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1.
J Biol Regul Homeost Agents ; 35(3): 1029-1040, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34155876

RESUMEN

Proliferation of vascular smooth muscle cells (VSMCs) participates in multiple cardiovascular disorders, while the mechanism remains unclear. This study aims to investigate the effects of insulin on VSMC. Insulin was used to stimulate rat VSMCs, and the effects on cell cycle and proliferation were subsequently analyzed using flow cytometry. Furthermore, AP-1 and SM-α overexpression vectors were constructed and transfected into VSMCs. AP-1 and SM-α were inhibited by SR11302 and SM-α siRNA, respectively. The mRNA and protein expression levels were subsequently detected using the reversetranscription quantitative polymerase chain reaction and western blotting, respectively. AP-1 and SM-α gene promoter binding sites were determined using luciferase and chromatin immunoprecipitation assays. As a result, we found that high dose of insulin promoted proliferation of VSMCs and increased the percentage of cells in the S phase by downregulating AP-1. AP-1 was identified to bind to the SM-α gene promoter at locus 2-177 to upregulate SM-α gene expression. Inhibition of AP-1 led to the decrease of SM-α expression. Overexpression of SM-α directly suppressed proliferation of VSMCs, while knocking it down promoted the process. Therefore, this study revealed that insulin downregulated the expression of the SM-α gene by inhibiting AP-1, which in turn facilitated proliferation of VSMCs.


Asunto(s)
Músculo Liso Vascular , Factor de Transcripción AP-1 , Actinas , Animales , Proliferación Celular , Células Cultivadas , Insulina/farmacología , Miocitos del Músculo Liso , Ratas , Factor de Transcripción AP-1/genética
2.
Zhonghua Zhong Liu Za Zhi ; 40(2): 99-104, 2018 Feb 23.
Artículo en Zh | MEDLINE | ID: mdl-29502368

RESUMEN

Objective: To explore relationships between the enrichment of ETBF, Fn, Hp in feces, tissues and colorectal cancer. Methods: Feces, lesion tissue and adjacent tissue from 24 patients with colorectal cancer and 31 patients with adenomas were collected, and we collected Feces and tissue of 20 healthy control persons. Then the copy numbers of enterotoxigenic B. fragilis (ETBF), Fusobacterium nucleatum (Fn) and Helicobacter pylori (Hp) were determined by quantitative real-time PCR. Immunohistochemical method was used to examine the expression intensity of EGFR and p53, and the relationships between different expression intensity of EGFR, p53 and the numbers of three bacterias. Results: In the feces, copy numbers of ETBF and Fn were as follous: colorectal cancer group>adenomas group>healthy control group (P<0.05). Copy numbers of Hp were as follous: colorectal cancer group>healthy control group (P<0.01); adenomas group>healthy control group (P<0.01). In the tissue, copy numbers of ETBF, Fn were as follows: colorectal cancer group>adenomas group>healthy control group (P<0.05). Copy numbers of Hp were as follows: colorectal cancer group>healthy control group (P<0.01); adenomas group>healthy control group (P<0.01). Copy numbers of those three bacteria in the lesion tissue and the adjacent tissue had no significant difference. This happened both in colorectal cancer group and adenomas group. The different expression intensity of EGFR, p53 and the number of three bacteria showed no obviously statistical correlation(P>0.05). Conclusion: Adenomatous polyp and colorectal cancer patients show high enrichment of ETBF, Fn and Hp in both feces and tissues. ETBF, Fn and Hp probably contribute to the development of adenomatous polyp and colorectal cancer. Trial registration Chinese Clinical Trial Registry, ChiCTR-BOC-17012509.


Asunto(s)
Adenoma/microbiología , Bacteroides fragilis , Neoplasias Colorrectales/microbiología , Heces/microbiología , Fusobacterium nucleatum , Helicobacter pylori , Estudios de Casos y Controles , Humanos , Reacción en Cadena en Tiempo Real de la Polimerasa
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