Autophagy plays a protective role in cell death of osteoblasts exposure to lead chloride.

Abstract:

:Lead (Pb) is a toxic heavy metal widespreadly used in industrial field. Prior studies showed that Pb exposure had detrimental effects on osteoblasts. The mechanisms underlying Pb-induced damage are complex. Autophagy can protect cells from various cytotoxic stimuli. In the present study, the aim of our research was to investigate whether Pb could activate autophagy to play a protective role against osteoblasts apoptosis. Our results indicated that PbCl2 induced autophagy and autophagic flux in MC3T3-E1 murine osteoblastic cell by RT-PCR, western blot, as well as fluorescence microscopy analysis of GFP-LC3, AO and MDC staining. Pb increased the apoptosis of osteoblasts, evidenced by western blot and Hoechst 33258 staining assessment. In addition, inhibiting autophagy by 3-MA further increased the osteoblasts apoptosis after Pb exposure, showed by flow cytometry and Hoechst 33258 staining. Furthermore, phosphorylation of mTOR and p70S6K was inhibited by Pb exposure, indicating that Pb might induce autophagy in osteoblasts via inhibiting mTOR pathway. Altogether, these evidence suggested that Pb exporsure promoted autophagy flux in osteoblasts. The activation of autophagy by Pb played a protective role in osteoblasts apoptosis, which might be mediated through the mTOR pathway.

journal_name

Toxicol Lett

journal_title

Toxicology letters

authors

Lv XH,Zhao DH,Cai SZ,Luo SY,You T,Xu BL,Chen K

doi

10.1016/j.toxlet.2015.09.014

subject

Has Abstract

pub_date

2015-12-03 00:00:00

pages

131-40

issue

2

eissn

0378-4274

issn

1879-3169

pii

S0378-4274(15)30053-9

journal_volume

239

pub_type

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