E now possess a new reagent which will assist in determining the signal transduction pathways

E now possess a new reagent which will assist in determining the signal transduction pathways and mechanisms by which CCN2/CTGF stimulates collagen deposition by gingival fibroblasts. Data consist of the exciting observation that CCN2/CTGF increases collagen deposition without growing the development of these cultures. By contrast TGF-1 stimulated both growthNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptJ Cell Biochem. Author manuscript; obtainable in PMC 2006 Might 15.Heng et al.Pageand collagen deposition. TGF-1 has been shown previously to stimulate the proliferation of apparently confluent regular human primary dermal fibroblasts [Clark et al., 1997]. The absence of a mitogenic impact of CCN2/CTGF on confluent human fibroblasts distinguishes it from the effects of TGF-1. The absence of a mitogenic impact along with the presence of a modest collagen matrix stimulating effect by CTGF/CCN2 seem most likely to contribute to tissue fibrosis by successfully increasing the deposition of a collagenous extracellular matrix over time. This could in the end result in a tissue containing greater levels of deposited collagen than would occur in the absence of CTGF/CCN2. Drug induced gingival fibrosis can be a situation triggered by three classifications of drugs [Trackman and Kantarci, 2004]. Phenytoin, an anti-seizure medication, causes by far the most fibrotic lesions, and is accompanied by elevated levels of CTGF [Uzel et al., 2001]. Towards the extent that CTGF IL-1 alpha Proteins Species contributes to gingival fibrosis and for the extent that these mechanisms apply to other tissues, insights into mechanisms by which CTGF promotes collagen deposition are likely to become of fantastic significance. One can begin to envision the development of anti-fibrotic therapeutic techniques determined by E1 Enzymes Proteins web inhibition of CCN2/CTGF interactions with functionally critical binding partners for instance 61 integrins.Acknowledgements Investigation was supported by the following grants: NIH/NIDCR DE11004 and M01 RR00533. We thank Dr. Michael Davey for performing preliminary research related to creating the collagen deposition assay.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
NIH Public AccessAuthor ManuscriptJ Am Acad Dermatol. Author manuscript; obtainable in PMC 2012 July 1.Published in final edited kind as: J Am Acad Dermatol. 2011 July ; 65(1): 254. doi:ten.1016/j.jaad.2010.09.016.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptThe mucocutaneous and systemic phenotype of dermatomyositis sufferers with antibodies to MDA5 (CADM-140): A retrospective studyDavid Fiorentino, MD, PhDa, Lorinda Chung, MD, MSb, Jeff Zwerner, MD, PhDc, Antony Rosen, MDd, and Livia Casciola-Rosen, PhDdaDepartment bDepartmentof Dermatology, Stanford University School of Medicine, Stanford, California of Veterans Affairs Palo Alto Health Care Program, Palo Alto, California cDepartment of Pathology, Stanford University College of Medicine, Stanford, California dDivision of Rheumatology, Johns Hopkins University College of Medicine, Baltimore, MarylandAbstractBackground–Dermatomyositis (DM) is often a multisystem autoimmune disease, in which serologic evidence of immune responses to disease-specific antigenic targets is found in around 50 to 70 of individuals. Lately, melanoma differentiation-associated gene five (MDA5) has been identified as a DM-specific autoantigen that seems to be targeted in patients with DM and mild or absent muscle inflammation and with an elevated threat of interstitial lung dis.