Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis without Helicobacter pylori infection

Abstract

Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.

Cytokine-Producing Potential of Blood Cells and Serum Cytokines in Patients With Chronic Atrophic Gastritis

“…15, 3 2013 Введение Считается, что развитие аденокарцином же-лудка представляет взаимосвязанные между со-бой патогенетические звенья (каскад Correa): поверхностный (неатрофический) гастрит -атрофический гастрит -кишечная метапла-зия -дисплазия -рак [7], поэтому хронический атрофический гастрит (ХАГ), являющийся рас-пространенным заболеванием желудочно-ки-шечного тракта, относят к предраковым состо-яниям желудка [26,29]. ХАГ характеризуется, помимо атрофии, воспалительными изменени-ями в слизистой оболочке желудка (СОЖ) [2], которые сопровождаются продолжительной ста-дией регенерации в условиях длительно сохра-няющейся гипоксии и активации внеклеточного протеолиза с ускорением процесса мобилизации и деления незрелых эпителиальных клеток, с бло-кированием их созревания и увеличением гене-тической нестабильности с нарастанием числа мутаций [3,25].…”

Mitochondria metabonomics of Huangqi Jianzhong Tang against chronic atrophic gastritis

“…It is widely accepted that gastric carcinogenesis is a continuous process starting from non‐atrophic gastritis to chronic atrophic gastritis (CAG; i.e. loss of specialized glands), to metaplasia and dysplasia, and finally to adenocarcinoma (Zhang, Hou, Wu, & Li, 2012). Reducing the risk of gastric cancer by improving CAG in patients is seen as a significant treatment option (Xu, Qin, & Liu, 2020).…”

Molecular Pathological Epidemiology in Helicobacter Pylori Infection and Risk of Chronic Atrophic Gastritis

“…The authors found that patients with CAG had the lower serum PGR than those without CAG, and the optimal PGR cut-off values for predicting CAG of the antrum and of the corpus were 4.9 and 3.5, respectively [30] . One comparative proteomics analysis showed that up-regulation of ribosomal protein S12 (RPS12) and down-regulation of proteasome activator subunit 1 (PSME1) were involved in the development of CAG [31] . Another analysis of genomic expression profiles found that five genes were associated with H. pylori-related CAG, including ATP6V0B, ATP6V1G1, ATP6V1F, NDUFV2 and NDUFS5 [32] .…”