Arancha R. Gortázar

ORCID: 0000-0001-5072-3141
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About
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Research Areas
  • Bone Metabolism and Diseases
  • Bone health and treatments
  • Bone health and osteoporosis research
  • Knee injuries and reconstruction techniques
  • Osteoarthritis Treatment and Mechanisms
  • Mesenchymal stem cell research
  • Tendon Structure and Treatment
  • Immune cells in cancer
  • Wnt/β-catenin signaling in development and cancer
  • Caveolin-1 and cellular processes
  • Genetic and Kidney Cyst Diseases
  • Biomarkers in Disease Mechanisms
  • MicroRNA in disease regulation
  • Phagocytosis and Immune Regulation
  • Amino Acid Enzymes and Metabolism
  • Periodontal Regeneration and Treatments
  • Protease and Inhibitor Mechanisms
  • Hedgehog Signaling Pathway Studies
  • Cytokine Signaling Pathways and Interactions
  • Chemical Synthesis and Analysis
  • S100 Proteins and Annexins
  • Genetic Syndromes and Imprinting
  • Growth Hormone and Insulin-like Growth Factors
  • Parathyroid Disorders and Treatments
  • Cell Adhesion Molecules Research

Universidad San Pablo CEU
2012-2024

Indiana University School of Medicine
2015

Institute of Cell Biology and Neurobiology
2015

Xiaomi (China)
2015

Ross School
2015

Indiana University – Purdue University Indianapolis
2015

Comunidad de Madrid
2010

Central Arkansas Veterans Healthcare System
2007-2008

University of Arkansas for Medical Sciences
2007-2008

Hospital Universitario Fundación Jiménez Díaz
2002-2008

The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators senescence. mice, these instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. cell metabolic failure induces the accumulation circulating cytokines, resembles...

10.1126/science.aax0860 article EN Science 2020-05-21

Osteocytes, former osteoblasts buried within bone, are thought to orchestrate skeletal adaptation mechanical stimuli. However, it remains unknown whether hormones control homeostasis through actions on osteocytes. Parathyroid hormone (PTH) stimulates bone remodeling and may cause loss or gain depending the balance between resorption formation. Herein, we demonstrate that transgenic mice expressing a constitutively active PTH receptor exclusively in osteocytes exhibit increased mass...

10.1371/journal.pone.0002942 article EN cc-by PLoS ONE 2008-08-12

Skeletal aging results in apoptosis of osteocytes, cells embedded bone that control the generation/function forming and resorbing cells. Aging also decreases connexin43 (Cx43) expression bone; osteocytic Cx43 deletion partially mimics skeletal phenotype old mice. Particularly, increase osteocyte apoptosis, osteoclast number resorption on endocortical surfaces. We examined herein molecular signaling events responsible for recruitment triggered by deficiency. Cx43-silenced MLO-Y4 (Cx43def)...

10.1111/acel.12586 article EN cc-by Aging Cell 2017-03-19

Apoptosis of osteocytes and osteoblasts precedes bone resorption loss with reduced mechanical stimulation, receptor activator NF-κB ligand (RANKL) expression is increased unloading in mice. Because are major RANKL producers, we hypothesized that apoptotic signal to neighboring increase expression, which, turn, increases osteoclastogenesis resorption. The traditional bisphosphonate (BP) alendronate (Aln) or IG9402, a BP analog does not inhibit resorption, prevented the osteocyte apoptosis...

10.1074/jbc.m115.642090 article EN cc-by Journal of Biological Chemistry 2015-06-18

Osteocyte viability is a critical determinant of bone strength and promoted by both mechanical stimulation activation the Wnt signaling pathway. Earlier studies demonstrated that stimuli promote survival osteocytes activating ERKs. Here, we show there interaction between caveolin-1/ERK Wnt/β-catenin pathways in transduction cues into osteocyte survival. Thus, ERK nuclear translocation anti-apoptosis induced are abolished antagonist Dkk1 β-catenin degradation stimulator Axin2. Conversely,...

10.1074/jbc.m112.437921 article EN cc-by Journal of Biological Chemistry 2013-01-30

Abstract Background Bone is one of the major target tissues for Insulin-like Growth Factor I (IGF-I). Low doses IGF-I were able to improve liver-associated osteopenia. In present work, a model partial deficiency was used in order provide insight into mechanisms beneficial actions replacement therapy bone. Methods Several proteins involved osteoblastic/osteocyte and osteoclastic differentiation activity studied three experimental groups: control (CO) group (wild type mice, Igf +/+ , n = 10),...

10.1186/1479-5876-11-271 article EN cc-by Journal of Translational Medicine 2013-10-25

There is an unmet need to understand the mechanisms underlying skeletal deterioration in diabetes mellitus (DM) and develop therapeutic approaches treat bone fragility diabetic patients. We demonstrate herein that mice with type 1 DM induced by streptozotocin exhibited low mass, inferior mechanical material properties, increased resorption, decreased formation, apoptosis of osteocytes, expression osteocyte-derived formation inhibitor Sost/sclerostin. Further, short treatment parathyroid...

10.1002/jbmr.3007 article EN Journal of Bone and Mineral Research 2016-09-28

Type 1 diabetes mellitus (T1D) is associated with bone loss. Given that the Wnt/β‐catenin pathway a major regulator of accrual, we assessed this in mice streptozotozin‐induced T1D. In diabetic mouse long bones, found alterations favouring suppression by using PCR arrays and β‐catenin immunostaining. Downregulation sclerostin, an inhibitor pathway, also occurred, related to increased osteocyte apoptosis. Our data show both N‐ C‐terminal parathyroid hormone‐related peptide fragments might...

10.1016/j.febslet.2010.05.047 article EN FEBS Letters 2010-06-01

Abstract Parathyroid hormone‐related protein (PTHrP) (107–139), in contrast to the N‐terminal fragment PTHrP (1–36), has been shown interact with vascular endothelial growth factor (VEGF) system modulate human osteoblast differentiation. In this study, we evaluated whether interaction might affect osteoblastic cell survival. Pre‐incubation (107–139) for 1–24 h dose‐dependently (0.1–100 nM) inhibited dexamethasone‐ or etoposide‐induced death MG‐63 cells and osteoblast‐like from trabecular...

10.1002/jcp.21547 article EN Journal of Cellular Physiology 2008-07-23

Abstract Osteocytes have a major role in the control of bone remodeling. Mechanical stimulation decreases osteocyte apoptosis and promotes accrual, whereas skeletal unloading is deleterious both respects. PTH1R ablation or overexpression osteocytes mice produces trabecular loss increases mass, respectively. The latter effect was related to decreased apoptosis. Here, putative activation protection conferred by mechanical assessed. Osteocytic MLO-Y4 cells were subjected stimuli represented...

10.1002/jbmr.2439 article EN Journal of Bone and Mineral Research 2014-12-22

Abstract Mechanical stimulation of primary cilia in osteocytes and osteoblasts has been proposed as a mechanism that participates bone cell survival skeletal remodeling. Among different signaling pathways stimulated by cilia, the hedgehog pathway associated with regulation development. Parathyroid hormone (PTH)‐related protein (PTHrP) through PTH 1 receptor (PTH1R) also regulates remodeling during We hypothesize PTH1R concomitantly regulate aim to describe mechanisms mediate these effects...

10.1002/jcp.29636 article EN Journal of Cellular Physiology 2020-02-10

Abstract Osteocytes respond to mechanical forces controlling osteoblast and osteoclast function. Mechanical stimulation decreases osteocyte apoptosis promotes bone formation. Primary cilia have been described as potential mechanosensors in cells. Certain osteogenic responses induced by fluid flow (FF) vitro are decreased primary inhibition MLO‐Y4 osteocytes. The parathyroid hormone (PTH) receptor type 1 (PTH1R) modulates osteoblast, osteoclast, effects upon activation PTH or PTH‐related...

10.1002/jcp.30849 article EN Journal of Cellular Physiology 2022-08-07

Mechanical loading plays a key role in bone formation and maintenance. While unloading induces osteocyte apoptosis loss vivo, mechanical stimuli prevents death through mechanism involving β-catenin accumulation ERK nuclear translocation. Vascular endothelial growth factor (VEGF) has crucial formation, but its interaction with osteocytes is not completely understood. Of interest, VEGF receptor 2 (VEGFR2) recently been shown to mediate the response of cells. The present study aimed evaluate...

10.1002/jcp.24734 article EN Journal of Cellular Physiology 2014-08-07

Abstract The infrapatellar fat pad (IPFP) is a periarticular adipose knee tissue. This tissue contains large number of mesenchymal stem cells (MSCs). In the present work, we wanted to study IPFP MSCs and their relationship differences in two groups, anterior cruciate ligament (ACL) ruptures knees ostheoarthrosis (OA). 42 patients with OA or ACL rupture were analyzed. Isolation, primary culture, genetic proteomic from performed. Gene expression IL‐6, tumor necrosis factor (TNF), IL‐8, HSPA1A...

10.1002/jcp.28532 article EN Journal of Cellular Physiology 2019-03-25

Abstract Osteocytes are the main cells of bone tissue and play a crucial role in formation resorption. Recent studies have indicated that Diabetes Mellitus (DM) affects mass potentially causes higher fracture risk. Previous work on osteocyte cell cultures has demonstrated mechanotransduction is impaired after culture under diabetic pre-conditioning with high glucose (HG), specifically osteoclast recruitment differentiation. The aim this study was to analyze extracellular metabolic changes...

10.1038/s41598-018-38154-6 article EN cc-by Scientific Reports 2019-02-19

Abstract Meniscus had two areas with different vascular supply. Cells of the and synovium were monolayer cultivated. We analyzed expression genes Col1, Col 2A, MMP‐2, MMP‐13, aggrecan in a baseline state after incubation VEGF, TGF‐β, FGF, IGF. found that growth factors used produced major increase MMP‐13 all three areas. In area, stimulation MMP‐3 was by while synovial avascular areas, it caused TGF‐β. MMP‐2 only stimulated area 2A IGF, whereas 1 VEGF. The or meniscus, behave differently...

10.1002/jor.22110 article EN Journal of Orthopaedic Research® 2012-03-23

Aim In the osteoarthritis (OA) disease, all structures of joint are involved. The infrapatellar Hoffa fat pad is rich in macrophages and granulocytes, which also represents a source adipose mesenchymal progenitor cells (ASC) cells. our study, we analyze how OA affects ability ASC-derived from Hoffa's to differentiate into chondrocytes. Material methodology We took knee samples tissue proximal thigh 6 patients diagnosed with severe another an anterior cruciate ligament (ACL) rupture without...

10.1177/1947603516686144 article EN Cartilage 2017-01-10

Parathyroid hormone (PTH)-related protein (PTHrP) seems to affect bone resorption by interaction with cytokines, among them interleukin-6 (IL-6). Recent studies suggest that nuclear factor (NF)-κB activation has an important role in resorption. We assessed whether the N-terminal fragment of PTHrP, and its C-terminal region, unrelated PTH, can activate NF-κB, relationship IL-6 gene induction different rat human osteoblastic cell preparations. Here we present molecular data demonstrating both...

10.1074/jbc.m111013200 article EN cc-by Journal of Biological Chemistry 2002-08-01
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