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Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model.
Int J Mol Sci 2017; 18(8)IJ

Abstract

Galectin-3 (Gal-3) is involved in cardiovascular fibrosis and aortic valve (AV) calcification. We hypothesized that Gal-3 pharmacological inhibition with modified citrus pectin (MCP) could reduce aortic and AV remodeling in normotensive rats with pressure overload (PO). Six weeks after aortic constriction, vascular Gal-3 expression was up-regulated in male Wistar rats. Gal-3 overexpression was accompanied by an increase in the aortic media layer thickness, enhanced total collagen, and augmented expression of fibrotic mediators. Further, vascular inflammatory markers as well as inflammatory cells content were greater in aorta from PO rats. MCP treatment (100 mg/kg/day) prevented the increase in Gal-3, media thickness, fibrosis, and inflammation in the aorta of PO rats. Gal-3 levels were higher in AVs from PO rats. This paralleled enhanced AV fibrosis, inflammation, as well as greater expression of calcification markers. MCP treatment prevented the increase in Gal-3 as well as fibrosis, inflammation, and calcification in AVs. Overall, Gal-3 is overexpressed in aorta and AVs from PO rats. Gal-3 pharmacological inhibition blocks aortic and AV remodeling in experimental PO. Gal-3 could be a new therapeutic approach to delay the progression and the development of aortic remodeling and AV calcification in PO.

Authors+Show Affiliations

Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. jaime.ibarrola.ulzurrun@navarra.es.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. ernesto_mart@hotmail.com.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. jr.sadaba.sagredo@navarra.es.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. varriet8@hotmail.com.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. amaiagpu@hotmail.com.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. virginia.alvarez.asiain@navarra.es.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. amaya.fernandez.decelis@navarra.es.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. alicia.gainza.calleja@navarra.es.Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigations Cliniques-Plurithématique 1433, UMR 1116 Université de Lorraine, CHRU de Nancy, French-Clinical Research Infrastructure Network (F-CRIN) INI-CRCT, Nancy 54500, France. p.rossignol@chu-nancy.fr.Department of Physiology, School of Medicine, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), Universidad Complutense, Madrid 28040, Spain. vcara@ucm.es.Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona 31008, Spain. natalia.lopez.andres@navarra.es. Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigations Cliniques-Plurithématique 1433, UMR 1116 Université de Lorraine, CHRU de Nancy, French-Clinical Research Infrastructure Network (F-CRIN) INI-CRCT, Nancy 54500, France. natalia.lopez.andres@navarra.es.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28758988

Citation

Ibarrola, Jaime, et al. "Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model." International Journal of Molecular Sciences, vol. 18, no. 8, 2017.
Ibarrola J, Martínez-Martínez E, Sádaba JR, et al. Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model. Int J Mol Sci. 2017;18(8).
Ibarrola, J., Martínez-Martínez, E., Sádaba, J. R., Arrieta, V., García-Peña, A., Álvarez, V., ... López-Andrés, N. (2017). Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model. International Journal of Molecular Sciences, 18(8), doi:10.3390/ijms18081664.
Ibarrola J, et al. Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model. Int J Mol Sci. 2017 Jul 31;18(8) PubMed PMID: 28758988.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model. AU - Ibarrola,Jaime, AU - Martínez-Martínez,Ernesto, AU - Sádaba,J Rafael, AU - Arrieta,Vanessa, AU - García-Peña,Amaia, AU - Álvarez,Virginia, AU - Fernández-Celis,Amaya, AU - Gainza,Alicia, AU - Rossignol,Patrick, AU - Cachofeiro Ramos,Victoria, AU - López-Andrés,Natalia, Y1 - 2017/07/31/ PY - 2017/06/14/received PY - 2017/07/28/revised PY - 2017/07/28/accepted PY - 2017/8/1/entrez PY - 2017/8/2/pubmed PY - 2018/4/18/medline KW - Galectin-3 KW - aorta KW - pressure overload KW - valve JF - International journal of molecular sciences JO - Int J Mol Sci VL - 18 IS - 8 N2 - Galectin-3 (Gal-3) is involved in cardiovascular fibrosis and aortic valve (AV) calcification. We hypothesized that Gal-3 pharmacological inhibition with modified citrus pectin (MCP) could reduce aortic and AV remodeling in normotensive rats with pressure overload (PO). Six weeks after aortic constriction, vascular Gal-3 expression was up-regulated in male Wistar rats. Gal-3 overexpression was accompanied by an increase in the aortic media layer thickness, enhanced total collagen, and augmented expression of fibrotic mediators. Further, vascular inflammatory markers as well as inflammatory cells content were greater in aorta from PO rats. MCP treatment (100 mg/kg/day) prevented the increase in Gal-3, media thickness, fibrosis, and inflammation in the aorta of PO rats. Gal-3 levels were higher in AVs from PO rats. This paralleled enhanced AV fibrosis, inflammation, as well as greater expression of calcification markers. MCP treatment prevented the increase in Gal-3 as well as fibrosis, inflammation, and calcification in AVs. Overall, Gal-3 is overexpressed in aorta and AVs from PO rats. Gal-3 pharmacological inhibition blocks aortic and AV remodeling in experimental PO. Gal-3 could be a new therapeutic approach to delay the progression and the development of aortic remodeling and AV calcification in PO. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/28758988/Beneficial_Effects_of_Galectin_3_Blockade_in_Vascular_and_Aortic_Valve_Alterations_in_an_Experimental_Pressure_Overload_Model_ L2 - http://www.mdpi.com/resolver?pii=ijms18081664 DB - PRIME DP - Unbound Medicine ER -