[Involvement of chemokine CXCL16 in myocardial infarction and its influence on phagocytic activity of macrophage in vitro]

Zhonghua Yi Xue Za Zhi. 2014 Jan 21;94(3):218-22.
[Article in Chinese]

Abstract

Objective: To explore whether chemokine CXCL16 is up-regulated after myocardial infarction and promotes the phagocytic activity of macrophage in vitro.

Methods: Forty wild-type mice were randomly separated into 2 groups (n = 20 each). Group A had the ligation of left anterior descending coronary artery while group B underwent a sham operation. Electrocardiogram was used to assess whether the operation was successful or not. Three days after surgery, 10 animals of each group were sacrificed and the serum level of CXCL16 was detected by enzyme-linked immunosorbent assay (ELISA). Twenty-eight days after surgery, cardiac function of the remaining mice was measured by small animal ultrasound. Then the animals were sacrificed. Hematoxylin and eosin (HE) staining and immunohistochemical staining of cardiac paraffin section were used to observe the inflammation and detect the expression of CXCL16 in cardiac tissue after myocardial infarction. To explore the function of CXCL16 in vitro, primary murine monocytes were separated from bone marrow, cultured to differentiate into macrophages and transfected with adenovirus vectors over-expressing CXCL16 or control adenovirus vectors. After stimulation by debris of cardiac cells, the phagocytic uptake by macrophages was evaluated by flow cytometry.

Results: The model of myocardial infarction was successfully established. ELISA showed that the serum level of CXCL16 was elevated 3 days after myocardial infarction [(1 079 ± 176) vs (611 ± 37) pg/ml, P = 0.032]. HE and immunohistochemical staining demonstrated that the infiltration of macrophages increased during an early stage of myocardial infarction and decreased at the late stage. The CXCL16 level was up-regulated 3 days after myocardial infarction and returned to normal level at Day 28. Furthermore, macrophages transfected with adenovirus over-expressing CXCL16 showed stronger phagocytic activity compared with control (17.11% ± 0.87% vs 7.91% ± 0.71%, P < 0.01).

Conclusion: CXCL16 is up-regulated after myocardial infarction in mice. And an in vitro over-expression of CXCL16 promotes the macrophage phagocytosis of cardiac debris.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Chemokine CXCL6 / metabolism*
  • Disease Models, Animal
  • Macrophages / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / metabolism*
  • Myocardial Infarction / metabolism*
  • Phagocytosis*

Substances

  • Chemokine CXCL6