title: [In vitro stimulation of retinoic acid syndrome by rotary cell culture system and its relationship with expression of CXCR4 and SDF-1 alpha].
abstract: OBJECTIVE
  To explore the molecular mechanism and prevention of retinoic acid syndrome (RAS).
  
  
  METHODS
  SDF-1 alpha mRNA from healthy adult lung tissue was measured by RT-PCR, CXCR4 protein expression on the cell membrane of APL cells induced by ATRA (APL-ATRA) was tested by FCM, and the rotary cell culture system (RCCS) was used to build a modal for in vitro stimulation of APL-ATRA infiltrating human lung tissue. The ability of APL-ATRA in adhesion, migration and infiltration was observed by interference from DEX, Ara-C and DNR.
  
  
  RESULTS
  The APL-ATRA cells could evidently infiltrate into normal lung tissue. Mean fluorescence intensity (MFI) of CXCR4 on the cell membrane of APL-ATRA cells was 30.6 +/- 1.8, which was much higher than that on unspecialized APL cells (9.8 +/- 4.2). SDF-1 alpha mRNA expression was detected positive in all 6 lung tissue. Contrary to the control groups, DEX could dramatically restrain the ability of APL-ATRA cells in adhesion and migration [(27.2 +/- 2.6)% vs. (46.0 +/- 3.0)%, (28.1 +/- 4.0)% vs. (48.2 +/- 3.0)%], while Ara-C and DNR could distinctly depress the ability in adhesion, migration and infiltration [(28.1 +/- 3.0)%, (30.2 +/- 3.2)% vs. (46.0 +/- 3.0)%; (29.0 +/- 4.0)%, (23.0 +/- 5.2)% vs. (48.2 +/- 3.0)%; (16.8 +/- 7.6)%, (17.1 +/- 6.0)% vs. (43.6 +/- 5.0)%].
  
  
  CONCLUSIONS
  In vitro APL-ATRA cells can infiltrate into the human lung tissue. High expression of CXCR4 on APL-ATRA and SDF-1 alpha in the lung tissue may be one of the molecular mechanisms of the lung infiltration and RAS. DEX, Ara-C and DNR can dramatically restrain the ability of APL-ATRA cells in adhesion, migration and infiltration.
authors.affiliation: The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Zhou
authors.forename: Long-hu
authors.initials: LH
authors.lastname: Hu
authors.forename: Zhe
authors.initials: Z
authors.lastname: Cui
authors.forename: Gui-fang
authors.initials: GF
authors.lastname: Wang
authors.forename: Jin-mei
authors.initials: JM
authors.lastname: Li
authors.forename: Yan-hong
authors.initials: YH
authors.lastname: Zhao
authors.forename: Sheng-jin
authors.initials: SJ
authors.lastname: Fan
authors.forename: Li-min
authors.initials: LM
authors.lastname: Li
authors.forename: Feng-lin
authors.initials: FL
authors.lastname: Cao
authors.forename: Xue-ying
authors.initials: XY
authors.lastname: Han
mesh_terms: D000293:Adolescent; D000328:Adult; D002448:Cell Adhesion; D018929:Cell Culture Techniques; D002465:Cell Movement; D054377:Chemokine CXCL12 / Q000235:genetics / Q000378:metabolism*; D002648:Child; D005260:Female; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D019718:Receptors, CXCR4 / Q000235:genetics / Q000378:metabolism*; D014212:Tretinoin / Q000009:adverse effects*; D014407:Tumor Cells, Cultured
chemical_list: D054377:Chemokine CXCL12; D019718:Receptors, CXCR4; D014212:Tretinoin