli, Campylobacter jejuni, and Arcanobacterium pyogenes and tested them with appropriate antibodies and Eub338 FISH probe. The sandwich is an effective and simple method to prepare bacterial histological controls fixed and processed in the same way as the diagnostic tissues.
Expression analysis of Dickkopf-related protein 3 (Dkk3) suggests its pleiotropic roles for a secretory glycoprotein in adult mouse
Journal of Molecular Histology - Tập 48 - Trang 29-39 - 2016
Junji Inoue, Hirofumi Fujita, Tetsuya Bando, Yoichi Kondo, Hiromi Kumon, Hideyo Ohuchi
Dickkopf-related protein 3 (Dkk3) is the third member of the Dkk gene family and identical to the gene, whose expression was reduced in immortalized cells. Therefore, its another name is reduced expression in immortalized cells. Since the intratumoral introduction of Dkk3 inhibits tumor growth in mouse models of cancers, Dkk3 is likely a tumor suppressor gene. However, the functions of Dkk3 in vivo remain unclear. As the first step to decipher the physiological roles of this gene, we examined the expression pattern of Dkk3 in various tissues from adult mice. In situ hybridization showed that Dkk3 mRNA was detected in the brain, retina, heart, gastrointestinal tract, adrenal glands, thymus, prostate glands, seminal vesicles, testes, and ovaries in a regionally specific manner. Furthermore, we raised anti-mouse Dkk3 antibody and performed immunohistochemistry. Cytoplasmic localization of Dkk3 protein was observed in the cells of the adrenal medulla, while Dkk3 immunoreactivity was observed in the lumen of the stomach and intestine, implying that the Dkk3 protein may be secreted into the lumen of the gastrointestinal tract. These results suggest that Dkk3 has pleiotropic roles for a secretory glycoprotein that acts primarily in the gastrointestinal tract, thymus, endocrine and reproductive organs of the mouse.
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