Li Wang

Nanjing Normal University, Nanjing, Jiangsu Sheng, China

Are you Li Wang?

Claim your profile

Publications (4)18.37 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE: The purpose of the present study was to investigate human papillomavirus (HPV) infection and evaluate the risk factors for occurrence of HPV infection in the prevention of HPV-related cancers in Northwestern China. MATERIALS AND METHODS: In a cross-sectional study, 402 rural women, ages 20 to 60 years in the rural areas of Shiquan County in the Shaanxi Province of China between August 2009 and July 2010 were interviewed and examined, and specimens were collected to identify the HPV type using the polymerase chain reaction. RESULTS: The prevalence rate of HPV was 12.6% (47/373). Coinfections with more types of HPV were detected in 38.3% (18/47) of HPV-positive subjects. There was an age-dependent prevalence, showing the highest prevalence among women in the study between ages 20 and 29 years (18.2%, 8/44). Human papillomavirus 35 was the most common type of infection found, occurring in 5.1% (19/373) of the HPV-positive samples, followed by HPV-16 (4.6%, 17/373), HPV-58 E7 (4.0%, 15/373), HPV-18 (1.6%, 6/373), HPV-31 (0.5%, 2/373), and HPV-33 (0.3%, 1/373). More than 1 previous abortion and women with vaginitis were associated with the increased risk of HPV infection (χ = 4.71, p < .05; χ = 9.703, p < .01). CONCLUSION: The prevalence rate of HPV among women in the study was 12.6%, and HPV-35 was the most common type of HPV infection in the study in Shaanxi Province. Women with more than 1 previous abortion and vaginitis had more HPV prevalence, and HPV infection could coincide with pregnancy.
    Journal of Lower Genital Tract Disease 08/2012; · 1.21 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: MicroRNAs (miRNAs) are a class of small non-coding RNAs that repress the expression of their target genes post-transcriptionally. MiRNAs participate in the regulation of a variety of biological processes, including development and diseases. However, the functional role and molecular mechanism by which miRNAs regulate skeletal muscle development and differentiation are not fully understood. In this report, we identified miR-23a as a key regulator of skeletal muscle differentiation. Using bioinformatics analyses, miR-23a is predicted to target multiple adult fast myosin heavy chain (Myh) genes, including Myh 1, 2 and 4. Luciferase reporter assays show that miR-23a directly targets the 3' untranslated regions (UTRs) of these mRNAs. Interestingly, the expression level of mature miR-23a is inversely correlated with myogenic progression in mouse skeletal muscle. Both gain- and loss-of-function studies using C2C12 myoblasts demonstrate that miR-23a inhibits myogenic differentiation. These findings therefore reveal a novel role of miR-23a in regulating myogenic differentiation via inhibiting the expression of fast myosin heavy chain isoforms.
    Experimental Cell Research 07/2012; 318(18):2324-34. · 3.56 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Mutations in smooth muscle cell (SMC)-specific isoforms of α-actin and β-myosin heavy chain, two major components of the SMC contractile unit, cause familial thoracic aortic aneurysms leading to acute aortic dissections (FTAAD). To investigate whether mutations in the kinase that controls SMC contractile function (myosin light chain kinase [MYLK]) cause FTAAD, we sequenced MYLK by using DNA from 193 affected probands from unrelated FTAAD families. One nonsense and four missense variants were identified in MYLK and were not present in matched controls. Two variants, p.R1480X (c.4438C>T) and p.S1759P (c.5275T>C), segregated with aortic dissections in two families with a maximum LOD score of 2.1, providing evidence of linkage of these rare variants to the disease (p = 0.0009). Both families demonstrated a similar phenotype characterized by presentation with an acute aortic dissection with little to no enlargement of the aorta. The p.R1480X mutation leads to a truncated protein lacking the kinase and calmodulin binding domains, and p.S1759P alters amino acids in the α-helix of the calmodulin binding sequence, which disrupts kinase binding to calmodulin and reduces kinase activity in vitro. Furthermore, mice with SMC-specific knockdown of Mylk demonstrate altered gene expression and pathology consistent with medial degeneration of the aorta. Thus, genetic and functional studies support the conclusion that heterozygous loss-of-function mutations in MYLK are associated with aortic dissections.
    The American Journal of Human Genetics 11/2010; 87(5):701-7. · 11.20 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: As an anti-oxidant molecule, heme oxygenase-1 (HO-1) has been implicated in the protection of lung injury by cigarette smoke (CS). The mechanisms regulating its expression have not been defined. In this report, the role of early growth response 1 (EGR-1) in the regulation of Ho-1 expression was investigated. In C57BL/6 mice with CS exposure, HO-1 was greatly increased in bronchial epithelial cells and alveolar inflammatory cells. In primary cultured mouse lung fibroblasts and RAW264.7 cells exposed to cigarette smoke water extract (CSE), an increase in HO-1 protein level was detected. In addition, CSE induced HO-1 expression was decreased in Egr-1 deficient mouse embryo fibroblasts (Egr-1(-/-) MEFs). Nuclear localization of EGR-1 was examined in mouse lung fibroblasts after exposure to CSE. Luciferase reporter activity assays showed that the enhancer region of the Ho-1 gene containing a proposed EGR-1 binding site was responsible for the induction of HO-1. A higher increase of alveolar mean linear intercept (Lm) was observed in lung tissues, and a larger increase in the number of total cells and monocytes/macrophages from bronchial alveolar lavage fluid was found in CS-exposed mice by loss of function of EGR-1 treatment. In summary, the present data demonstrate that EGR-1 plays a critical role in HO-1 production induced by CS.
    Biochemical and Biophysical Research Communications 05/2010; 396(2):388-93. · 2.41 Impact Factor