Bárbara Victoria Fernández García (Spain)

INSTITUTO DE INVESTIGACIONES BIOMEDICAS ALBERTO SOLS CSIC-UAM Biochemistry
Born in Madrid (1992), she obtained her Degree in Pharmacy from the Complutense University, with special mention of Industrial Itinerary. She completed her Final Degree Project on Phosphazenes (Department of Inorganic Chemistry); as well as months of supervised internships at pharmacy office and at the San Carlos Clinical Hospital. She finished her Master in Microbiology and Parasitology: Research and Development, also at the Complutense University. She remained collaborating in the Department of Microbiology in different projects, such as the SWI program for the discovery of new antibiotics-producing microbial strains and the dissemination of the rational use of antimicrobials. Having published several scientific publications, she has participated in numerous projects, conferences, courses and teaching activities. She has presented many communications at conferences, winning awards for the best communication. Since 2017, Victoria has been a contracted predoctoral researcher at the Alberto Sols Biomedical Research Institute (IIB), CSIC. Working in the Lisardo Boscá's group, where she is preparing her doctoral thesis and is involved in different projects, she is scientist at the Center for Biomedical Research Network (CIBER) and integrated in the CIBERCV. She is a member of scientific societies, such as the EAS, EACVI, Council on Cardiovascular Genomics, SEM and SEBBM.

Author Of 1 Presentation

 Conference Calendar

O066 - Macrophages, Smooth Muscle Cells and Nod1 inhibition in advanced stages of Atherosclerosis: a clue to plaque stabilization and atherothrombosis attenuation (ID 11)

Session Type
Vascular Biology
Session Name
Workshop: Extracellular matrix components: guardians of vascular health (ID 12)
Session Time
10:30 - 12:00
Date
Wed, 02.06.2021
Room
Live Streamed
Lecture Time
11:11 - 11:19
Presenter

Abstract

Background and Aims

Macrophages and Smooth Muscle Cells (SMCs) are well known to have a preeminent role in plaque necrosis and rupture. These events, added to inflammation and thin layers of collagen unchain atherothrombosis, the main cause of Acute Coronary Syndromes (ACs). Pattern recognition receptor Nucleotide-Binding Oligomerization Domain-1 (NOD1) has previously been linked to inflammation and cardiovascular diseases. The aim of this work was to unveil the function of NOD1 in the plaque stabilization phenomena in the late stages of the disease.

Methods

Athero-prone Apoe-/-Nod1-/- against Apoe-/-mice were treated with high fat diet for 16 weeks in order to characterized the advanced lesions in the aortic sinus. Proliferation, apoptosis and foam cell formation were assessed in the atheroma lesions and in primary cell cultures of macrophages and vascular SMCs. In addition, human coronary arteries were employed. Cell procedures, flow cytometry, immunofluorescences, histochemistry techniques, qRT-PCR, western blot and kinetic colorimetric assays were performed.

Results

ORO stained aorta showed a reduction in the atheroma of the double-knockout mice. NOD1 staining in human atherosclerotic coronary arteries was enhanced near lipid deposition areas and NOD1 expression was higher in Macrophages (MAC3 marker) and SMCs (Smooth Muscle α-actin marker) of these plaques. We also demonstrated that NOD1 deletion or inhibition reduced myeloid cells infiltration, macrophage and SMCs apoptosis, fibrous caps and collagen content. Interestingly, Nod1-/-SMCs presented higher proliferation rates.

Conclusions

To conclude, here we determine that both macrophages and SMCs are subjected to NOD1 regulation under advanced atherogenesis condition, triggering plaque vulnerability and thus promoting atherothrombosis and ACS.

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Presenter of 1 Presentation

 Conference Calendar

O066 - Macrophages, Smooth Muscle Cells and Nod1 inhibition in advanced stages of Atherosclerosis: a clue to plaque stabilization and atherothrombosis attenuation (ID 11)

Session Type
Vascular Biology
Session Name
Workshop: Extracellular matrix components: guardians of vascular health (ID 12)
Session Time
10:30 - 12:00
Date
Wed, 02.06.2021
Room
Live Streamed
Lecture Time
11:11 - 11:19
Presenter

Abstract

Background and Aims

Macrophages and Smooth Muscle Cells (SMCs) are well known to have a preeminent role in plaque necrosis and rupture. These events, added to inflammation and thin layers of collagen unchain atherothrombosis, the main cause of Acute Coronary Syndromes (ACs). Pattern recognition receptor Nucleotide-Binding Oligomerization Domain-1 (NOD1) has previously been linked to inflammation and cardiovascular diseases. The aim of this work was to unveil the function of NOD1 in the plaque stabilization phenomena in the late stages of the disease.

Methods

Athero-prone Apoe-/-Nod1-/- against Apoe-/-mice were treated with high fat diet for 16 weeks in order to characterized the advanced lesions in the aortic sinus. Proliferation, apoptosis and foam cell formation were assessed in the atheroma lesions and in primary cell cultures of macrophages and vascular SMCs. In addition, human coronary arteries were employed. Cell procedures, flow cytometry, immunofluorescences, histochemistry techniques, qRT-PCR, western blot and kinetic colorimetric assays were performed.

Results

ORO stained aorta showed a reduction in the atheroma of the double-knockout mice. NOD1 staining in human atherosclerotic coronary arteries was enhanced near lipid deposition areas and NOD1 expression was higher in Macrophages (MAC3 marker) and SMCs (Smooth Muscle α-actin marker) of these plaques. We also demonstrated that NOD1 deletion or inhibition reduced myeloid cells infiltration, macrophage and SMCs apoptosis, fibrous caps and collagen content. Interestingly, Nod1-/-SMCs presented higher proliferation rates.

Conclusions

To conclude, here we determine that both macrophages and SMCs are subjected to NOD1 regulation under advanced atherogenesis condition, triggering plaque vulnerability and thus promoting atherothrombosis and ACS.

Hide