Proteomics Reveals the Secrets of Child Growth Retardation

Vitamin B2 deficiency can lead to a variety of clinical abnormalities, including growth retardation, pharyngitis, cleft lip, anemia, kidney damage, neurasthenia, and even tumorigenesis. This article aims to study the effects of vitamin B2 deficiency on HepG2 cell activity and proliferation and related mechanisms by means of proteomics.

Sample Resource

HepG2 cells were cultured for a period of time in a medium containing 12.76 nmol/L vitamin B2, and then transferred to a medium containing 0.76, 3.76, 6.76, 12.76, 24.76, 48.76 nmol/L vitamin B2, and the cells were collected after 96 hours of culture.

Research Technique

Label-free protein quantitative analysis

Conventional cytology experiment

Research Results

A. Cellular activity, apoptosis and glutathione reductase determination

Under the condition of vitamin B2 deficiency (the vitamin B2 concentration is 0.76, 3.76, 6.76 nmol/L), the cell activity was significantly decreased. When the concentration was higher than 12.76 nmol/L, the cell activity was not affected. The trend of apoptosis experiment results is similar. In addition, when the vitamin B2 concentration is lower than 12.76 nmol/L, the activity of glutathione reductase (the activity coefficient of which is commonly used to evaluate the nutritional status of vitamin B2) was also significantly lowered.

B. Label-free protein quantitative analysis

A total of 3,730 proteins were identified in the paper, of which 85 proteins were only found in HepG2 cells under vitamin B2 deficient culture conditions. 275 proteins were only found in HepG2 cells under ample vitamin B2 culture conditions. GO analysis of the above 360 proteins revealed that most proteins are involved in the process of phosphate metabolism, embryonic development of chordate, protein phosphorylation, and so on. Among them, 37 proteins were differentially expressed in HepG2 cells under vitamin B2 deficiency culture conditions (±2 fold, p