Matrilin-2 regulates proliferation, apoptosis and cell cycle during radiation-induced injury in HPAEpiC cell

  • Biochem Biophys Res Commun. 2017 Apr 8;485(3):577-583. doi: 10.1016/j.bbrc.2016.12.022.
Junming Luo  1 Menglan Zhang  1 Hong Huang  1 Yichun Wang  2 Xin Yuan  3 Siqing Ma  4 Jingshi Liu  2 Shiying Zhou  1 Shukun Zhang  5
Affiliations
  • 1. Department of Pathology, Qinghai People's Provincial Hospital, Xining 810007, Qinghai Province, People's Republic of China.
  • 2. Department of Anesthesiology, Hunan Provincial Tumor Hospital, Central South University, Changsha 410013, Hunan Province, People's Republic of China.
  • 3. Department of Internal Medicine, Qinghai People's Provincial Hospital, Xining 810007, Qinghai Province, People's Republic of China.
  • 4. Department of Critical Care Medicine, Qinghai People's Provincial Hospital, Xining 810007, Qinghai Province, People's Republic of China.
  • 5. Department of Pathology, Qinghai People's Provincial Hospital, Xining 810007, Qinghai Province, People's Republic of China. Electronic address: [email protected].
Abstract

Radiation pulmonary injury is related to the accumulation of extracellular matrix proteins in the alveolar interstitial space. Matrilin-2 as a component of extracellular filamentous networks, present higher level in the lung tissue from irradiated mice and irradiated pulmonary epithelial cell line, HPAEpiC cells. Knockdown of endogenous matrilin-2 prevents the Apoptosis of HPAEpiC cell induced by the irradiation injury. Consistently, over-expression of matrilin-2 reduced the proliferation and induced Apoptosis of HPAEpiC cells. Matrilin-2 promotes the expression of p21 via increasing the transcriptional activity of p53, by which induces the G1 phase arresting in HPAEpiC cells. In summary, matrilin-2, increased by irradiation, reduced the proliferation and induces Apoptosis of pulmonary epithelial cells via p53/p21 pathway.

Keywords
Apoptosis; Cell cycle; Matrilin-2; Proliferation; Radiation pulmonary injury.