ABSTRACT
The remodelling of the extracellular matrix plays an important role in skeletal muscle development and regeneration. Syndecan-4 is a cell surface proteoglycan crucial for muscle differentiation. Syndecan-4-/- mice have been reported to be unable to regenerate following muscle damage. To investigate the consequences of the decreased expression of Syndecan-4, we have studied the in vivo and in vitro muscle performance and the excitation-contraction coupling machinery in young and aged Syndecan-4+/- (SDC4) mice. In vivo grip force was decreased significantly as well as the average and maximal speed of voluntary running in SDC4 mice, regardless of their age. The maximal in vitro twitch force was reduced in both EDL and soleus muscles from young and aged SDC4 mice. Ca2+ release from the sarcoplasmic reticulum decreased significantly in the FDB fibres of young SDC4 mice, while its voltage dependence was unchanged regardless of age. These findings were present in muscles from young and aged mice as well. On C2C12 murine skeletal muscle cells, we have also found altered calcium homeostasis upon Syndecan-4 silencing. The decreased expression of Syndecan-4 leads to reduced skeletal muscle performance in mice and altered motility in C2C12 myoblasts via altered calcium homeostasis. The altered muscle force performance develops at an early age and is maintained throughout the life course of the animal until old age.
Subject(s)
Muscle, Skeletal , Syndecan-4 , Animals , Mice , Calcium/metabolism , Muscle Contraction/physiology , Muscle Fibers, Skeletal/metabolism , Muscle, Skeletal/metabolism , Sarcoplasmic Reticulum/metabolism , Syndecan-4/genetics , Syndecan-4/metabolismABSTRACT
L-aminoguanidine (AG) is an inhibitor frequently used for investigating plant abiotic stress responses; however, its exact mode of action is not well understood. Many studies used this compound as a specific diamine oxidase inhibitor, whereas other studies used it for reducing nitric oxide (NO) production. Recent studies suggest its antiglycation effect; however, this remains elusive in plants. This review summarises our current knowledge about different targets of AG in plants. Our recommendation is to use AG as a modulator of polyamine-related mechanisms rather than a specific inhibitor. In the future overall investigation is needed to decipher the exact mechanisms of AG. More careful application of AG could give more insight into plant abiotic stress responses.
ABSTRACT
Astaxanthin is a lipid-soluble carotenoid influencing lipid metabolism, body weight, and insulin sensitivity. We provide a systematic analysis of acute and chronic effects of astaxanthin on different organs. Changes by chronic astaxanthin feeding were analyzed on general metabolism, expression of regulatory proteins in the skeletal muscle, as well as changes of excitation and synaptic activity in the hypothalamic arcuate nucleus of mice. Acute responses were also tested on canine cardiac muscle and different neuronal populations of the hypothalamic arcuate nucleus in mice. Dietary astaxanthin significantly increased food intake. It also increased protein levels affecting glucose metabolism and fatty acid biosynthesis in skeletal muscle. Inhibitory inputs innervating neurons of the arcuate nucleus regulating metabolism and food intake were strengthened by both acute and chronic astaxanthin treatment. Astaxanthin moderately shortened cardiac action potentials, depressed their plateau potential, and reduced the maximal rate of depolarization. Based on its complex actions on metabolism and food intake, our data support the previous findings that astaxanthin is suitable for supplementing the diet of patients with disturbances in energy homeostasis.
Subject(s)
Action Potentials/drug effects , Anabolic Agents/pharmacology , Energy Metabolism/drug effects , Animals , Dogs , Eating/drug effects , Hypothalamus/drug effects , Hypothalamus/metabolism , Lipid Metabolism/drug effects , Mice , Muscle, Skeletal/drug effects , Muscle, Skeletal/metabolism , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Organ Specificity/drug effects , Signal Transduction/drug effects , Xanthophylls/pharmacologyABSTRACT
Several clinical studies indicate that smoking predisposes its consumers to esophageal inflammatory and malignant diseases, but the cellular mechanism is not clear. Ion transporters protect esophageal epithelial cells by maintaining intracellular pH at normal levels. In this study, we hypothesized that smoking affects the function of ion transporters, thus playing a role in the development of smoking-induced esophageal diseases. Esophageal cell lines were treated with cigarettesmoke extract (CSE), and the viability and proliferation of the cells, as well as the activity, mRNA and protein expression of the Na+/H+ exchanger-1 (NHE-1), were studied. NHE-1 expression was also investigated in human samples. For chronic treatment, guinea pigs were exposed to tobacco smoke, and NHE-1 activity was measured. Silencing of NHE-1 was performed by using specific siRNA. CSE treatment increased the activity and protein expression of NHE-1 in the metaplastic cells and decreased the rate of proliferation in a NHE-1-dependent manner. In contrast, CSE increased the proliferation of dysplastic cells independently of NHE-1. In the normal cells, the expression and activity of NHE-1 decreased due to in vitro and in vivo smoke exposure. Smoking enhances the function of NHE-1 in Barrett's esophagus, and this is presumably a compensatory mechanism against this toxic agent.
