Carlos Villalobos

ORCID: 0000-0002-0429-3846
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Ion channel regulation and function
  • Mitochondrial Function and Pathology
  • Alzheimer's disease research and treatments
  • Ion Channels and Receptors
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Hypothalamic control of reproductive hormones
  • Stress Responses and Cortisol
  • Growth Hormone and Insulin-like Growth Factors
  • Biochemical Analysis and Sensing Techniques
  • Cholinesterase and Neurodegenerative Diseases
  • Pituitary Gland Disorders and Treatments
  • Protein Kinase Regulation and GTPase Signaling
  • Adenosine and Purinergic Signaling
  • Receptor Mechanisms and Signaling
  • Tryptophan and brain disorders
  • Vitamin D Research Studies
  • Pancreatic function and diabetes
  • Regulation of Appetite and Obesity
  • Nicotinic Acetylcholine Receptors Study
  • bioluminescence and chemiluminescence research
  • Endoplasmic Reticulum Stress and Disease
  • Periodontal Regeneration and Treatments
  • Estrogen and related hormone effects
  • Lipid Membrane Structure and Behavior

Consejo Superior de Investigaciones Científicas
2015-2024

Universidad de Valladolid
2015-2024

Instituto de Biomedicina y Genética Molecular de Valladolid
2015-2024

International Committee of the Red Cross
2017

Medical University of South Carolina
1997-2002

Dysregulation of intracellular Ca(2+) homeostasis may underlie amyloid beta peptide (Abeta) toxicity in Alzheimer's Disease (AD) but the mechanism is unknown. In search for this we found that Abeta(1-42) oligomers, assembly state correlating best with cognitive decline AD, not Abeta fibrils, induce a massive entry neurons and promote mitochondrial overload as shown by bioluminescence imaging targeted aequorin individual neurons. oligomers also permeability transition, cytochrome c release,...

10.1371/journal.pone.0002718 article EN cc-by PLoS ONE 2008-07-22

Toll-like receptors (TLRs) are transmembrane pattern-recognition of the innate immune system recognizing diverse pathogen-derived and tissue damage-related ligands. It has been suggested that TLR signaling contributes to pathogenesis age-related, neurodegenerative diseases, including Alzheimer's disease (AD). AD is associated oligomers amyloid β peptide (Aβo) cause intracellular Ca2+ dishomeostasis neuron cell death in rat hippocampal neurons. Here we assessed interplay between inflammation...

10.1186/s12974-017-0802-0 article EN cc-by Journal of Neuroinflammation 2017-01-30

Alzheimer's disease (AD) is the most common neurodegenerative disorder and strongly associated to aging. AD has been related excess of neurotoxic oligomers amyloid β peptide (Aβo), loss intracellular Ca2+ homeostasis mitochondrial damage. However, intimate mechanisms underlying pathology remain obscure. We have reported recently that long-term cultures rat hippocampal neurons resembling aging are prone damage induced by Aβo while short-term cultured cells young not. In addition, we also...

10.3389/fncel.2019.00022 article EN cc-by Frontiers in Cellular Neuroscience 2019-02-08

The active vitamin D metabolite 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) inhibits proliferation and promotes differentiation of colon cancer cells through the activation receptor (VDR), a transcription factor nuclear superfamily. Additionally, 1,25(OH)2D3 has several nongenomic effects uncertain relevance. We show that induces transcription-independent Ca2+ influx RhoA–Rho-associated coiled kinase (ROCK). This requires VDR is followed by p38 mitogen-activated protein (p38MAPK) mitogen-...

10.1083/jcb.200803020 article EN cc-by-nc-sa The Journal of Cell Biology 2008-11-17

Abstract Background Loss-of-function mutations in PTEN-induced kinase 1 (PINK1) have been linked to familial Parkinson’s disease, but the underlying pathogenic mechanism remains unclear. We previously reported that loss of PINK1 impairs mitochondrial respiratory activity mouse brains. Results In this study, we investigate how respiration using cultured primary fibroblasts and neurons. found intact mitochondria −/− cells recapitulate defect isolated from brains, suggesting these are a valid...

10.1186/1750-1326-7-22 article EN cc-by Molecular Neurodegeneration 2012-05-25

Recent results indicate that Ca2+ transport by organella contributes to shaping signals and exocytosis in adrenal chromaffin cells. Therefore, accurate measurements of [Ca2+] inside cytoplasmic are essential for a comprehensive analysis the redistribution follows cell stimulation. Here we have studied changes endoplasmic reticulum, mitochondria, nucleus imaging aequorins targeted these compartments cells stimulated brief depolarizing pulses with high K+ solutions. We find entry through...

10.1096/fj.01-0630com article EN The FASEB Journal 2002-03-01

We have studied the effects of cytochrome P450 inhibitors on entry Ca2∗ and Mn2∗, used here as a surrogate for Ca2+ channels, in fura-2-loaded GH3 pituitary cells bovine chromaffin depolarized with high-K∗ solutions. Imidazole antimycotics were potent (econazole > miconazole clotrimazole ketoconazole). α-Naphtoflavone isosafrole, but not metyrapone, also inhibited Mn2∗ induced by depolarization. This inhibitory profile most resembles that reported IA-type P450. However, carbon monoxide (CO),...

10.1096/fasebj.6.9.1319362 article EN The FASEB Journal 1992-06-01

Nuñez J, Sanz‐Blasco S, Vignoletti F, Muñoz Arzate H, Villalobos C, L, Caffesse RG, Sanz M. Periodontal regeneration following implantation of cementum and periodontal ligament‐derived cells. J Periodont Res 2012; 47: 33–44. © 2011 John Wiley & Sons A/S Background Objective: The bone defects is often unsatisfactory could be largely improved by cell therapy. Therefore, the purpose this study was to evaluate regenerative potential implanting canine cementum‐derived cells (CDCs) (PDLDCs) in...

10.1111/j.1600-0765.2011.01402.x article EN Journal of Periodontal Research 2011-09-12

Store‐operated Ca 2+ entry (SOCE) is a ubiquitous influx pathway involved in control of multiple cellular and physiological processes including cell proliferation. Recent evidence has shown that SOCE depends critically on mitochondrial sinking entering to avoid ‐dependent inactivation. Thus, role mitochondria proliferation could be anticipated. We show here activation induces cytosolic high [Ca ] domains are large enough sensed avidly taken up by pool nearby mitochondria. Prevention...

10.1113/jphysiol.2005.100586 article EN The Journal of Physiology 2005-12-09

The most important risk factor for Alzheimer’s disease (AD) is aging. Neurotoxicity in AD has been linked to dyshomeostasis of intracellular Ca2+ induced by small aggregates the amyloid-β peptide 1-42 (Aβ42 oligomers). However, how aging influences susceptibility neurotoxicity Aβ42 oligomers unknown. In this study, we used long-term cultures rat hippocampal neurons, a model neuronal vitro aging, investigate contribution dishomeostasis and neuron cell death oligomers. addition, tested whether...

10.3233/jad-151189 article EN Journal of Alzheimer s Disease 2016-07-22

Colorectal cancer (CRC) cells undergo the remodeling of intracellular Ca2+ homeostasis, which contributes to hallmarks such as enhanced proliferation, invasion and survival. includes critical changes in store-operated entry (SOCE) store content. Some have been investigated at molecular level. However, since nearly 100 genes are involved transport, a comprehensive view CRC is lacking. We used Next Generation Sequencing (NGS) investigate differences expression 77 selected gene transcripts...

10.3390/ijms18050922 article EN International Journal of Molecular Sciences 2017-04-27

Anthocyanins are pigments with antihyperglycemic properties, and they potential candidates for developing functional foods the therapy or prevention of Diabetes mellitus type 2 (DM2). The mechanism these beneficial effects anthocyanins are, however, hard to explain, given their very low bioavailability due poor intestinal absorption. We propose that free fatty acid receptor 1 (FFA1, also named GPR40), is involved in an inhibitory effect anthocyanidin delphinidin over glucose show direct on...

10.3390/ijms18040750 article EN International Journal of Molecular Sciences 2017-04-05

The classic view for hypothalamic regulation of anterior pituitary (AP) hormone secretion holds that release each AP is controlled specifically by a corresponding hypothalamic-releasing (HRH). In this scenario, binding given HRH (thyrotropin-, growth hormone-, corticotropin-, and luteinizing hormone-releasing hormones) to specific receptors in its target cell increases the concentration cytosolic Ca 2+ ([Ca ] i ), thereby selectively stimulating appropriate hormone. However, “paradoxical”...

10.1073/pnas.94.25.14132 article EN Proceedings of the National Academy of Sciences 1997-12-09
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