The glycosaminoglycan (GAG) molecules are a group of high molecular weight, negatively charged polysaccharides present abundantly in the mammalian organism. By their virtue of ion and water binding capacity, they may affect the redistribution of body fluids and ultimately the blood pressure. Data from the literature suggests that the mitogens Vascular Endothelial Growth Factor (VEGF)-A and VEGF-C are able to regulate the amount and charge density of GAGs and their detachment from the cell surface. Based on these findings we investigated the relationship between the level of dietary sodium intake, the expression levels of VEGF-A and VEGF-C, and the amount of the skin GAGs hyaluronic acid and chondroitin sulfate in an in vivo rat model. Significant correlation between dietary sodium intake, skin sodium levels and GAG content was found. We confirmed the GAG synthesizing role of VEGF-C but failed to prove that GAGs are degraded by VEGF-A. No significant difference in blood pressure was registered between the different dietary groups. A quotient calculated form the ion and water content of the skin tissue samples suggests that - in contrast to previous findings - the osmotically inactive ions and bound water fractions are proportional.

• MeSH
• glykosaminoglykany metabolismus   MeSH
• krysa rodu rattus MeSH
• kůže účinky léků   metabolismus   MeSH
• náhodné rozdělení MeSH
• potkani Wistar MeSH
• sodík dietní aplikace a dávkování   MeSH
• sodík fyziologie   MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Hypoxia-inducible factor-1alpha (HIF-1alpha) transcriptionally regulates expression of several target genes in protecting tissues against hypoxia. With hypoxic stress, vascular endothelial growth factor (VEGF) is a signal protein produced by cells and further contributes to improvement of vascular functions and restoring the oxygen supply to tissues. In this current study, we first hypothesized that the protein levels of HIF-1alpha and VEGF are reduced in skeletal muscles of plateau animals [China Qinghai-Tibetan plateau pikas (ochotona curzoniae)] in response to hypoxia as compared with control animals [normal lowland Sprague-Dawley (SD) rats]. We further hypothesized that HIF-1alpha plays a role in regulating expression of VEGF in skeletal muscle. Note that HIF-1alpha and VEGF were determined by using two-site immunoenzymatic assay (ELISA) methods. Our results demonstrated that hypoxic stress induced by exposure of lower O(2) (6 h) significantly increased the levels of HIF-1alpha and VEGF in the oxidative and glycolytic muscles of SD rats and pikas (P<0.05 vs. normoxic conditions). Notably, the increases in HIF-1alpha and VEGF were significantly less in pikas (P<0.05, vs. SD controls) than in SD rats. In addition, a linear relationship was observed between amplified HIF-1alpha and VEGF in oxidative muscle (r=0.76 and P<0.01) and glycolytic muscle (r=0.72 and P<0.01) and inhibiting HIF-1alpha significantly decreased expression of VEGF induced by hypoxic stress in skeletal muscles (P<0.05). Overall, our findings suggest that (1) responsiveness of HIF-1alpha and VEGF in skeletal muscles to hypoxic stress is blunted in plateau animals, and (2) HIF-1alpha has a regulatory effect on VEGF under hypoxic environment.

• MeSH
• faktor 1 indukovatelný hypoxií - podjednotka alfa biosyntéza   MeSH
• hypoxie metabolismus   MeSH
• kosterní svaly metabolismus   MeSH
• krysa rodu rattus MeSH
• Lagomorpha metabolismus   MeSH
• potkani Sprague-Dawley MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Acute respiratory distress syndrome (ARDS) is a serious medical condition occurring in patients with polytrauma, pulmonary or non-pulmonary sepsis, pneumonia and many other circumstances. It causes inflammation of the lung parenchyma leading to impaired gas exchange with a systemic release of inflammatory mediators, causing consequential lung tissue injury, hypoxemia and frequently multiple organ failure. The aim of current study was to describe expression of inflammatory markers (myeloperoxidase, CD163 and vascular endothelial growth factor) by the cells in acute phase of ARDS. The lung samples of a 20-year-old man who had suffered a serious motorbike accident were obtained for histological examination. He died on the seventh day as a consequence of respiratory failure. Our results imply that expression of CD163 was restricted to activated alveolar macrophages and monocytes. Immunopositivityof MPO was observed in neutrophil granulocytes within lung alveoli and lung blood vessels. Myeloperoxidase positivity was observed in alveolar macrophages, too. Vascular endothelial growth factor was expressed in cytoplasm of neutrophil granulocytes, monocytes, small-sized alveolar macrophages and type II pneumocytes localized mostly inside lung alveoli. On the contrary, no positivity was observed in lung endothelial cells of blood vessels.

• MeSH
• alveolární makrofágy imunologie   metabolismus   MeSH
• antigeny diferenciační myelomonocytární biosyntéza   MeSH
• CD antigeny biosyntéza   MeSH
• dopravní nehody MeSH
• imunohistochemie MeSH
• lidé MeSH
• mimosilniční motorová vozidla MeSH
• mladý dospělý MeSH
• monocyty imunologie   metabolismus   MeSH
• neutrofily imunologie   metabolismus   MeSH
• peroxidasa biosyntéza   MeSH
• pneumocyty imunologie   metabolismus   MeSH
• receptory buněčného povrchu biosyntéza   MeSH
• syndrom dechové tísně imunologie   metabolismus   patologie   MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   MeSH
• Check Tag
• lidé MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• práce podpořená grantem MeSH

BACKGROUND: Vascular endothelial growth factor (VEGF) is not only a potent angiogenic factor but it also promotes axonal outgrowth and proliferation of Schwann cells. The aim of the present study was to quantitatively assess reinnervation of musculocutaneous nerve (MCN) stumps using motor and primary sensory neurons after plasmid phVEGF transfection and end-to-end (ETE) or end-to-side (ETS) neurorrhaphy. The distal stump of rat transected MCN, was transfected with plasmid phVEGF, plasmid alone or treated with vehiculum and reinnervated following ETE or ETS neurorrhaphy for 2 months. The number of motor and dorsal root ganglia neurons reinnervating the MCN stump was estimated following their retrograde labeling with Fluoro-Ruby and Fluoro-Emerald. Reinnervation of the MCN stumps was assessed based on density, diameter and myelin sheath thickness of regenerated axons, grooming test and the wet weight index of the biceps brachii muscles. RESULTS: Immunohistochemical detection under the same conditions revealed increased VEGF in the Schwann cells of the MCN stumps transfected with the plasmid phVEGF, as opposed to control stumps transfected with only the plasmid or treated with vehiculum. The MCN stumps transfected with the plasmid phVEGF were reinnervated by moderately higher numbers of motor and sensory neurons after ETE neurorrhaphy compared with control stumps. However, morphometric quality of myelinated axons, grooming test and the wet weight index were significantly better in the MCN plasmid phVEGF transfected stumps. The ETS neurorrhaphy of the MCN plasmid phVEGF transfected stumps in comparison with control stumps resulted in significant elevation of motor and sensory neurons that reinnervated the MCN. Especially noteworthy was the increased numbers of neurons that sent out collateral sprouts into the MCN stumps. Similarly to ETE neurorrhaphy, phVEGF transfection resulted in significantly higher morphometric quality of myelinated axons, behavioral test and the wet weight index of the biceps brachii muscles. CONCLUSION: Our results showed that plasmid phVEGF transfection of MCN stumps could induce an increase in VEGF protein in Schwann cells, which resulted in higher quality axon reinnervation after both ETE and ETS neurorrhaphy. This was also associated with a better wet weight biceps brachii muscle index and functional tests than in control rats.

• MeSH
• dextrany diagnostické užití   MeSH
• fluoresceiny diagnostické užití   MeSH
• genetická terapie metody   MeSH
• krysa rodu rattus MeSH
• mícha patologie   MeSH
• modely nemocí na zvířatech MeSH
• nemoci periferního nervového systému patologie   terapie   MeSH
• nervová vlákna myelinizovaná patologie   MeSH
• nervus musculocutaneus metabolismus   patologie   fyziologie   MeSH
• neurologické vyšetření MeSH
• neurony metabolismus   patologie   MeSH
• potkani Wistar MeSH
• přední končetina patofyziologie   MeSH
• regenerace nervu genetika   fyziologie   MeSH
• rhodaminy diagnostické užití   MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   metabolismus   terapeutické užití   MeSH
• velikost orgánu fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Hindlimb unweighting (HU) leads to capillary regression in skeletal muscle. However, the molecular mechanism(s) remains to be elucidated. To gain insight into the regulation of this process, we investigated gene expression of hypoxia-inducible factor-1? (HIF-1?), vascular endothelial growth factor (VEGF), angiopoietin, and their receptors in the atrophied muscle induced by HU. The hindlimbs of mice were unweighted by tailsuspension and then the gastrocnemius muscles were isolated after 10 days. To assess the capillary distribution, the capillary endothelium in frozen transverse sections was identified by staining for alkaline phosphatase. The mRNA levels were analyzed using a real-time reverse transcription-polymerase chain reaction. After 10 days of HU, the number of capillaries around a muscle fiber was significantly decreased by 19.5 %, suggesting that capillary regression appears to occur. The expression of HIF- 1? was significantly down-regulated after 10 days of HU. The expression of VEGF remained unchanged, whereas those of Flt-1, KDR/Flk-1, and neuropilin-1 were significantly down-regulated, suggesting that VEGF signaling through these receptors would be attenuated. The expression of angiopoietin-1, and -2, as well as their receptor, Tie-2 were also significantly down-regulated, suggesting that angiopoietin-1 signaling through Tie-2 would be attenuated. These findings suggest that alterations in expression of VEGF, angiopoietins, and their receptors may be associated with capillary regression after HU.

• Klíčová slova
• Angiogenic factor, Capillary regression, Hindlimb unweighting, Muscle atrophy,
• MeSH
• angiopoetin-1 biosyntéza   MeSH
• angiopoetin-2 biosyntéza   MeSH
• faktor 1 indukovatelný hypoxií - podjednotka alfa biosyntéza   MeSH
• financování organizované MeSH
• histocytochemie MeSH
• kapiláry fyziologie   MeSH
• komplementární DNA biosyntéza   genetika   MeSH
• kosterní svaly fyziologie   metabolismus   MeSH
• myši MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• receptory buněčného povrchu metabolismus   MeSH
• receptory vaskulárního endoteliálního růstového faktoru biosyntéza   MeSH
• RNA biosyntéza   genetika   MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   MeSH
• zadní končetina - imobilizace fyziologie   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH

• MeSH
• Escherichia coli genetika   MeSH
• finanční podpora výzkumu jako téma MeSH
• fyziologická neovaskularizace fyziologie   MeSH
• genetická terapie MeSH
• látky indukující angiogenezi metabolismus   MeSH
• protein - isoformy genetika   MeSH
• vaskulární endoteliální růstový faktor A biosyntéza   MeSH