[Effects of methyl β cyclodextrin on the proliferation and transdifferentiation of type II alveolar epithelial cells].

Objective: To study the destructive effects of the membrane lipid microdomain with methyl β cyclodextrin (MβCD) on the proliferation, transdifferentiation and cell cycle of type II alveolar epithelial cell (AEC II).

Methods: The membrane lipid microdomain of AEC II was destroyed by MβCD (MβCD interference group) in vitro, and then cultured with DMEM as control. Cell number was counted with hemacytometer; the proliferation rate was measured by methyl thiazolyl tetrazolium (MTT); flow cytometry was used to assay the cell cycle. The expressions of AEC II specific surfactant protein-C (SP-C) and AECI specific aquaporin 5 (AQP5) were detected by immunofluorescence and Western blotting analyses.

Results: Compared with control group, cell number and the cell proliferation was decreased in MβCD interference group at 24, 48 and 72 hours after interaction [cell numbers (×10(6)/ml): 2.74±0.56 vs. 8.05±0.92, 4.45±0.68 vs. 10.52±0.81, 7.82±0.59 vs. 11.39±0.81; MTT results (A value): 0.25±0.20 vs. 0.45±0.02, 0.35±0.03 vs. 0.54±0.28, 0.48±0.04 vs. 0.59±0.05, all P<0.01]. MβCD could increase the percentage of cells in G0/G1 phases and decreased the percentage in S phases at 24 hours [G0/G1 phases: (60.06±1.65)% vs. (43.43±3.59)%; S phases: (16.20±2.17)% vs. (34.07±2.63)%, both P<0.05 ]. Incubation of AEC II with MβCD resulted in up regulation of the expression of SP-C (0.54±0.04 vs. 0.47±0.03, 0.19±0.03 vs. 0.06±0.02) and down regulation of AQP5 (0.30±0.04 vs. 0.43±0.06, 0.39±0.04 vs. 0.59±0.04) at 48 hours and 72 hours after interaction (P<0.05 or P<0.01).

Conclusion: The destruction of membrane lipid microdomain by the MβCD can inhibit proliferation and transdifferentiation of AEC II, and induce cell cycle arrest in G1 phase.