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Articles by D Luo
Total Records ( 3 ) for D Luo
  Z. J Ou , W Wei , D. D Huang , W Luo , D Luo , Z. P Wang , X Zhang and J. S. Ou

l-Arginine can attenuate pulmonary hypertension (PH) by a mechanism that are not fully understood. This study investigated the molecule mechanism of l-arginine attenuating PH. Sprague Dawley rats were treated with monocrotaline (MCT) with or without l-arginine for 3 or 5 wk. Right ventricular systolic pressure (RVSP), right heart hypertrophy, survival rate, pulmonary artery wall thickness, nitric oxide (NO) concentration, and superoxide anion (O2·–) generation in the lung were measured. Expressions of endothelial nitric oxide synthase (eNOS) and heat shock protein 90 (HSP90), phosphorylation of eNOS at Ser1177, and the association of eNOS and HSP90 in the lung were determined by Western blot and immunoprecipitation experiments. MCT increased RVSP, right heart hypertrophy, mortality, pulmonary artery wall thickness, and O2·– generation and decreased eNOS and HSP90 expression and association, phosphorylation of eNOS at Ser1177, and NO production. l-Arginine decreased RVSP, right heart hypertrophy, mortality, O2·– generation, and pulmonary artery wall thickness and increased NO production. l-Arginine increased eNOS expression, phosphorylation of eNOS at Ser1177, and association of eNOS and HSP90 without significantly altering HSP90 expression. l-Arginine may act through three pathways, providing a substrate for NO generation, preserving eNOS expression/phosphorylation, and maintaining the association of eNOS and HSP90, which allows restoration of eNOS activity and coupling activity, to maintain the balance between NO and O2·– and delay the development of PH.

  Z Han , Z Hong , C Chen , Q Gao , D Luo , Y Fang , Y Cao , T Zhu , X Jiang , Q Ma , W Li , L Han , D Wang , G Xu , S Wang , L Meng , J Zhou and D. Ma

Tumor cells acquire the ability to proliferate uncontrollably, resist apoptosis, sustain angiogenesis and evade immune surveillance. Signal transducer and activator of transcription (STAT) 3 regulates all of these processes in a surprisingly large number of human cancers. Consequently, the STAT3 protein is emerging as an ideal target for cancer therapy. This paper reports the generation of an oncolytic adenovirus (M4), which selectively blocks STAT3 signaling in tumor cells as a novel therapeutic strategy. M4 selectively replicated in tumor cells and expressed high levels of antisense STAT3 complementary DNA during the late phase of the viral infection in a replication-dependent manner. The viral progeny yield of M4 in tumor cells was much higher than that of the parent adenoviral mutants, Ad5/dE1A. M4 effectively silenced STAT3 and its target genes in tumor cells while sparing normal cells and exhibited potent antitumoral efficacy in vitro and in vivo. Systemic administration of M4 significantly inhibited tumor growth in an orthotopic gastric carcinoma mouse model, eliminated abdominal cavity metastases and prolonged survival time. In summary, M4 has low toxicity and great potential as a therapeutic agent for different types of cancers.

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