Changqing Li

Changqing Li


Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 March 2020 in Journal of Pharmacological and Toxicological Methods
Verified
Journal Article
Closed access
LHLu Hong
Lu Hong
Zongkui WangZongkui Wang
Zongkui Wang
鑫魏鑫 魏
鑫 魏
JSJianyou Shi
Jianyou Shi
CLChangqing Li
Changqing Li

1 March 2019 in Journal of Proteomics
Verified
Journal Article
Closed access
Zongkui WangZongkui Wang
Zongkui Wang
FLFengjuan Liu
Fengjuan Liu
SYShengliang Ye
Shengliang Ye
PJPeng Jiang
Peng Jiang
XYXiaochuan Yu
Xiaochuan Yu
CLChangqing Li
Changqing Li

Verified
Journal Article
Open access
PDF file
Zongkui WangZongkui Wang
Zongkui Wang
PJPeng Jiang
Peng Jiang
FLFengjuan Liu
Fengjuan Liu
XDXi Du
Xi Du
LMLi Ma
Li Ma
CLChangqing Li
Changqing Li
Growth differentiation factor 11 (GDF11), belonging to the transforming factor-β superfamily, regulates anterior-posterior patterning and inhibits neurogenesis during embryonic development. However, recent studies recognized GDF11 as a rejuvenating (or anti-ageing) factor to reverse age-related cardiac hypertrophy, repair injured skeletal muscle, promote cognitive function, etc. The effects of GDF11 are contradictory and the mechanism of action is still not well clarified. The objective of the present study was to investigate effects of GDF11 on PC12 neural stem cells in vitro and to reveal the underlying mechanism. We systematically assessed the effects of GDF11 on the life activities of PC12 cells. GDF11 significantly suppressed cell proliferation and migration, promoted differentiation and apoptosis, and arrested cell cycle at G2/M phase. Both TMT-based proteomic analysis and phospho-antibody microarray revealed PI3K-Akt pathway was enriched when treated with GDF11. Inhibition of ALK5 or PI3K obviously attenuated the effects of GDF11 on PC12 neural stem cells, which exerted that GDF11 regulated neural stem cells through ALK5-dependent PI3K-Akt signaling pathway. In summary, these results demonstrated GDF11 could be a negative regulator for neurogenesis via ALK5 activating PI3K-Akt pathway when it directly acted on neural stem cells.


9 December 2022 in PeerJ
Verified
Journal Article
Open access
PDF file
BLBin Liu
Bin Liu
DDDemei Dong
Demei Dong
ZWZongkui Wang
Zongkui Wang
YGYang Gao
Yang Gao
DYDing Yu
Ding Yu
CLChangqing Li
Changqing Li
Background and objectives: The adverse effects of plasma donation on the body has lowered the odds of donation. The aim of this study was to investigate the prevalence of abnormal serum calcium and total serum protein related to plasma donation, identify the influencing factors, and come up with suggestions to make plasma donation safer. Methods: Donors from 10 plasmapheresis centers in five provinces of China participated in this study. Serum samples were collected before donation. Serum calcium was measured by arsenazo III colorimetry, and the biuret method was used for total serum protein assay. An automatic biochemical analyzer was used to conduct serum calcium and total serum protein tests. Results: The mean serum calcium was 2.3 ± 0.15 mmol/L and total serum protein was 67.75 ± 6.02 g/L. The proportions of plasma donors whose serum calcium and total serum protein were lower than normal were 20.55% (815/3,966) and 27.99% (1,111/3,969), respectively. There were significant differences in mean serum calcium and total serum protein of plasma donors with different plasma donation frequencies, gender, age, regions, and body mass index (BMI), (all p < 0.05). Logistic regression analysis revealed that donation frequencies, age, BMI and regions were significantly associated with a higher risk of low serum calcium level, and donation frequencies, gender, age and regions were significant determinants factors of odds of abnormal total serum protein. Conclusions: Donation frequencies, gender, age, regions, and BMI showed different effects on serum calcium and total serum protein. More attention should be paid to the age, donation frequency and region of plasma donors to reduce the probability of low serum calcium and low total serum protein.

3 December 2022 in Clinical Proteomics
Verified
Journal Article
Open access
PDF file
RZRong Zhang
Rong Zhang
FLFengjuan Liu
Fengjuan Liu
SYShengliang Ye
Shengliang Ye
XDXi Du
Xi Du
LMLi Ma
Li Ma
CLChangqing Li
Changqing Li
Background: High blood glucose level is one of the main characteristics of diabetes mellitus. Based on previous studies, it is speculated longevity families may have certain advantages in blood glucose regulation. However, limited information on these items has been reported. The purpose of this study was to profile differences of plasma proteomics between longevity subjects (with normal fructosamine (FUN) level) and non-longevity area participants (with exceeding standard FUN level). Methods: In this study, a TMT-based proteomics analysis was used to profile differences of plasma proteomics between longevity subjects (with normal FUN level) and non-longevity area participants (with exceeding standard FUN level). Results were validated by Luminex detection. Results: A total of 155 differentially expressed proteins (DEPs) were identified between these two groups. The DEPs related to blood glucose regulation were mainly involved in glycolysis/gluconeogenesis, pyruvate metabolism and propanoate metabolism, and most of the DEPs were contained in carbohydrate metabolism, PI3K-Akt pathway, glucagon signaling pathway and inflammatory response. Validation by Luminex detection confirmed that CD163 was down-regulated, and SPARC, PARK 7 and IGFBP-1 were up-regulated in longevity participants. Conclusions: This study not only highlighted carbohydrate metabolism, PI3K-Akt pathway, glucagon signaling pathway and inflammatory response may play important roles in blood glucose regulation, but also indicated that YWHAZ, YWHAB, YWHAG, YWHAE, CALM3, CRP, SAA2, PARK 7, IGFBP1 and VNN1 may serve as potential biomarkers for predicting abnormal blood glucose levels.