International CCN Society

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International CCN Society

Paris, France
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Perbal A.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2017

The recent publication of a commentary article by Dadkhah et al. (J Cell Commun Signal 11:181–185, 2017) which addressed issues raised by the citation of questionable scientific papers in current databases and the recent retraction of manuscripts dealing with the biological properties of the CCN1 protein by Lin et al. (J Biol Chem 291(53):27433, 2016) prompted us to examine how this situation reflects an evolution of the original citation system, endangering scientific communication. We argue that the increasing number of publication retractions that have been witnessed over several years is a direct consequence of the bias created by the inconsistency of citation metrics. © 2017, The International CCN Society.


Perbal A.,International CCN Society | Perbal B.,French National Center for Scientific Research
Journal of Cell Communication and Signaling | Year: 2016

The CCN family of proteins is composed of six members, which are now well recognized as major players in fundamental biological processes. The first three CCN proteins discovered were designated CYR61, CTGF, and NOV because of the context in which they were identified. Both CYR61 and CTGF were discovered in normal cells, whereas NOV was identified in tumors. Soon after their discovery, it was established that they shared important and unique structural features and distinct biological properties. Based on these structural considerations, the three proteins were proposed to belong to a family that was designated CCN by P. Bork. Hence the CCN1, CCN2 and CCN3 acronyms. The family grew to six members a few years later with the description of three proteins WISP-1, WISP-2 and WISP-3 (CCN4, CCN5 and CCN6), that shared the same tetramodular and conserved structural features. With the functions of the CCN proteins being uncovered, this raised a nomenclature problem. A scientific committee convened in Saint Malo (France) proposed to apply the CCN nomenclature to the six members of the family. Although the unified nomenclature was proposed in order to avoid serious misconceptions and lack of precision associated with the use of the old acronyms, the acceptance of the new acronyms has taken time. In order to evaluate how the use of disparate nomenclatures have had an impact on the CCN protein field, we conducted a survey of the articles that have been published in this area since the discovery of the first CCN proteins and inception of the field. We report in this manuscript the confusion and serious deleterious scientific consequences that have stemmed from a disorganized usage of several unrelated acronyms. The conclusions that we have reached call for a unification that needs to overcome personal habits and feelings. Instead of allowing the CCN field to fully crystalize and gain the recognition that it deserves the usage of many different acronyms represents a danger that everyone must fight against in order to avoid its deliquescence. We hope that the considerations discussed in the present article will encourage all authors working in the CCN field to work jointly and succeed in building a strong and coherent CCN scientific community that will benefit all of us. © 2016 The International CCN Society


PubMed | International CCN Society and French National Center for Scientific Research
Type: Journal Article | Journal: Journal of cell communication and signaling | Year: 2016

The CCN family of proteins is composed of six members, which are now well recognized as major players in fundamental biological processes. The first three CCN proteins discovered were designated CYR61, CTGF, and NOV because of the context in which they were identified. Both CYR61 and CTGF were discovered in normal cells, whereas NOV was identified in tumors. Soon after their discovery, it was established that they shared important and unique structural features and distinct biological properties. Based on these structural considerations, the three proteins were proposed to belong to a family that was designated CCN by P. Bork. Hence the CCN1, CCN2 and CCN3 acronyms. The family grew to six members a few years later with the description of three proteins WISP-1, WISP-2 and WISP-3 (CCN4, CCN5 and CCN6), that shared the same tetramodular and conserved structural features. With the functions of the CCN proteins being uncovered, this raised a nomenclature problem. A scientific committee convened in Saint Malo (France) proposed to apply the CCN nomenclature to the six members of the family. Although the unified nomenclature was proposed in order to avoid serious misconceptions and lack of precision associated with the use of the old acronyms, the acceptance of the new acronyms has taken time. In order to evaluate how the use of disparate nomenclatures have had an impact on the CCN protein field, we conducted a survey of the articles that have been published in this area since the discovery of the first CCN proteins and inception of the field. We report in this manuscript the confusion and serious deleterious scientific consequences that have stemmed from a disorganized usage of several unrelated acronyms. The conclusions that we have reached call for a unification that needs to overcome personal habits and feelings. Instead of allowing the CCN field to fully crystalize and gain the recognition that it deserves the usage of many different acronyms represents a danger that everyone must fight against in order to avoid its deliquescence. We hope that the considerations discussed in the present article will encourage all authors working in the CCN field to work jointly and succeed in building a strong and coherent CCN scientific community that will benefit all of us.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2015

Previous studies have indicated that the expression of CCN3, a member of the CCN family of proteins, was tightly regulated during central nervous development and was associated with acquisition of cognitive functions in rats (Perbal, Mol Pathol 54(2):57–79, 2001; Su et al. Sheng Li Xue Bao 52(4):290–294, 2000) therefore suggesting that CCN3 might be involved in higher levels of physiological communication in the brain. In spite of the considerable amount of progress made into the understanding of neuronal organization and communication, reducing the knowledge gap between brain cellular biology and behavioral studies remains a huge challenge. Mind-to-mind communication has been the subject of numerous science fiction writings, intense research and emotional debates for many years. Scientists have tried for a long time to achieve transmission of messages between living subjects via non intrusive protocols. Thanks to the great progress made in imagery and neurosciences, another dimension of neuronal function in communication has now been documented. Two recent experimental demonstrations of direct brain to brain communication without physical contact (Grau et al. (2014) Conscious brain-to-brain communication in humans using non-invasive technologies. PLoS One. Aug 19;9(8)- - Rao et al. (2014) A direct brain-to-brain interface in humans. PLoS One. Nov 5;9(11)) pave the road to more sophisticated applications that could profoundly affect communications of humans with other humans, animals and machines. Although the wide use of such applications might seem a long way off, they raise quite a number of ethical, legal and societal issues. © 2015, The International CCN Society.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2012

A critical look at a recently published manuscript reporting the role of CCN3 in the regulation of clear cell renal cell carcinoma (RCC) biology raises several scientific concerns, and reveals flaws in the reviewing process which appear to have resulted in the dissemination of conclusions that are not supported by proper experimental procedures. In the example presented here, the observed biological effects are attributed to a high molecular weight "CCN3" protein which is detected by a single commercial antibody that was not shown in the experimental conditions used by the authors to be a valid reagent capable of stringently detecting the "canonical" CCN3 protein. Experiments establishing that inhibiting the production of high molecular weight "CCN3" protein would reverse these biological effects were not performed. The case discussed here clearly demonstrates that unreliable data can go through peer reviewing and be published. As the data can end up being cited and used as a potential reference by new investigators in the field, we believe that such data can throw roadblocks across the scientific path of inquiry and mislead investigations. We therefore raise awareness for the need of a more stringent peer reviewing process in which assurance can be had that the strength and precision of the data have been thoroughly checked by experts in the CCN field, and previous work properly referenced. © The International CCN Society 2012.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2014

The Nuts and Bolts section of our Journal (mirrored on the ICCNS society web site), is meant to provide a very practical way to share useful information, that goes beyond the scope of cell signaling and basic CCN protein biology. Considering the number of requests we have had for information related to protection of Intellectual Property (IP), I am pleased to initiate what will be a series of articles that will focus on various IP topics. The inaugural topic is the protection of computer programs. Some colleagues may wonder how and why the patentability of computer programs is a topic of interest for scientists working on CCN proteins . . . As a matter of fact, to assist us in analyzing the potential involvement of CCN3 in human genetic diseases, we considered developing a computer program designed to analyze large amounts of data. Sharing the concepts and the computer program raised concerns regarding IP and protection of the software that we would handle. We believe that many colleagues have encountered similar problems. This article provides a short focus on computer program patentability. It is aimed to provide basic legal information, and to help our readers in understanding the process. It is not intended to replace IP counselors or technology transfer departments. Future articles will address other practical aspects of IP protection. © 2014 The International CCN Society.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2014

The considerable advances of genome sequencing over the past decades have had a profound impact on our daily life and opened up new avenues for the public to have access to their genetic information and learn more about their ancestry, genealogy and other traits that make each of us unique individuals. A very large number of individual single nucleotide polymorphisms (SNPs) have been associated to diseases whereas others have no known phenotype. For example, among the SNPs mapped within ccn1(cyr61), ccn2(ctgf), ccn3(nov), ccn4(wisp-1), ccn5(wisp-2) and ccn6 (wisp-3), only mutations within ccn4 were associated to PPD (the autosomal recessive skeletal disorder Progressive Pseudorheumatoid Dysplasia). On the occasion of this JCCS special issue on the roles of hormetic responses in adaptation, and response of living species to the modifications of their environment, it appeared that it was a good time to briefly review a topic that has been the subject of passionate discussions for the past few years, that is Direct to Consumer genetic tests (DTC GT). Based on the use of DNA analysis and identification of polymorphisms, DTC GT have been developed by several companies in the USA and in countries where there was no legal obstacle for customers to have direct access to their genetic information and manage their healthcare. Problems that arose and decisions that have been taken by regulatory agencies are presented and discussed in this editorial. The « freeze » of health-oriented DTC GT in the USA neither implies the end of DNA analysis nor « fun » applications, which are not aimed at providing risks estimates for particular illnesses. As shown in the example which is discussed in this editorial, DTC GT for cosmetic applications might be considered a fun application of great interest for companies such as L’Oréal, who recently developed the Makeup Genius mobile application. Other fun applications of DTC GT are discussed but there is no doubt that nothing will stop progress and it is most probable than within a few years from now all the tensions raised about these procedures will vanish to the profit and benefit of consumers. In any case, this will only be possible through an intensive communication effort, because …communication is the key ! © 2014, The International CCN Society.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2013

In this Editorial, I would like to provide our readers with a brief mid-year update about our activities and efforts to bring together researchers working on intercellular signaling proteins at international meetings. The roots emerged about 20 years ago in the discovery of three genes originally designated cyr61, ctgf, and nov. The proteins encoded by these genes were first proposed to constitute a family of proteins (CCN) which now comprises 6 members (CCN1, CCN2, CCN3, CCN4-6) including the wisp proteins. These proteins were recognized to share a striking structural organization and a high degree of identity although they exhibited quite distinct biological properties. After historical considerations regarding the reasons for using the CCN acronym, and how the ICCNS publishing landscape that drove the ICCNS from Cell Communication and Signaling to the Journal of Cell Communication and Signaling, this short update will focus on the 7th edition of the International Workshop on the CCN family of genes to be held in Nice, Oct 16-19, 2013. © 2013 The International CCN Society.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2012

There is increasing evidence that metalloproteinases are involved in neuropathic pain [Dev et al., Expert Opin Investig Drugs 19:455-468 2010] Hence, the identification of molecules that can regulate MMP9 and MMP2 is warranted. In a recent publication, Kular et al. (2012) claim that CCN3 functions to decrease inflammatory pain via the regulation of two metalloproteinases, MMP2 and MMP9, in response to experimentally-induced inflammation. Their conclusion is based on the following observations: i) the expression of CCN3 was reduced following induction of pain by subcutaneous injection of complete Freund's adjuvent in rat's paw, ii) an inhibition of MMP9 decreased CFA-associated mechanical allodynia, iii) inhibition of CCN3 expression by siRNA led to an upregulation of MMP2 in the dorsal horn of the spinal cord (DHSC) and MMP9 in the dorsal root ganglia (DRG), iv) a partial effect of CCN3 on CFA-induced expression of MMP9 and MMP2 in DRG and DHSC following intrathecal injection of CCN3. Unfortunately, the conclusion of this study is weakened by the lack of experimental evidence showing a direct relationship between the expression of CCN3 and MMPs. Furthermore, several results contained in this manuscript only confirm data that were previously established by others. Owing to the wide range of activities which have been attributed to CCN3 (Perbal, Mol Pathol 54:57-79 2001, Brigstock, J Endocrinol 178:169-175 2003, Perbal, Lancet 363 (9402):62-64 2004, Perbal, Cell Commun Signal 4:6 2006, Holbourn et al. Trends Biochem Sci. 33:461-473 2008, Leask and Abraham, J Cell Sci 119:4803-4810 2006, Jun and Lau, Nat Rev Drug Discov 10:945-963 2011, Rachfal and Brigstock, Vitam Horm 70:69-103 2005), the mechanisms underlying the potential role of CCN3 in the expression of these MMPs in the context of inflammatory pain must be thoroughly studied before a meaningful conclusion can be reached. Indeed, Kular et al. description of variations in CCN3, MMP9 and MMP2 levels occurring simultaneously is not sufficient to draw a functional relationship between these three proteins. It should be noted that the expression of CCN3 was already reported to repress MMP9 (Benini et al., Oncogene 24:4349-4361 2005, Fukunaga-Kalabis et al., Oncogene 27:2552-2560 2008) and the roles of CCN3 in inflammatory processes has been extensively documented in the past few years (Bleau et al., Front Biosci 10:998-1009 2005, Lin et al., J Biol Chem 280:8229-8237 2005, Perbal, Cell Commun Signal 4:6 2006, Hughes et al., Diabetologia 50:1089-1098 2007, Lin et al., J Cell Commun Signal 4:141-153 2010, Pasmant et al., J Neuropathol Exp Neurol 69:60-69 2010, Shimoyama et al., Thromb Vasc Biol 30:675-682 2010, Lemaire et al., J Invest Dermatol 130:2517 2010, Chen and Lau, J Cell Commun Signal 4:63-69 2010, Le Dréau et al., Glia 58:1510-1521 2010, Rittié et al. J Cell Commun Signal 5:69-80 2011, Janune et al., J Cell Commun Signal 5:167-171 2011). In addition, the expression of CCN3 in the neurons of dorsal root ganglia and dorsal horn of the spinal horn in rat and human has also been documented (Su et al., C R Acad Sci III 321:883-892 1998, Mol Pathol 54:184-191 2001, Kocialkowski et al., Anat Embryol (Berl) 203:417-427 2001). Implication of CCN3 in cognitive functions (Su et al., Sheng Li Xue Bao 52:290-294 2000) and the possible involvement of CCN3 in the regulation of pain was already suggested almost a decade ago (Perbal, Expert Rev Mol Diagn 3:597-604 2003, Perbal et al., Mol Pathol 56:80-85 2003) with the demonstration of cell-specific effects of CCN3 on intracellular calcium stores and inhibition of anionic channels by CCN3 (Li et al., Mol Pathol 55:250-261 2002, Lombet et al., Cell Commun Signal 1:1 2003, Perbal, Expert Rev Mol Diagn 3:597-604 2003, Perbal et al., Mol Pathol 56:80-85 2003). Aside from these general aspects, and in the light of the potential participation of CCN3 in the whole process of pain sensing, the reader would have appreciated the discussion in this manuscript not being essentially a flat summary of the data presented, but a more thorough discussion of the possible role for CCN3 in the regulation of MMPs and its significance in the context of the wide biological functions of CCN3. © The International CCN Society 2012.


Perbal B.,International CCN Society
Journal of Cell Communication and Signaling | Year: 2013

The CCN family of proteins includes six members presently known as CCN1, CCN2, CCN3, CCN4, CCN5 and CCN6. These proteins were originally designated CYR61, CTGF, NOV, and WISP-1, WISP-2, WISP-3. Although these proteins share a significant amount of structural features and a partial identity with other large families of regulatory proteins, they exhibit different biological functions. A critical examination of the progress made over the past two decades, since the first CCN proteins were discovered brings me to the conclusion that most of our present knowledge regarding the functions of these proteins was predicted very early after their discovery. In an effort to point out some of the gaps that prevent us to reach a comprehensive view of the functional interactions between CCN proteins, it is necessary to reconsider carefully data that was already published and put aside, either because the scientific community was not ready to accept them, or because they were not fitting with the « consensus » when they were published. This review article points to avenues that were not attracting the attention that they deserved. However, it is quite obvious that the six members of this unique family of tetra-modular proteins must act in concert, either simultaneously or sequentially, on the same sites or at different times in the life of living organisms. A better understanding of the spatio-temporal regulation of CCN proteins expression requires considering the family as such, not as a set of single proteins related only by their name. As proposed in this review, there is enough convincing pieces of evidence, at the present time, in favor of these proteins playing a role in the coordination of multiple signaling pathways, and constituting a Centralized Communication Network. Deciphering the hierarchy of regulatory circuits involved in this complex system is an important challenge for the near future. In this article, I would like to briefly review the concept of a CCN family of proteins and critically examine the progress made over the past 10 years in the understanding of their biological functions and involvement in both normal and pathological processes. © 2013 The International CCN Society.

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