98 research outputs found
Effect of Short-Time Exposures to Nickel and Lead on Brain Monoamine Oxidase from Danio rerio and Poecilia reticulata
No full textThe aim of this work was to verify, in two small size freshwater teleosts Danio rerio and Poecilia reticulata, the effects of short-time exposures (24 and 72 h) to a sublethal dose (500 mu g/L) of nickel and lead, on brain monoamine oxidase (MAO), an important neural enzyme. The 24-h treatment using both metals caused a strong reduction of MAO activity in D. rerio brain, whereas causing a slight MAO activity stimulation in P reticulata brain. The same treatment in both species did not affect the brain MAO mRNA production as showed by RT-PCR. Extending the duration of treatment as far as 72 h, partly (D. rerio) or completely (P. reticulata) reversed the metal effects on brain MAO activity suggesting that mechanisms to neutralize the metals had been activated. (C) 2008 Wiley Periodicals, Inc. Environ Toxicol 24: 309-313, 2009
Pattern recognition receptors, peroxisome proliferator activated receptor (PPARgamma)and related genes in mice smooth muscle cells.
No full textCellular and molecular mechanisms of phenotypic switch in gastrointestinal smooth muscle
No full textAs a general rule, smooth muscle cells (SMC) are able to switch from a contractile phenotype to a less mature synthetic phenotype. This switch is accompanied by a loss of differentiation with decreased expression of contractile markers, increased proliferation as well as the synthesis and the release of several signaling molecules such as pro-inflammatory cytokines, chemotaxis-associated molecules, and growth factors. This SMC phenotypic plasticity has extensively been investigated in vascular diseases, but interest is also emerging in the field of gastroenterology. It has in fact been postulated that altered microenvironmental conditions, including the composition of microbiota, could trigger the remodeling of the enteric SMC, with phenotype changes and consequent alterations of contraction and impairment of gut motility. Several molecular actors participate in this phenotype remodeling. These include extracellular molecules such as cytokines and extracellular matrix proteins, as well as intracellular proteins, for example, transcription factors. Epigenetic control mechanisms and miRNA have also been suggested to participate. In this review key roles and actors of smooth muscle phenotypic switch, mainly in GI tissue, are described and discussed in the light of literature data available so far. J. Cell. Physiol. 231: 295-302, 2016.As a general rule, smooth muscle cells (SMC) are able to switch from a contractile phenotype to a less mature synthetic phenotype. This switch is accompanied by a loss of differentiation with decreased expression of contractile markers, increased proliferation as well as the synthesis and the release of several signaling molecules such as pro-inflammatory cytokines, chemotaxis-associated molecules, and growth factors. This SMC phenotypic plasticity has extensively been investigated in vascular diseases, but interest
is also emerging in the field of gastroenterology. It has in fact been postulated that altered microenvironmental conditions, including the composition of microbiota, could trigger the remodeling of the enteric SMC, with phenotype changes and consequent alterations of contraction and impairment of gut motility. Several molecular actors participate in this phenotype remodeling. These include extracellular molecules such as cytokines and extracellular matrix proteins, as well as intracellular proteins, for example, transcription factors. Epigenetic control mechanisms and miRNA have also been suggested to participate. In this review key roles and actors of smooth muscle phenotypic switch, mainly in GI tissue, are described and discussed in the light of literature data available so far
The gut brain axis. interactions between enteric microbiota, central and enteric nervous systems
No full textThe gut-brain axis (GBA) consists of bidirectional communication between the central and the enteric nervous system, linking emotional and cognitive centers of the brain with peripheral intestinal functions. Recent advances in research have described the importance of gut microbiota in influencing these interactions. This interaction between microbiota and GBA appears to be bidirectional, namely through signaling from gut-microbiota to brain and from brain to gut-microbiota by means of neural, endocrine, immune, and humoral links. In this review we summarize the available evidence supporting the existence of these interactions, as well as the possible pathophysiological mechanisms involved. Most of the data have been acquired using technical strategies consisting in germ-free animal models, probiotics, antibiotics, and infection studies. In clinical practice, evidence of microbiota-GBA interactions comes from the association of dysbiosis with central nervous disorders (i.e. autism, anxiety-depressive behaviors) and functional gastrointestinal disorders. In particular, irritable bowel syndrome can be considered an example of the disruption of these complex relationships, and a better understanding of these alterations might provide new targeted therapies
Microbiota, Innate Immune System, and Gastrointestinal Muscle Ongoing Studies
No full textAim: To test the activities of culture-extracted or commercially available toll-like receptors (TLRs) ligands to establish their direct impact on target gastrointestinal motor cells. Methods: Short-term and long-term effects of Shigella flexneri M90T and Escherichia coil K-2 strains-extracted lipopolysaccharides (LPS), commercially highly purified LPS (E. coli 0111:B4 and EH100), and Pam2CSK4 and Pam3CSK4, which bind TLR2/6 and TLR1/2 heterodimers, respectively, have been assessed on pure primary cultures of colonic human smooth muscle cells (HSMC). Results: Pathogenic Shigella-LPS and nonpathogenic E. coli K-2-LPS induced a time-dependent decrease of resting cell length and acetylcholine-induced contraction, with both alterations occurring rapidly and being more pronounced in response to the former. However, their effects differed, prolonging HSMC exposure with Shigella-LPS effects maintained throughout the 4 hours of observation compared with E. coli K-2-LPS, which disappeared after 60 minutes of incubation. Similar differences in magnitude and time dependency of myogenic effects were observed between pure TLR4 and TLR2/1 or TLR2/6 ligands. The specific activation of TLR4 with LPS from pathogen or nonpathogen E. coli, 0111:B4 and EH100, respectively, induced smooth muscle alterations that progressively increased, prolonging incubation, whereas TLR2 ligands induced short-term alterations, of a lesser magnitude, which decreased over time. The real-time polymerase chain reaction analysis showed that HSMC express mRNA for TLR1, 2, 4, and 6, substantiating a direct effect of TLR ligands on human colonic smooth muscle. Conclusions: This study highlights that bacterial products can directly affect gastrointestinal motility and that TLRs subtypes may differ in their cellular activity
Inflammatory Cytokines-Induced Modulation of Human Colonic Smooth Muscle Contractile Phenotype
No full textExpression of Gram+ sensing toll-like receptors in human colonic smooth muscle cells: a possible mechanism for prebiotics beneficial effect.
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