The mechanisms underlying the cardiac effects of modified citrus pectin in obese rats with myocardial ischemia: Role of galectin-3.

Background: Modified citrus pectin (MCP) is used as a nutritional supplement that inhibits galectin-3 activity, a central player in the cardiac damage associated with different pathological situations. In fact, we have previously observed that MCP improved cardiac function in obese infarcted rats that was associated with a reduction in cardiac fibrosis. Therefore, the aim of the present study was to further explore whether this effect could involve the modulation of gene expression of ECM components and their mediators as well as whether it could affect another two mechanisms involved in cardiac damage: mitochondrial dynamics and autophagic flux.

Effect of resistance exercise training on plasma neurofilaments in multiple sclerosis: a proof of concept for future designs.

Multiple sclerosis (MS) is a dysimmune and neurodegenerative disease of the central nervous system that continues to be one of the main causes of non-traumatic disability in young people despite the recent availability of highly effective drugs. Exercise-based interventions seem to have a positive impact on the course of the disease although pathophysiological mechanisms responsible for this benefit remain unclear. This is a longitudinal study to examine the effects of a short-term training program on neurofilament plasma levels, a biomarker of axonal destruction, measured using the ultrasensitive single molecule array (SiMoA).

Milk fat globule membrane concentrate as a nutritional supplement prevents age-related cognitive decline in old rats: A lipidomic study of synaptosomes.

Aging is associated with a decline in cognitive abilities, mainly in memory and executive functioning. A similar but premature deterioration in cognitive capacities is the hallmark of mild cognitive impairment, Alzeimer's disease and dementia. The biochemical mechanisms that cause these neurodegenerative disorders are poorly understood.

Manipulation of Transmembrane Transport by Synthetic K Ionophore Depsipeptides and Its Implications in Glucose-Stimulated Insulin Secretion in β-Cells.

The cyclic depsipeptide cereulide toxin it is a very well-known potassium electrogenic ionophore particularly sensitive to pancreatic beta cells. The mechanistic details of its specific activity are unknown. Here, we describe a series of synthetic substituted cereulide potassium ionophores that cause impressive selective activation of glucose-induced insulin secretion in a constitutive manner in rat insulinoma INS1E cells.

Alterations in cholesterol metabolism as a risk factor for developing Alzheimer's disease: Potential novel targets for treatment.

Alzheimer's disease (AD) is the most common form of dementia and it is characterized by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain. However, the complete pathogenesis of the disease is still unknown. High level of serum cholesterol has been found to positively correlate with an increased risk of dementia and some studies have reported a decreased prevalence of AD in patients taking cholesterol-lowering drugs.

Mitochondrial control of store-operated Ca channels in cancer: Pharmacological implications.

Intracellular Ca is a pleiotropic second messenger involved in control of different cell and physiological functions including long-term processes such as cell proliferation, migration and survival. Agonist-induced Ca entry in most cells, especially in non-excitable cells including epithelial cells, is mediated by store-operated Ca entry (SOCE), a Ca entry pathway activated by agonist-induced release of Ca from intracellular stores in the endoplasmic reticulum (ER). This pathway is modulated also by mitochondria which, acting as Ca sinks, take up Ca, thus limiting Ca-dependent inactivation of Ca-release activated Ca channels (CRAC).

Insulin degrading enzyme is up-regulated in pancreatic β cells by insulin treatment.

Insulin Degrading Enzyme (IDE) is an endopeptidase that degrades insulin and glucagon. Ide gene has been associated with type-2 diabetes mellitus (DM2). However, the physiological role(s) of IDE in glucose homeostasis and its potential therapeutic benefit remain not completely known.

Is it All Said for NSAIDs in Alzheimer's Disease? Role of Mitochondrial Calcium Uptake.

Objectives: Epidemiological data suggest that non-steroidal anti-inflammatory drugs (NSAIDs) may protect against Alzheimer's disease (AD). Unfortunately, recent trials have failed in providing compelling evidence of neuroprotection. Discussion as to why NSAIDs effectivity is uncertain is ongoing.

Mitochondria sustain store-operated currents in colon cancer cells but not in normal colonic cells: reversal by non-steroidal anti-inflammatory drugs.

Tumor cells undergo a critical remodeling of intracellular Ca homeostasis that contribute to important cancer hallmarks. Store-operated Ca entry (SOCE), a Ca entry pathway modulated by mitochondria, is dramatically enhanced in colon cancer cells. In addition, most cancer cells display the Warburg effect, a metabolic switch from mitochondrial metabolism to glycolysis that provides survival advantages.

Calcium signaling and cell cycle: Progression or death.

Cytosolic Ca concentration levels fluctuate in an ordered manner along the cell cycle, in line with the fact that Ca is involved in the regulation of cell proliferation. Cell proliferation should be an error-free process, yet is endangered by mistakes. In fact, a complex network of proteins ensures that cell cycle does not progress until the previous phase has been successfully completed.

Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer.

Colorectal cancer (CRC) cells undergo the remodeling of intracellular Ca homeostasis, which contributes to cancer hallmarks such as enhanced proliferation, invasion and survival. Ca remodeling includes critical changes in store-operated Ca entry (SOCE) and Ca store content. Some changes have been investigated at the molecular level.

The Calcium-Sensing Receptor in Health and Disease.

The extracellular calcium-sensing receptor (CaSR) is a unique G protein-coupled receptor (GPCR) activated by extracellular Ca and by other physiological cations including Mg, amino acids, and polyamines. CaSR is the most important master controller of the extracellular Ca homeostatic system being expressed at high levels in the parathyroid gland, kidney, gut and bone, where it regulates parathyroid hormone (PTH) secretion, vitamin D synthesis, and Ca absorption and resorption, respectively. Gain and loss of function mutations in the CaSR are responsible for severe disturbances in extracellular Ca metabolism.

A new procedure for amyloid β oligomers preparation enables the unambiguous testing of their effects on cytosolic and mitochondrial Ca(2+) entry and cell death in primary neurons.

Oligomers of the amyloid β peptide (Aβo) are becoming the most likely neurotoxin in Alzheimer's disease. Controversy remains on the mechanisms involved in neurotoxicity induced by Aβo and the targets involved. We have reported that Aβo promote Ca(2+) entry, mitochondrial Ca(2+) overload and apoptosis in cultured cerebellar neurons.

Stem Cell Therapy for Corneal Epithelium Regeneration following Good Manufacturing and Clinical Procedures.

Objective: To evaluate outcomes of cultivated limbal epithelial transplantation (CLET) for management of ocular surface failure due to limbal stem cell deficiency (LSCD).

Design: Prospective, noncomparative, interventional case series and extensive comparison with recent similar studies.

Participants: Twenty eyes with LSCD underwent CLET (11 autologous; 9 allogeneic) and were followed up for 3 years.

A reciprocal shift in transient receptor potential channel 1 (TRPC1) and stromal interaction molecule 2 (STIM2) contributes to Ca2+ remodeling and cancer hallmarks in colorectal carcinoma cells.

We have investigated the molecular basis of intracellular Ca(2+) handling in human colon carcinoma cells (HT29) versus normal human mucosa cells (NCM460) and its contribution to cancer features. We found that Ca(2+) stores in colon carcinoma cells are partially depleted relative to normal cells. However, resting Ca(2+) levels, agonist-induced Ca(2+) increases, store-operated Ca(2+) entry (SOCE), and store-operated currents (ISOC) are largely enhanced in tumor cells.

Intracellular Ca(2+) remodeling during the phenotypic journey of human coronary smooth muscle cells.

Vascular smooth muscle cells undergo phenotypic switches after damage which may contribute to proliferative disorders of the vessel wall. This process has been related to remodeling of Ca(2+) channels. We have tested the ability of cultured human coronary artery smooth muscle cells (hCASMCs) to return from a proliferative to a quiescent behavior and the contribution of intracellular Ca(2+) remodeling to the process.