MARIA CLAUDIA COSTA IRIGOYEN
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/65, Hospital das Clínicas, Faculdade de Medicina
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/65, Hospital das Clínicas, Faculdade de Medicina
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
- Molecular mapping of the regenerative niche in a murine model of myocardial infarction(2012) ALVES, Gabriela Dornelles; PAZZINE, Mariana; BRAGA, Luisa Maria Gomes De Macedo; IRIGOYEN, Maria Claudia; ANGELIS, Katia De; IKUTA, Nilo; CAMASSOLA, Melissa; NARDI, Nance BeyerAdult stem cells are distributed through the whole organism, and present a great potential for the therapy of different types of disease. For the design of efficient therapeutic strategies, it is important to have a more detailed understanding of their basic biological characteristics, as well as of the signals produced by damaged tissues and to which they respond. Myocardial infarction (MI), a disease caused by a lack of blood flow supply in the heart, represents the most common cause of morbidity and mortality in the Western world. Stem cell therapy arises as a promising alternative to conventional treatments, which are often ineffective in preventing loss of cardiomyocytes and fibrosis. Cell therapy protocols must take into account the molecular events that occur in the regenerative niche of MI. In the present study, we investigated the expression profile of ten genes coding for chemokines or cytokines in a murine model of MI, aiming at the characterization of the regenerative niche. MI was induced in adult C57BL/6 mice and heart samples were collected after 24 h and 30 days, as well as from control animals, for quantitative RT-PCR. Expression of the chemokine genes CCL2, CCL3, CCL4, CCL7, CXCL2 and CXCL10 was significantly increased 24 h after infarction, returning to baseline levels on day 30. Expression of the CCL8 gene significantly increased only on day 30, whereas gene expression of CXCL12 and CX3CL1 were not significantly increased in either ischemic period. Finally, expression of the IL-6 gene increased 24 h after infarction and was maintained at a significantly higher level than control samples 30 days later. These results contribute to the better knowledge of the regenerative niche in MI, allowing a more efficient selection or genetic manipulation of cells in therapeutic protocols.
- Moderate exercise training promotes adaptations in coronary blood flow and adenosine production in normotensive rats(2011) ROQUE, Fernanda R.; SOCI, Ursula Paula Reno; ANGELIS, Katia De; COELHO, Marcele A.; FURSTENAU, Cristina R.; VASSALLO, Dalton V.; IRIGOYEN, Maria Claudia; OLIVEIRA, Edilamar M.OBJECTIVES: Aerobic exercise training prevents cardiovascular risks. Regular exercise promotes functional and structural adaptations that are associated with several cardiovascular benefits. The aim of this study is to investigate the effects of swimming training on coronary blood flow, adenosine production and cardiac capillaries in normotensive rats. METHODS: Wistar rats were randomly divided into two groups: control (C) and trained (T). An exercise protocol was performed for 10 weeks and 60 min/day with a tail overload of 5% bodyweight. Coronary blood flow was quantified with a color microsphere technique, and cardiac capillaries were quantified using light microscopy. Adenine nucleotide hydrolysis was evaluated by enzymatic activity, and protein expression was evaluated by western blot. The results are presented as the means +/- SEMs (p<0.05). RESULTS: Exercise training increased the coronary blood flow and the myocardial capillary-to-fiber ratio. Moreover, the circulating and cardiac extracellular adenine nucleotide hydrolysis was higher in the trained rats than in the sedentary rats due to the increased activity and protein expression of enzymes, such as E-NTPDase and 5'-nucleotidase. CONCLUSIONS: Swimming training increases coronary blood flow, number of cardiac capillaries, and adenine nucleotide hydrolysis. Increased adenosine production may be an important contributor to the enhanced coronary blood flow and angiogenesis that were observed in the exercise-trained rats; collectively, these results suggest improved myocardial perfusion.
article 1 Citação(ões) na Scopus Treinamento físico de natação promove remodelamento cardíaco e melhora a perfusão sanguínea no músculo cardíaco de SHR via mecanismo dependente de adenosina(2011) BARROS, Juliana Goncalves de; REDONDO, Fernanda Roque; ZAMO, Fernanda de Souza; MATTOS, Katt Cristina; ANGELIS, Katia De; IRIGOYEN, Maria Claudia; OLIVEIRA, Edilamar Menezes dePhysical training (PT) has been used as non-pharmacological therapy for hypertension treatment and swimming physical training is recognized for yielding cardiac remodeling in experiments. However, little is known on the effects of adenosine (Ado) resulting from PT as hypertension prevention and treatment. Objective: To evaluate cardiac remodeling and the role of adenosine in cardiac blood flow distribution (BF) to the myocardium after aerobic PT on SHR. Methods: 28 male SHR, babies and adults, were submitted to swimming training protocol during 10 weeks (5 times a week - 1 h a day). Colored micro spheres protocols were used to evaluate blood flow, morphological techniques were used to evaluate cardiac hypertrophy and biochemical analysis were performed to verify enzyme activity in the adenosine formation. Results: PT attenuated the evolution of hypertension in the SHR babies group (S: 145 2; T: 140 2mmHg), HR was lower in adult SHR (S: 340 4; T: 321 6bpm) and CH increased in both groups (TB: 12%; TA: 10%). At basal condition, BF was increased in trained babies (S: 4.745 +/- 2.145; T: 6.970 +/- 2.374mi/heart) and higher vasodilatation response was observed due to adenosine infusion (S: 18.946 +/- 6.685; T: 25.045 +/- 7.031mi/heart). In this group, the PT promoted a higher 5'-nucleotidase enzyme activity leading to a higher adenosine formation (S: 0.45 +/- 0.09; T: 1.01 +/- 0.05). Conclusion: The swimming training developed CH as well as increased adenosine formation, leading to higher coronary blood flow, and its important role in hypertension regulation was demonstrated.- Cholinergic stimulation with pyridostigmine modulates a heart-spleen axis after acute myocardial infarction in spontaneous hypertensive rats(2021) BANDONI, Robson Luiz; CHOQUE, Pamela Nithzi Bricher; DELLE, Humberto; MORAES, Tercio Lemos de; PORTER, Maria Helena Mattos; SILVA, Bruno Durante da; NEVES, Gizele Alves; IRIGOYEN, Maria-Claudia; ANGELIS, Katia de; PAVLOV, Valentin A.; ULLOA, Luis; CONSOLIM-COLOMBO, Fernanda MarcianoThe mechanisms regulating immune cells recruitment into the heart during healing after an acute myocardial infarction (AMI) have major clinical implications. We investigated whether cholinergic stimulation with pyridostigmine, a cholinesterase inhibitor, modulates heart and spleen immune responses and cardiac remodeling after AMI in spontaneous hypertensive rats (SHRs). Male adult SHRs underwent sham surgery or ligation of the left coronary artery and were randomly allocated to remain untreated or to pyridostigmine treatment (40 mg/kg once a day by gavage). Blood pressure and heart rate variability were determined, and echocardiography was performed at day six after MI. The heart and spleen were processed for immunohistochemistry cellular analyses (CD3(+) and CD4(+) lymphocytes, and CD68(+) and CD206(+) macrophages), and TNF levels were determined at day seven after MI. Pyridostigmine treatment increased the parasympathetic tone and T CD4(+) lymphocytes in the myocardium, but lowered M1/M2 macrophage ratio towards an anti-inflammatory profile that was associated with decreased TNF levels in the heart and spleen. Treatment with this cholinergic agent improved heart remodeling manifested by lower ventricular diameters and better functional parameters. In summary, cholinergic stimulation by pyridostigmine enhances the parasympathetic tone and induces anti-inflammatory responses in the heart and spleen fostering cardiac recovery after AMI in SHRs.
- Insulin Treatment Does Not Prevent EARLY Autonomic Cardiovascular and Diastolic Dysfunctions in Streptozotocin-Induced Diabetic Rats(2024) FREITAS, Sarah C. F.; DUTRA, Marina R. H.; DOURADO, Paulo M. M.; MIRANDA, Victor Hugo de Martins; SANTOS, Camila P. dos; SANCHES, Iris C.; IRIGOYEN, Maria-Claudia; ANGELIS, Katia DeRecent studies have found increased cardiovascular mortality risk in patients with type 1 diabetes when compared to normoglycemic people, even when they were kept under good glycemic control. However, the mechanisms underlying this condition have yet to be fully understood. Using streptozotocin (STZ)-induced diabetic rats, we evaluated the effects of insulin replacement therapy on cardiac, autonomic, inflammatory, and oxidative stress parameters. Daily treatment with insulin administrated subcutaneously in the STZ-diabetic rats showed a reduction in hyperglycemia (>250 mg/dL) to normalized values. The insulin treatment was effective in preventing alterations in cardiac morphometry and systolic function but had no impact on diastolic function. Also, the treatment was not able to prevent the impairment of baroreflex-tachycardic response and systolic arterial pressure variability (SAP-V). A correlation was found between improvement of these autonomic parameters and higher levels of IL-10 and lower levels of oxidized glutathione. Our findings show that insulin treatment was not able to prevent diastolic, baroreflex, and SAP-V dysfunction, suggesting an outstanding cardiovascular risk, even after obtaining a good glycemic control in STZ-induced diabetic rats. This study shed light on a relatively large population of diabetic patients in need of other therapies to be used in combination with insulin treatment and thus more effectively manage cardiovascular risk.