ObjectiveTo summarize the progress of study on the relationship between endoplasmic reticulum stress and cell proliferation and provide evidence with reliable evidence-based data to the experiment on the field of tissue damage repair, organ proliferation, and regeneration.MethodThe relevant literatures about the progress of multiple signaling pathways related to the endoplasmic reticulum stress in the cell proliferation and injury repair in recent years were reviewed.ResultsThe endoplasmic reticulum stress participated in the process of proliferation and regeneration in the intestinal epithelial cells, skeletal muscle cells, islet cells, and hepatocytes through different pathways, which involved the three pathways of unfolded protein reaction that interacted with interleukin-6, tumor necrosis factor-α, vascular endothelial growth factor, Wnt, etc.ConclusionsAlthough endoplasmic reticulum stress has been widely debated in the field of determining cell fate, after we reviewed recent studies on endoplasmic reticulum stress in maintaining cell survival and promoting cell proliferation, the complexity, diversity, and importance of the endoplasmic reticulum stress in promoting cell proliferation have been presented in front of us. It not only promotes cell proliferation through the classical signaling pathway with Wnt protein, but also acts to repair tissue and promote proliferation by interacting with Musashi protein independently of the Notch pathway. The complex reaction pathway interacts with different stimulating factors in different cells, providing research directions and exploration possibilities for cell proliferation, injury repair, and organ regeneration, reveales the critical role of endoplasmic reticulum stress in cell proliferation.
ObjectiveTo investigate the role of endoplasmic reticulum stress in liver regeneration after associating liver partition and portal vein ligation for staged hepatectomy (ALPPS).MethodsSeventy-two C57bl/6 mice were randomly divided into ALPPS group, portal vein ligation group (PVL group), and sham operation group (Sham group), 24 mice in each group. And then one-stage ALPPS operation, simple PVL, and sham operation will be performed. Six mice were randomized selected of the three groups on the 1st, 2nd, 4th, and 7th day after surgery, respectively, the liver weight to body weight ratio (FLR/BW) of each group was measured, and the liver tissues were taken for immunohistochemical staining to calculate the proportion of Ki-67 positive cells, Western blot was used to detect the expression levels of X-box binding protein 1 (XBP1) and inositol-requiring enzyme 1α (IRE1α) proteins.Results① FLR/BW: On the 4th day and the 7th day after operation, the FLR/BW of the Sham group, PVL group, and ALPPS group increased in sequence at the same time, and the difference between the three groups was statistically significant (P<0.05). ② Ki-67 positive cell ratio: On the 2nd day after operation, the ratio of Ki-67 positive cells in the Sham group, PVL group, and ALPPS group increased sequentially, and the difference between the two groups was statistically significant (P<0.05). On the 4th day after operation, the ratio of Ki-67 positive cells in the PVL group and the ALPPS group were still higher than that of the Sham group (P<0.05). ③ Expression levels of XBP1 and IRE1α: On the 2nd and 4th postoperative day, the expression levels of XBP1 and IRE1α in the ALPPS group were higher than those in the Sham group and the PVL group (P<0.05). On the 7th day after surgery, the expression levels of XBP1 and IRE1α in the ALPPS group were higher than those in the Sham group (P<0.05), while compared with the PVL group, the expression level of XBP1 in the ALPPS group was still higher (P<0.05).ConclusionsALPPS-induced liver regeneration is more advantageous than traditional PVL in mice. It may be attributed to the obvious endoplasmic reticulum stress activation after ALPPS leading to the up-regulation of IRE1α-XBP1 expression, which is involved in the regulation of hepatocyte cell cycle and promotes hepatocyte proliferation, thus promoting rapid liver regeneration.