Inflammation accelerates lipid dysregulation mediated cardiac fibrosis through enhancing myocardial endothelial-to-mesenchymal transition / 中华心血管病杂志
Chinese Journal of Cardiology
;
(12): 602-606, 2013.
Artículo
en Chino
| WPRIM
| ID: wpr-261487
ABSTRACT
<p><b>OBJECTIVE</b>Dyslipidemia and chronic inflammation are risk factors of cardiac fibrosis. This study was aimed to investigate their possible synergetic effects and underlying mechanisms on progression of cardiac fibrosis in apolipoprotein E knockout (ApoE -/-) mice.</p><p><b>METHODS</b>Twenty-four ApoE-/- mice were divided into normal chow diet (control), high fat diet (HFD group), and HFD plus subcutaneously injection of 10% casein (inflammation group) for 8 weeks. Lipid profile and serum amyloid A (SAA) were examined by clinical biochemical assays and Enzyme-Linked Immunosorbent Assay, respectively. Hematoxylin-eosin staining (HE) and Masson staining were used to evaluate the myocardial accumulation of lipid and collagen. Collagen I protein expression was detected by immunohistochemical staining. Endothelial-to-mesenchymal transition related protein expressions were determined by Western blot.</p><p><b>RESULTS</b>Serum SAA level was significantly higher in inflammation group [(127.42 ± 26.99) ng/ml] than in control [(15.40 ± 7.62) ng/ml] and HFD [(8.17 ± 0.72) ng/ml] group (all P < 0.01).However serum levels of triglyceride, total cholesterol, and low density lipoprotein (LDL) cholesterol were significantly higher in HFD group than in inflammation and control groups[TG (7.53 ± 2.05) mmol/L vs. (3.43 ± 0.79) mmol/L; TC (27.80 ± 3.99) mmol/L vs. (14.94 ± 1.92) mmol/L;LDL-C (11.56 ± 2.56) mmol/L vs. (9.46 ± 1.31) mmol/L, all P < 0.05) . Foam cell formation in cardiac vessels, myocardial collagen deposit, protein expressions of collagen I, CD31, and alpha-smooth muscle actin (α-SMA) were all significantly higher in inflammation group than in HFD group (all P < 0.05) suggesting that inflammation contributes to the phenotype endothelial-to-mesenchymal transition in heart.</p><p><b>CONCLUSION</b>Inflammation exacerbates dyslipidemia mediated cardiac fibrosis in ApoE-/- mice partly through enhancing myocardial endothelial-to-mesenchymal transition.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Patología
/
Apolipoproteínas E
/
Fibrosis
/
Proteína Amiloide A Sérica
/
Ratones Noqueados
/
Modelos Animales de Enfermedad
/
Metabolismo de los Lípidos
/
Transición Epitelial-Mesenquimal
/
Genética
/
Inflamación
Tipo de estudio:
Estudio pronóstico
/
Factores de riesgo
Límite:
Animales
Idioma:
Chino
Revista:
Chinese Journal of Cardiology
Año:
2013
Tipo del documento:
Artículo
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