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Showing papers by "Jian Wang published in 2008"


Journal ArticleDOI
TL;DR: This is the first study demonstrating a critical role for miRNAs in modulating TGF-β-dependent inhibition of myogenesis, and provides a novel mechanism of the genetic regulation of T GF-β signaling during skeletal muscle differentiation.
Abstract: MicroRNAs (miRNAs) have recently been proposed as a versatile class of molecules involved in regulation of a variety of biological processes. However, the role of miRNAs in TGF-β-regulated biological processes is poorly addressed. In this study, we found that miR-24 was upregulated during myoblast differentiation and could be inhibited by TGF-β1. Using both a reporter assay and Northern blot analysis, we showed that TGF-β1 repressed miR-24 transcription which was dependent on the presence of Smad3 and a Smads binding site in the promoter region of miR-24. TGF-β1 was unable to inhibit miR-24 expression in Smad3-deficient myoblasts, which exhibited accelerated myogenesis. Knockdown of miR-24 led to reduced expression of myogenic differentiation markers in C2C12 cells, while ectopic expression of miR-24 enhanced differentiation, and partially rescued inhibited myogenesis by TGF-β1. This is the first study demonstrating a critical role for miRNAs in modulating TGF-β-dependent inhibition of myogenesis, and provides a novel mechanism of the genetic regulation of TGF-β signaling during skeletal muscle differentiation.

246 citations


Journal ArticleDOI
TL;DR: The results provide further support for the importance of SOCE in HPV and suggest that HPV is greater in distal than proximal PA because greater numbers and activation of SOCC indistal PASMC generate bigger increases in [Ca(2+)](i).
Abstract: Hypoxic pulmonary vasoconstriction (HPV) requires Ca2+ influx through store-operated Ca2+ channels (SOCC) in pulmonary arterial smooth muscle cells (PASMC) and is greater in distal than proximal pu...

113 citations


Journal ArticleDOI
TL;DR: The results suggest that the inhibition of K(v) channel expression and rise in [Ca(2+)](i) during chronic hypoxia may be the result of HIF-1-dependent induction of ET-1.
Abstract: Prolonged exposure to decreased oxygen tension causes contraction and proliferation of pulmonary arterial smooth muscle cells (PASMCs) and pulmonary hypertension. Hypoxia-induced inhibition of volt...

106 citations


Journal ArticleDOI
TL;DR: High mobility group protein-B1 (HMGB1), a chromosomal protein, was identified as a novel HNF1α-interacting protein and raised the intriguing possibility that HMGB1 is a new cofactor of H NF1α and participates in HNF 1α-mediated transcription regulation through protein–protein interaction.
Abstract: Hepatocyte nuclear factor (HNF)-1α is one of the liver-enriched transcription factors involved in many tissue-specific expressions of hepatic genes. The molecular mechanisms for determining HNF1α-mediated transactivation have not been explained fully. To identify unknown proteins that interact with HNF1α, we developed a co-IP-MS strategy to search HNF1α interactions, and high mobility group protein-B1 (HMGB1), a chromosomal protein, was identified as a novel HNF1α-interacting protein. In vitro glutathione S-transferase pull-down and in vivo co-immunoprecipitation studies confirmed an interaction between HMGB1 and HNF1α. The protein–protein interaction was mediated through the HMG box domains of HMGB1 and the homeodomain of HNF1α. Furthermore, electrophoretic mobility shift assay and chromatin-immunoprecipitation assay demonstrated that HMGB1 was recruited to endogenous HNF1α-responsive promoters and enhanced HNF1α binding to its cognate DNA sequences. Moreover, luciferase reporter analyses showed that HMGB1 potentiated the transcriptional activities of HNF1α in cultured cells, and downregulation of HMGB1 by RNA interference specifically affected the HNF1α-dependent gene expression in HepG2 cell. Taken together, these findings raise the intriguing possibility that HMGB1 is a new cofactor of HNF1α and participates in HNF1α-mediated transcription regulation through protein–protein interaction.

36 citations


Journal ArticleDOI
TL;DR: In this article, the authors use an international comparative perspective to examine how the health of China's population and other aspects of health system performance changed during the reform era and draw on standard public finance and health economics theory, as well as the more recent incomplete-contracting theory of property rights, to summarize the comparative advantages of government and market for financing and delivery of health services.

32 citations


Journal ArticleDOI
TL;DR: Results indicate that induced TRPC1 expression increases PP2A activity through Ca2+ influx and that increasedPP2A sensitizes IECs to apoptosis as a result of NF-kappaB inactivation.
Abstract: Transient receptor potential canonical-1 (TRPC1) functions as a store-operated Ca2+ channel in intestinal epithelial cells (IECs), and induced TRPC1 expression sensitizes IECs to apoptosis by inhib

24 citations


Journal ArticleDOI
Jian Wang1, Yu Cao1, Min Chen1, Jin Sun1, A. Mitev1 
TL;DR: A new finite point device modeling technique that can speed up the analysis procedure, a new parametric reduction method and a novel Chebyshev Affine Arithmetic (CAA) based performance bound estimation approach are described.
Abstract: As feature size goes below 70 nm, process variation introduced device mismatch may cause over 40% performance variations and circuit failures especially for analog/mixed-signal designs. The location dependent correlations among devices and the large number of devices in some practical designs make it difficult to predict performance corners accurately and efficiently. This paper aims to provide an overview of possible methodologies and approaches that model and analyze device mismatch. In particular, the paper describes a new finite point device modeling technique that can speed up the analysis procedure, a new parametric reduction method and a novel Chebyshev Affine Arithmetic (CAA) based performance bound estimation approach.

7 citations


Journal Article
TL;DR: OSA-18 QOL survey had better reliability and validity, and was applicable for life quality assessment in OSAHS children, and could help clinical diagnosis of OSA HS in children and give quantitative evaluation for therapeutic measure.
Abstract: OBJECTIVE One of the objective of the study was to evaluate the reliability and validity of 18 items survey (OSA-18) which was made for disease specific quality of life in children with obstructive sleep apnea The other was to explore whether OSA-18 could be used as a well appreciation method on OSAHS in children's quality of life before and after surgery METHOD First, one hundred and twenty-two children's parents were interviewed with this survey scales and the survey scales was assessed by split-half reliability, retest reliability, internal consistency, construct validity and content validity Second,OSA-18 was used to evaluate the QOL of 122 children within 4 weeks before PSG and in 6 to 12 months after operation RESULT OSA-18 has a satisfactory internal consistency Global Cronbach's alpha coefficient were 0939 All domains and items Cronbach's alpha coefficients > 06; also has a well retest reliability, coefficient correlation of pearson equal 0 619 Construct validity and content validity were satisfactory The impact of pediatric OSAHS on QOL was moderate and severe in 7705% patients pre-operation However, it was only 2869% after surgery OSA-18 total scores, every domain and item score were significant decrease CONCLUSION OSA-18 QOL survey had better reliability and validity, and was applicable for life quality assessment in OSAHS children OSA-18 QOL survey could help clinical diagnosis of OSAHS in children and give quantitative evaluation for therapeutic measure

2 citations