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During the past decade there has been a substantial increase in macroautophagy (herein simply referred to as autophagy) research due to a growing understanding of this process, coupled with improved new techniques for its detection. Autophagy (auto — self, phagy — eating) is defined as a fundamental lysosomal catabolic pathway responsible for degrading long-lived proteins, protein aggregates, oxidised lipids, damaged organelles, and even microbial invaders. Although autophagy occurs at basal levels in normal conditions, many different forms of metabolic stress, including starvation, hypoxia, high temperature, high culture density, hormones, and growth factor deprivation can dramatically stimulate an autophagic response. Autophagy plays a critical role in maintaining cellular homeostasis and genomic integrity and therefore has been implicated in many physiological activities such development, differentiation, and tissue remodelling. Consequently, defects in autophagy have been linked to various human diseases such as neurodegenerative and muscle disorders, cancers, cardiac failure, and inflammatory disorders. This mini-review summarises current knowledge in a field of mammalian autophagy and considers the significance of autophagy in human physiology and pathology. (Folia Morphol 2013; 72, 2: 87–93)
 Inflammatory response has been recognized as a central feature in the development and progression of atherosclerosis, and VSMCs (Vascular Smooth Muscle Cells) - the main cellular component of media, play an important role in this process. Many reports indicate that the biologically active vitamin D metabolite - 1,25-dihydroxyvitamin D3 (1,25(OH)2D3 = calcitriol), besides its well established role in calcium homeostasis, plays an essential role in the regulation of the inflammation process. The aim of this study was to determine the regulatory effects of calcitriol, applied at two supra-physiological doses (10 nM and 100 nM), in VSMC culture. Secretion of the pro-inflammatory cytokines, IL-6 and TNF-α, was significantly attenuated in calcitriol-treated VSMC culture, but the level of anti-inflammatory TGF-β was generally unchanged. Since in advanced atherosclerosis lesions several cell types, including VSMCs, overproduce the HSP70 chaperone protein, we also checked the effects of calcitriol on its synthesis. The presence of 1,25(OH)2D3 did not affect HSP70 synthesis under physiological conditions but the synthesis of HSP70 in VSMCs exposed to heat shock was significantly inhibited by calcitriol (=100 nM). We observed that 1,25(OH)2D3 induced SOD 1 activity, stimulated the expression of IκB-α, and did not influence the level of NF-κB-p65 in VSMCs. The results of our study suggest that 1,25(OH)2D3 may serve as a natural anti-inflammatory agent and may therefore play a beneficial role in the physiology of VSMC in some contexts of atherosclerosis.
Pathophysiology of acute pancreatitis (AP) has not been clearly established; nevertheless, accumulating evidence implicates highly reactive oxygen species (ROS) as important mediators of exocrine tissue damage. In this study, we used a water-soluble radical initiator, 2,2’-azobis-(2-amidinopropane) dihydrochloride (AAPH), to investigate the consequences of oxidative stress insult to the rat pancreas. The detailed characterisation of acini ultrastructural changes in the early course (3, 6, 12, 24 h) of AAPH-induced pancreatitis (40 mg/1 kg body weight) was performed. Considerable damage to the mitochondria in acinar cells manifested by increased translucence of the matrix, partial destruction of cristae, and formation of myelin figures were noted. At the same time, focal dilation, degranulation of rough endoplasmic reticulum, and reduced number of zymogen granules was observed. The most prominent ultrastructural feature was accumulation of highly polymorphic cytoplasmic vacuoles in acinar cells. Double membrane-bound autophagosomes, different in size and shape, with sequestered organelles, autophagolysosomes, and large, empty, single-membrane-bound vacuoles were observed within the cytoplasm. The results indicate that intensive and impaired autophagy mediates pathological accumulation of vacuoles in acinar cells. The rat model of acute pancreatitis induced by AAPH is useful to investigate the early events of oxidative stress insult to the pancreas. (Folia Morphol 2012; 71, 3: 136–141)
The smooth muscle cells (SMCs) of the arterial media play a predominant role in functional and structural alterations of the arterial wall. The transition from the “contractile” to the “synthetic” phenotype appears to be an early critical event in the development of atherosclerotic disease. A number of observations suggest that 1,25(OH)₂D₃ (calcitriol) is of importance in maintaining normal cardiovascular function through its receptors in cardiac myocytes or aortal SMCs. The present study has focused on the microtubular (MT) network reorganisation after exposure to calcitriol. SMCs isolated by enzymatic digestion from the aortal media of neonatal rats were cultured on glass cover slips. 1 μM of 1,25(OH)₂D₃ was added to the culture medium every second day. The cytoskeletal features of SMCs after calcitriol were visualised by the immunofluorescence staining of α-tubulin. The alterations in α-tubulin expression and the distribution of microtubules related to the activities of the vascular smooth muscle cells, namely adhesion, migration, multilayer formation and cell division, were observed. A spindle shape, decreased cell adhesion, low expression of α-tubulin and a longitudinally arranged microtubular network manifested the high rate of SMC differentiation in the calcitriol-treated culture. A flat stellate morphology, high expression of α-tubulin and a radially distributed three-dimensional microtubular network were observed in the SMCs of the control culture. Destructive changes in the microtubular architecture which altered the cellular shape were evident in SMCs undergoing apoptosis. Cells with apoptotic features were more frequent in calcitriol-exposed culture. In contrast to the regular SMC divisions observed in the control culture, some of the mitotic cells exposed to calcitriol contained broader bipolar, multipolar or disordered spindles. These alterations in the SMCs’ microtubular cytoskeleton after calcitriol treatment were concomitant with changes in cell growth, differentiation and apoptosis, and may suggest a similarity to atherosclerotic plaque formation.
The influence of chronic ethanol intoxication on the terminal vascularization of particular hippocampal fields and layers was investigated in different age groups of rats. Thirty-six male Wistar rats aged 6 weeks were used in the study. For twelve months 24 of them drank only 25% ethanol — 12 starting at 6-week- -age and 12 at 3-month-age. The control group of 12 rats drank only water. As an effect of long-term ethanol exposure on hippocampal capillaries we observed the increase in the terminal vessel diameter and the decrease in microvascular length, surface, and volume densities. These changes varied between different age groups and between particular hippocampal regions. The observed age and regional differentiation of ethanol-related microvascular changes did not correlate well with the damaging effects of alcohol on corresponding neuronal elements, which emphasizes the very complicated pathogenesis of ethanol-induced injuries.
It is generally accepted that phospholipids of plasma membrane display lateral segregation into small microdomains commonly known as lipid rafts. Such lateral lipid organization is under the control of cholesterol. Cholesterol depletion evolved by methyl-β-cyclodextrin (MCD) has been found to induce further marked perturbation in lateral lipid organization, evidenced in the high field part of electron paramagnetic resonance spectra of plasma membranes labelled with a spectroscopic probe, namely 5-doxyl-stearic acid (5DOXS). Such perturbation of surface lipid topo-logy has been found to induce distinct changes in the mitochondrial morpho-logy, i.e. switch from filamentous form into small granular form. (Folia Morphol 2009; 68, 4: 244–246)
Many hypothalamic nuclei are involved in the regulation of food intake and energy homeostasis. An ultrastructural investigation of the hypothalamic ventromedial nucleus (VMN), a hypothetical “satiety centre” was performed to explore the morphological basis of altered feeding behaviour of old rats in an experimental model of fasting/refeeding. Young (5 months old, n = 12) and old (24 months old, n = 12) male Wistar rats were fasted for 48 hours, then refed for 24 hours and sampled thereafter. Brain tissue was fixed by perfusion, histological and ultrathin sections were obtained by routine methods. Although food intake was similar in control young and old rats, during refeeding old animals consumed less chow than young ones. The EM analysis of VMN neurones of old control rats revealed, besides typical age-related residual bodies, deep indentations of the nuclear envelope and the presence of long, undulating rough endoplasmic reticulum cisternae in the cell periphery. In both young and old rats fasting for 48 hours led to the expansion of Golgi complexes and increased folds of the nuclear envelope, which is suggestive of enhanced cellular activity of the VMN neurones. These fasting-induced alterations were sustained in the VMN neurones of refed rats in both age groups. The results showed that the VMN neurones of old control rats differ at the ultrastructural level from young ones. However, starvation and subsequent refeeding cause similar alterations in the hypothalamic neurones of “satiety centre” of both young and old rats.
In order to explore the morphological basis of the altered feeding behaviour of old rats, an ultrastructural investigation of the magnocellular neurons of the hypothalamic paraventricular nucleus (PVN) was performed. Young and old male Wistar rats, 5 and 24 months old, respectively, and with each age group comprising 12 animals, were divided into 3 groups. The rats in Group I were used as controls (normally fed), the rats of Group II were fasted for 48 hours and in Group III the rats were fasted for 48 hours and then refed for 24 hours. The brains were fixed by perfusion and histological and ultrathin sections were obtained by routine methods. Common features of the magnocellular PVN neurons of young and old rats were abundant Golgi complexes and short fragments of RER localised at the cell periphery. In contrast to young rats, the PVN neurons of old animals showed deep indentations of the nuclear envelope and agerelated residual bodies. In both age groups fasting for 48 hours led to the expansion of the Golgi complexes and dilatation of RER cisternae. In contrast to those in fed rats, RER cisternae in the neurons of old fasted animals were situated between the nuclear envelope and the Golgi zone. Prolonged RER cisternae were distributed in the peripheral cytoplasm of refed old rats. Our observations suggest that at the ultrastructural level the process of ageing does not change the responsiveness of magnocellular PVN neurons to fasting-refeeding.
Thymocytes exposed to the pro-oxidant tert–butyl-hydroperoxide (ButOOH) display a number of dramatic changes in morphology similar to those observed in the case of dexamethasone-treated cells. Both reagents induce nuclear chromatin peripheral aggregation below the nuclear membrane. Some nuclei themselves break up producing two or more fragments. ButOOH-treated cells are morphologically characterised by cell shrinkage, extensive surface blebbing and, finally, fragmentation into membrane–bound apoptotic bodies composed of cytoplasm and tightly packed with or without nuclear fragments. An increased level of lipid hydroxyperoxides was detected after exposure of thymocytes to ButOOH. Both oxidative stress markers and morphological damage to cells were prevented by the antioxidant 4-OH-TEMPO.
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