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Set7 Deletion Prevents Glucose Intolerance and Improves the Recovery of Cardiac Function After Ischemia and Reperfusion in Obese Female Mice.
Miranda, Juliane B; Lunardon, Guilherme; Lima, Vanessa M; de Oliveira Silva, Tábatha; Lino, Caroline A; Jensen, Leonardo; Irigoyen, Maria Cláudia; da Silva, Ivson Bezerra; Lu, Yao Wei; Liu, Jianming; Donato Júnior, Jose; Barreto-Chaves, Maria Luiza M; Wang, Da-Zhi; Diniz, Gabriela P.
Afiliación
  • Miranda JB; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Lunardon G; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Lima VM; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • de Oliveira Silva T; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Lino CA; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Jensen L; Hypertension Unit, Heart Institute, University of Sao Paulo, Sao Paulo, Brazil.
  • Irigoyen MC; Hypertension Unit, Heart Institute, University of Sao Paulo, Sao Paulo, Brazil.
  • da Silva IB; Department of Morphology, Federal University of Paraiba, Paraiba, Brazil.
  • Lu YW; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
  • Liu J; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
  • Donato Júnior J; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Barreto-Chaves MLM; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
  • Wang DZ; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
  • Diniz GP; Center for Regenerative Medicine, USF Health Heart Institute, University of South Florida, Tampa, FL, USA.
Cell Physiol Biochem ; 56(3): 293-309, 2022 Jun 30.
Article en En | MEDLINE | ID: mdl-35781359
BACKGROUND/AIMS: An obesogenic diet (high fat and sugar, low fiber) is associated with an increased risk for metabolic and cardiovascular disorders. Previous studies have demonstrated that epigenetic changes can modify gene transcription and protein function, playing a key role in the development of several diseases. The methyltransferase Set7 methylates histone and non-histone proteins, influencing diverse biological and pathological processes. However, the functional role of Set7 in obesity-associated metabolic and cardiovascular complications is unknown. METHODS: Wild type and Set7 knockout female mice were fed a normal diet or an obesogenic diet for 12 weeks. Body weight gain and glucose tolerance were measured. The 3T3-L1 cells were used to determine the role of Set7 in white adipogenic differentiation. Cardiac morphology and function were evaluated by histology and echocardiography. An ex vivo Langendorff perfusion system was used to model cardiac ischemia/reperfusion (I/R). RESULTS: Here, we report that Set7 protein levels were enhanced in the heart and perigonadal adipose tissue (PAT) of female mice fed an obesogenic diet. Significantly, loss of Set7 prevented obesogenic diet-induced glucose intolerance in female mice although it did not affect the obesogenic diet-induced increase in body weight gain and adiposity in these animals, nor did Set7 inhibition change white adipogenic differentiation in vitro. In addition, loss of Set7 prevented the compromised cardiac functional recovery following ischemia and reperfusion (I/R) injury in obesogenic diet-fed female mice; however, deletion of Set7 did not influence obesogenic diet-induced cardiac hypertrophy nor the hemodynamic and echocardiographic parameters. CONCLUSION: These data indicate that Set7 plays a key role in obesogenic diet-induced glucose intolerance and compromised myocardial functional recovery after I/R in obese female mice.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Intolerancia a la Glucosa Límite: Animals Idioma: En Revista: Cell Physiol Biochem Asunto de la revista: BIOQUIMICA / FARMACOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Alemania
Texto completo
Añadir a Mi BVS
Imprimir
XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Intolerancia a la Glucosa Límite: Animals Idioma: En Revista: Cell Physiol Biochem Asunto de la revista: BIOQUIMICA / FARMACOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Alemania