Cell line mixup causes retraction of paper on blood vessel damage
We’ve written before about retractions for cell lines that turn out not to be what researchers thought they were. In a few cases, that has involved contamination by HeLa cells, named for Henrietta Lacks. Today, we note the retraction of a paper whose authors, from Taiwan, thought they were using human muscle cells that line blood vessels when they were actually studying such cells from rat embryos.
Here’s the notice in the British Journal of Nutrition for “Molecular mechanism of green microalgae, Dunaliella salina, involved in attenuating balloon injury-induced neointimal formation”:
The article by Sheu et al. (1) has been retracted at the request of the authors. The cell lines were named as being human aortic smooth muscle cells (HASMCs). However, the authors have contacted us to state that these cells were in fact A10 cells from embryonic rats. Because of the fundamental nature of this error, the findings cannot be interpreted in the manner stated in the original article, and therefore this paper has been retracted. The authors apologise for this error.
For those wondering, Dunaliella salina is a green algae that lives in sea salt fields and produces high levels of beta-carotene. It is also sold by a neutraceutical company, which claims that “the benefits are endless.”
Here’s the original abstract of the paper:
The pathological mechanism of restenosis is primarily attributed to excessive proliferation of vascular smooth muscle cells (VSMC). The preventive effects of ethanol extract of Dunaliella salina (EDS) on balloon injury-induced neointimal formation were investigated. To explore its molecular mechanism in regulating cell proliferation, we first showed that EDS markedly reduced the human aortic smooth muscle cell proliferation via the inhibition of 5′-bromo-2′-deoxyuridine (BrdU) incorporation at 40 and 80 μg/ml. This was further supported by the G0/G1-phase arrest using a flow cytometric analysis. In an in vivo study, EDS at 40 and 80 μg/ml was previously administered to the Sprague–Dawley rats and found that the thickness of neointima, and the ratio of neointima:media were also reduced. EDS inhibited VSMC proliferation in a dose-dependent manner following stimulation of VSMC cultures with 15 % fetal bovine serum (FBS). Suppressed by EDS were 15 % FBS-stimulated intracellular Raf, phosphorylated extracellular signal-regulated kinases (p-Erk) involved in cell-cycle arrest and proliferating cell nuclear antigen. Phosphorylated focal adhesion kinase (p-FAK) was also suppressed by EDS. Also active caspase-9, caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels were increased by administration with EDS; the apoptotic pathway may play an important role in the regulatory effects of EDS on cell growth. These observations provide a mechanism of EDS in attenuating cell proliferation, thus as a potential intervention for restenosis.
The paper has been cited three times, including twice by the group that wrote it, according to Thomson Scientific’s Web of Knowledge.