E now have a new reagent that could support in determining the signal transduction pathways and mechanisms by which CCN2/CTGF stimulates collagen deposition by DYRK4 Inhibitor Species gingival fibroblasts. Information include the interesting observation that CCN2/CTGF increases collagen deposition without increasing the development of those cultures. By contrast TGF-1 stimulated each growthNIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptJ Cell Biochem. Author manuscript; offered in PMC 2006 May well 15.Heng et al.Pageand collagen deposition. TGF-1 has been shown previously to stimulate the proliferation of apparently confluent typical human primary dermal fibroblasts [Clark et al., 1997]. The absence of a mitogenic effect of CCN2/CTGF on confluent human fibroblasts distinguishes it from the effects of TGF-1. The absence of a mitogenic effect as well as the presence of a modest collagen matrix stimulating impact by CTGF/CCN2 appear most likely to contribute to tissue fibrosis by correctly increasing the deposition of a collagenous extracellular matrix over time. This could eventually result in a tissue containing greater levels of deposited collagen than would happen inside the absence of CTGF/CCN2. Drug induced gingival fibrosis is really a situation triggered by three classifications of drugs [Trackman and Kantarci, 2004]. Phenytoin, an anti-seizure medication, causes one of the most fibrotic lesions, and is accompanied by elevated levels of CTGF [Uzel et al., 2001]. Towards the extent that CTGF contributes to gingival fibrosis and to the extent that these mechanisms apply to other tissues, insights into mechanisms by which CTGF promotes collagen deposition are probably to be of terrific significance. One particular can start to envision the improvement of anti-fibrotic therapeutic strategies based on inhibition of CCN2/CTGF interactions with functionally crucial binding partners including 61 integrins.CCR2 Inhibitor custom synthesis Acknowledgements Investigation was supported by the following grants: NIH/NIDCR DE11004 and M01 RR00533. We thank Dr. Michael Davey for performing preliminary studies connected to building 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:10.1016/j.jaad.2010.09.016.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptThe mucocutaneous and systemic phenotype of dermatomyositis patients 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 College of Medicine, Stanford, California of Veterans Affairs Palo Alto Well being Care Program, Palo Alto, California cDepartment of Pathology, Stanford University School of Medicine, Stanford, California dDivision of Rheumatology, Johns Hopkins University College of Medicine, Baltimore, MarylandAbstractBackground–Dermatomyositis (DM) can be a multisystem autoimmune illness, in which serologic evidence of immune responses to disease-specific antigenic targets is identified in around 50 to 70 of sufferers. Not too long ago, melanoma differentiation-associated gene 5 (MDA5) has been identified as a DM-specific autoantigen that appears to be targeted in individuals with DM and mild or absent muscle inflammation and with an improved threat of interstitial lung dis.