Jiaqing Gong1, Yonghua Wang1, Yongkuan Cao1. 1. Center of General Surgery, The People's Liberation Army General Hospital of Chengdu Command Chengdu 610083, Sichuan Province, China.
Abstract
OBJECTIVE: To investigate the migratory path of stem cells in pancreatic tissues damaged by pancreatitis and to preliminarily identify stem cells that efficiently contribute to the repair of damaged pancreatic tissues. METHODS: An animal model of acute pancreatitis was established, in which rats in the experimental group were given intraperitoneal (IP) injections of caerulein. Before the rats were sacrificed, 5-bromo-2'-deoxyuridine (BrdU) was administered by IP injection to label proliferating pancreatic cells. The localization and distribution of the stem cell-specific marker proteins nestin and c-kit in pancreatic tissues were examined using an immunohistochemical approach, and proliferation-specific BrdU incorporation was also analyzed. RESULTS: (1) The nestin-positive cells first appeared in the pancreatic interlobar vessels, and then, were observed in the pancreatic acinar and islet tissues. (2) C-kit-positive cells were located only in the pancreatic islets. (3) BrdU-positive cells first appeared in the area surrounding the interlobular region, and then were diffusely distributed and filled the pancreatic lobules. CONCLUSIONS: (1) The stem cells, participated in the repair of damaged pancreatic tissue, appear firstly in the pancreatic interlobar vessels, then migrate toward the pancreatic lobules by using the interlobar vessels as channels and penetrate through the vascular endothelium into the pancreatic acinar tissues. A portion of the stem cells eventually penetrate into the islet tissue. (2) Exogenous stem cells, rather than the tissue-resident stem cells, efficiently contribute to the repair of damaged pancreatic tissues.
OBJECTIVE: To investigate the migratory path of stem cells in pancreatic tissues damaged by pancreatitis and to preliminarily identify stem cells that efficiently contribute to the repair of damaged pancreatic tissues. METHODS: An animal model of acute pancreatitis was established, in which rats in the experimental group were given intraperitoneal (IP) injections of caerulein. Before the rats were sacrificed, 5-bromo-2'-deoxyuridine (BrdU) was administered by IP injection to label proliferating pancreatic cells. The localization and distribution of the stem cell-specific marker proteins nestin and c-kit in pancreatic tissues were examined using an immunohistochemical approach, and proliferation-specific BrdU incorporation was also analyzed. RESULTS: (1) The nestin-positive cells first appeared in the pancreatic interlobar vessels, and then, were observed in the pancreatic acinar and islet tissues. (2) C-kit-positive cells were located only in the pancreatic islets. (3) BrdU-positive cells first appeared in the area surrounding the interlobular region, and then were diffusely distributed and filled the pancreatic lobules. CONCLUSIONS: (1) The stem cells, participated in the repair of damaged pancreatic tissue, appear firstly in the pancreatic interlobar vessels, then migrate toward the pancreatic lobules by using the interlobar vessels as channels and penetrate through the vascular endothelium into the pancreatic acinar tissues. A portion of the stem cells eventually penetrate into the islet tissue. (2) Exogenous stem cells, rather than the tissue-resident stem cells, efficiently contribute to the repair of damaged pancreatic tissues.