María Martín Estebané

María Martín Estebané
  • PhD
  • Postdoctoral Researcher at University of Granada

Postdoctoral Researcher

About

40
Publications
5,559
Reads
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505
Citations
Introduction
I am currently a postdoctoral researcher at the University of Granada. My research focuses on understanding the molecular mechanisms underlying neuroinflammation in neurodegenerative diseases.
Current institution
University of Granada
Current position
  • Postdoctoral Researcher
Additional affiliations
October 2013 - June 2015
University of Granada
Position
  • Lecturer
March 2021 - January 2022
Spanish National Research Council
Position
  • Postdoctoral Researcher
June 2018 - January 2021
University of Southampton
Position
  • Postdoctoral Researcher
Education
January 2012 - September 2017
University of Granada
Field of study
October 2010 - December 2011
University of Granada
Field of study
October 2005 - July 2010
University of Granada
Field of study

Publications

Publications (40)
Article
Full-text available
Microglial cell precursors located in the area of the base of the pecten and the optic nerve head (BP/ONH) start to enter the retina of quail embryos at the 7th day of incubation (E7), subsequently colonizing the entire retina by central-to-peripheral tangential migration, as previously shown by our group. The present study demonstrates a precise c...
Article
Full-text available
Alzheimer’s disease (AD) is the most common form of dementia, affecting two-thirds of people with dementia in the world. To date, no disease-modifying treatments are available to stop or delay the progression of AD. This chronic neurodegenerative disease is dominated by a strong innate immune response, whereby microglia plays a central role as the...
Article
Full-text available
The proliferation and activation of microglia, the resident macrophages in the brain, is a hallmark of many neurodegenerative diseases such as Alzheimer's disease (AD) and prion disease. Colony stimulating factor 1 receptor (CSF1R) is critically involved in regulating microglial proliferation, and CSF1R blocking strategies have been recently used t...
Preprint
Full-text available
The sustained proliferation of microglia is a key hallmark of Alzheimer's disease (AD), accelerating its progression. Here, we sought to understand the long-term impact of the early and prolonged microglial proliferation observed in AD, hypothesising that extensive and repeated cycling would engender a distinct transcriptional and phenotypic trajec...
Article
Full-text available
Alterations induced by maternal immune activation (MIA) during gestation impact the subsequent neurodevelopment of progeny, a process that in humans, has been linked to the development of several neuropsychiatric conditions. To undertake a comprehensive examination of the molecular mechanisms governing MIA, we have devised an in vitro model based o...
Preprint
Alterations induced by maternal immune activation (MIA) during gestation impact the subsequent neurodevelopment of progeny, a process that in humans, has been linked to the development of several neuropsychiatric conditions. To undertake a comprehensive examination of the molecular mechanisms governing MIA, we have devised an in vitro model based o...
Article
Full-text available
Microglia, the brain’s resident macrophages, shape neural development and are key neuroimmune hubs in the pathological signatures of neurodevelopmental disorders. Despite the importance of microglia, their development has not been carefully examined in the human brain, and most of our knowledge derives from rodents. We aimed to address this gap in...
Preprint
Full-text available
Microglia, the brain's resident macrophages, shape neural development and wiring, and are key neuroimmune hubs in the pathological signature of neurodevelopmental disorders. In the human brain, microglial development has not been carefully examined yet, and most of our knowledge derives from rodents. We established an unprecedented collection of 97...
Article
Full-text available
The sustained proliferation of microglia is a key hallmark of Alzheimer’s disease (AD), accelerating its progression. Here, we aim to understand the long-term impact of the early and prolonged microglial proliferation observed in AD, hypothesizing that extensive and repeated cycling would engender a distinct transcriptional and phenotypic trajector...
Preprint
Full-text available
The proliferation and activation of microglia, the resident macrophages in the brain, is a hallmark of many neurodegenerative diseases such as Alzheime's disease (AD) and prion disease. Colony stimulating factor 1 receptor (CSF1R) is critically involved in regulating microglial proliferation, and CSF1R blocking strategies have been recently used to...
Article
Full-text available
Poly(ADP-ribose)polymerases (PARPs) are a family of NAD⁺ consuming enzymes that play a crucial role in many cellular processes, most clearly in maintaining genome integrity. Here, we present an extensive analysis of the alteration of mitochondrial morphology and the relationship to PARPs activity after oxidative stress using an in vitro model of hu...
Data
PARP inhibition restores mitochondrial morphology 4 h after H2O2 treatment. (A) Percentage of type I (small globular; left graph) and type II (tubular including linear, twisted, branched and looped forms; right graph) of mitochondrial morphology prior to quantifying mitochondrial morphology with MicroP software. WRL68 cells pre-incubated 16 h with...
Data
Study of cytotoxic effects of PARPs inhibitors in WRL68 cells. Effects of PARPs inhibitors on the cell viability of WRL68 cells assessed by the MTT method. Cell viability was determined in WRL68 cells incubated with PJ34 or AG14361. To do so, hepatic cells were exposed for 40 h (16 h of pre-treatment and 24 h of post-incubation time) to different c...
Data
PARPs inhibitors block cellular PAR polymer formation. Immunofluorescence detection of PAR polymer (green) in WRL68 cells treated with H2O2 for 15 min in the absence or presence of the PJ34 inhibitor. Immunofluorescence images show that PAR polymer formation is blocked when PARPs inhibitors were used in oxidative treatment. Nuclei were counterstain...
Data
Morphology of mitochondria 4 h after H2O2 treatment. (A) Percentage of type I (small globular; left graph) and type II (tubular including linear, twisted, branched and looped forms; right graph) of mitochondrial morphology. Cells were treated with H2O2 for 30 min and then post-incubated for 4 h prior to quantifying mitochondrial morphology with Mic...
Article
Full-text available
The role of microglia during neurodegeneration remains controversial. We investigated whether microglial cells have a neurotoxic or neuroprotective function in the retina. Retinal explants from 10-day-old mice were treated in vitro with minocycline to inhibit microglial activation, with LPS to increase microglial activation, or with liposomes loade...
Article
PURPOSE. To study the incidence of DNA damage during postnatal development of the retina and its relationship with cell death. METHODS. DNA damage in the developing postnatal retina of C57BL/6 mice was assessed by determining the amount of 8-hydroxy-2'-deoxyguanosine (8-OHdG), indicative of DNA oxidation and related to the formation of DNA single-s...
Article
Full-text available
Inducible nitric oxide synthase (iNOS), which produce large amounts of nitric oxide (NO), is induced in macrophages and microglia in response to inflammatory mediators such as LPS and cytokines. Although iNOS is mainly expressed by microglia that become activated in different pathological and experimental situations, it was recently reported that u...
Article
Organotypic cultures of retinal explants allow the detailed analysis of microglial cells in a cellular microenvironment similar to that in the in situ retina, with the advantage of easy experimental manipulation. However, the in vitro culture causes changes in the retinal cytoarchitecture and induces a microglial response that may influence the res...

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