BRCC36 promotes intestinal mucosal barrier injury caused by BMP2 after ischemia reperfusion via inhibiting PPARγ signaling.

As one of the most common pathological changes in trauma and surgery practice, intestinal ischemia-reperfusion (I/R) injury is regarded as a major precipitating factor in the occurrence and development of fatal diseases. BRCA1-BRCA2-containing complex subunit 36 (BRCC36), a deubiquitinase, has been proved important in a variety of pathophysiological processes such as DNA repair, cell cycle regulation, tumorigenesis, and inflammatory response. However, the effect of BRCC36 on intestinal mucosal barrier injury after I/R has not been fully elucidated. Our research found that BRCC36 aggravated intestinal mucosal barrier injury caused by bone morphogenetic protein 2 after I/R by downregulating peroxisome proliferator-activated receptor-γ (PPARγ) signaling. These results suggested that BRCC36/PPARγ axis might serve as a potential therapeutic target for preventing intestinal mucosal barrier injury after I/R.

[Effects of Neurotrophin Receptor-interacting MAGE Homolog on Apoptosis of Intestinal Epithelial Cells].

OBJECTIVE: To explore whether neurotrophin receptor-interacting MAGE homolog (NRAGE) is involved in the intestinal ischemia-reperfusion (I/R) and its effect on the apoptosis of intestinal epithelial cells and the expression of occludin protein. METHODS: The level of NRAGE protein after the rat small intestine I/R was detected by immunohistochemical (IHC) In vivo. The level of NRAGE protein and mRNA in IEC-6 cells after hypoxia and reoxygenation were tested by Western blot and RT-PCR respectively in vitro. The IEC-6 cells were divided into four groups, including NRAGE overexpression by lentivirus infection (Lv-NRAGE group), interference (sh-NRAGE group), lentivirus control (Lv-control group), and normal control group without lentivirus infection (NC group). The apoptosis of IEC-6 cells after infection was analyzed by flow cytometry. The level of the tight junction protein occludin was detected by Western blot. RESULTS: The expression of NRAGE were highly increased in intestinal mucosa epithelial cells after I/R (P<0.01). The proteins and mRNA levels of NRAGE were increased after 6 h of hypoxia in IEC-6 cellsin vitro. Compared with the Lv-control group, the early apoptosis rate was raised (P<0.01) and the level of occludin was reduced (P<0.01) in Lv-NRAGE group; while the early apoptosis rate was reduced (P<0.01) and the level of occludin was raised in sh-NRAGE group(P<0.001). CONCLUSION: NRAGE may be involved in intestinal I/R and promote the apoptosis and decrease occludin expression of intestinal epithelial cells.

Relationship between Ki-67 and CD44 expression and microvascular formation in gastric stromal tumor tissues.

BACKGROUND: A gastric stromal tumor (GST) is a mesenchymal tumor that occurs in the gastrointestinal tract; its biological characteristics are highly complex. Clinically, the severity of a GST is often evaluated by factors such as risk classification, tumor size, and mitotic figures. However, these indicators are not very accurate. Even patients classified as low risk are also at risk of metastasis and recurrence. Therefore, more accurate and objective clinical biological behavior evaluations are urgently needed. AIM: To determine the relationship between Ki-67 and CD44 expression in GSTs and microvessel formation and prognosis. METHODS: Eighty-six GST tissue specimens from our hospital were selected for this study. The immunohistochemical staining technique was used to detect Ki-67, CD44, and microvessel density (MVD) in the collected samples to analyze the different risk grades and mitotic figures. In addition, this approach was used to determine the differences in the expression of Ki-67 and CD44 in GST tissues with varying lesion diameters. RESULTS: In GSTs with positive expression of the Ki-67 protein, the proportions of patients with medium-to-high risk and more than five mitotic counts were 24.07% and 38.89%, respectively. In GSTs with positive expression of the CD44 protein, the proportions of patients with medium-to-high risk and more than five mitotic counts were 23.73% and 38.98%, respectively. In GSTs with negative expression of the Ki-67 protein, these values were relatively high (3.70% and 11.11%, respectively). The MVD in GSTs with positive and negative expression of the CD44 protein was 15.92 ± 2.94 and 13.86 ± 2.98/Hp, respectively; the difference between the two groups was significant (P < 0.05). CONCLUSION: Ki-67 and CD44 expression in GSTs is correlated with the grade of tumor risk and mitotic figures. CD44 expression is correlated with microvessel formation in tumor tissues.