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Highly Accessed Letter

Response to 'TNF/TNFR signal transduction pathway-mediated anti-apoptosis and anti-inflammatory effects of sodium ferulate on IL-1β-induced rat osteoarthritis chondrocytes in vitro' - authors' reply

Jun Qin12, Liang Shang13, An-song Ping2, Jing Li1, Xiao-jun Li1, Hong Yu3, Jacques Magdalou4, Liao-bin Chen2* and Hui Wang1*

Author Affiliations

1 Department of Pharmacology, Basic Medical School, Wuhan University, Donghu Road 169, Wuhan 430071, China

2 Department of Orthopaedic Surgery, Zhongnan Hospital, Wuhan University, Donghu Road 169, Wuhan 430071, China

3 Department of Biochemistry, Basic Medical School, Wuhan University, Donghu Road 169, Wuhan 430071, China

4 UMR7561 CNRS-UHP, Laboratoire de Physiopathologie et Pharmacologie Articulaires, Faculté de Médecine, Vandoeuvre-lès-Nancy Cedex, Lorraine 54505, France

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Arthritis Research & Therapy 2013, 15:409  doi:10.1186/ar4227


See related research by Qin et al., http://arthritis-research.com/content/14/6/R242, and related letter by Ma et al., http://arthritis-research.com/content/15/3/408


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/15/3/409


Published:24 May 2013

© 2013 BioMed Central Ltd

Letter

We are pleased that our recent article published in Arthritis Research and Therapy could draw such great interest from the readers. The following is our response to Ma and colleagues' concerns [1].

In response to the first question, at the beginning of the research we had screened the entire apoptotic pathways using the Rat Apoptosis RT2 Profiler™ PCR Array (SABiosciences, Frederick, MD, USA), and the result (Table 1 in the original paper [2]) showed that mRNA expression of Bcl-2 family members regulating the intrinsic pathway did not appear to be significantly changed. We therefore subsequently focused on the extrinsic apoptotic pathway based on the screening data. This does not represent negligence of the intrinsic apoptotic pathway.

In response to the second question, there is not enough evidence to support the hypothesis that miRNAs are essential for the apoptotic process in osteoarthritis. Furthermore, it is even rare to see any study that indicates the anti-apoptosis effect of sodium ferulate is mediated by miRNAs. Confirmation of these factors is another scientific issue.

In response to the third question, we appreciate Ma and colleagues pointing out our inaccurate description. A correction has now been published to delete the sentence 'All of these results show that different concentrations of SF [sodium ferulate] from 125 to 1,000 μmol/l have no effect on normal chondrocyte viability' in the first section of Results [3].

Accordingly, we argue that it is not necessary to conduct the additional investigation on the intrinsic apoptotic pathway and the mechanism involved in miRNAs. This extra work recommended by Ma and colleagues would not enhance the persuasive capability of the conclusion in our paper.

Abbreviations

miRNA: microRNA.

Competing interests

The authors declare that they have no competing interests.

References

  1. Ma J, Li A, Zhu S, Cao XR, Pei GX: Response to 'TNF/TNFR signal transduction pathway-mediated anti-apoptosis and anti-inflammatory effects of sodium ferulate on IL-1β-induced rat osteoarthritis chondrocytes in vitro'. [http://arthritis-research.com/content/15/3/408] webcite

    Arthritis Res Ther 2013, 15:408. OpenURL

  2. Qin J, Shang L, Ping A-s, Li J, Li X-j, Yu H, Magdalou J, Chen L-b, Wang H: TNF/TNFR signal transduction pathway-mediated anti-apoptosis and anti-inflammatory effects of sodium ferulate on IL-1β-induced rat osteoarthritis chondrocytes in vitro.

    Arthritis Res Ther 2012, 14:R242. PubMed Abstract | BioMed Central Full Text OpenURL

  3. Qin J, Shang L, Ping AS, Li J, Li XJ, Yu H, Magdalou J, Chen LB, Wang H: Correction: TNF/TNFR signal transduction pathway-mediated anti-apoptosis and anti-inflammatory effects of sodium ferulate on IL-1β-induced rat osteoarthritis chondrocytes in vitro.

    Arthritis Res Ther 2013, 15:407. PubMed Abstract | BioMed Central Full Text OpenURL