Show simple item record

Matrix Metalloproteinase Induction by Relaxin Causes Cartilage Matrix Degradation in Target Synovial Joints

dc.contributor.authorKapila, Sunilen_US
dc.contributor.authorWang, Weien_US
dc.contributor.authorUston, Karen A.en_US
dc.date.accessioned2010-06-01T21:12:48Z
dc.date.available2010-06-01T21:12:48Z
dc.date.issued2009-04en_US
dc.identifier.citationKapila, Sunil; Wang, Wei; Uston, Karen (2009). "Matrix Metalloproteinase Induction by Relaxin Causes Cartilage Matrix Degradation in Target Synovial Joints." Annals of the New York Academy of Sciences 1160(1 Relaxin and Related Peptides Fifth International Conference ): 322-328. <http://hdl.handle.net/2027.42/74292>en_US
dc.identifier.issn0077-8923en_US
dc.identifier.issn1749-6632en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/74292
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=19416213&dopt=citationen_US
dc.format.extent167428 bytes
dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherBlackwell Publishing Incen_US
dc.rights© 2009 The New York Academy of Sciencesen_US
dc.subject.otherDegenerative Joint Diseaseen_US
dc.subject.otherFibrocartilageen_US
dc.subject.otherRelaxinen_US
dc.subject.otherEstrogenen_US
dc.subject.otherProgesteroneen_US
dc.subject.otherMatrix Metalloproteinasesen_US
dc.subject.otherExtracellular Matrixen_US
dc.titleMatrix Metalloproteinase Induction by Relaxin Causes Cartilage Matrix Degradation in Target Synovial Jointsen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelScience (General)en_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Orthodontics and Pediatric Dentistry, The University of Michigan, Ann Arbor, Michigan 48109-1078, USAen_US
dc.identifier.pmid19416213en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/74292/1/j.1749-6632.2009.03830.x.pdf
dc.identifier.doi10.1111/j.1749-6632.2009.03830.xen_US
dc.identifier.sourceAnnals of the New York Academy of Sciencesen_US
dc.identifier.citedreferenceFelson, D.T. & M.C. Nevitt. 1998. The effects of estrogen on osteoarthritis. Curr. Opin. Rheumatol. 10: 269 – 272.en_US
dc.identifier.citedreferenceVon Korff, M., S.F. Dworkin, L. Le Resche, et al. 1988. An epidemiologic comparison of pain complaints. Pain 32: 173 – 183.en_US
dc.identifier.citedreferenceWarren, M.P. & J.L. Fried. 2001. Temporomandibular disorders and hormones in women. Cells Tissues Organs 169: 187 – 192.en_US
dc.identifier.citedreferenceLipton, J.A., J.A. Ship & D. Larach-Robinson. 1993. Estimated prevalence and distribution of reported orofacial pain in the United States. J. Am. Dent. Assoc. 124: 115 – 121.en_US
dc.identifier.citedreferenceMilam, S.B., T.B. Aufdemorte, P.J. Sheridan, et al. 1987. Sexual dimorphism in the distribution of estrogen receptors in the temporomandibular joint complex of the baboon. Oral Surg. Oral Med. Oral Pathol. 64: 527 – 532.en_US
dc.identifier.citedreferenceAbubaker, A.O., W.F. Raslan & G.C. Sotereanos. 1993. Estrogen and progesterone receptors in temporomandibular joint discs of symptomatic and asymptomatic persons: a preliminary study. J. Oral Maxillofac. Surg. 51: 1096 – 1100.en_US
dc.identifier.citedreferenceYamada, K., K. Nozawa-Inoue, Y. Kawano, et al. 2003. Expression of estrogen receptor alpha (ER alpha) in the rat temporomandibular joint. Anat. Rec. A 274: 934 – 941.en_US
dc.identifier.citedreferenceWang, W., T. Hayami & S. Kapila. 2008. Female hormone receptors are differentially expressed in mouse fibrocartilages. Osteoarthritis Cartilage Epub ahead of print, 17 October 2008 posting date.en_US
dc.identifier.citedreferenceKapila, S. & Y. Xie. 1998. Targeted induction of collagenase and stromelysin by relaxin in unprimed and beta-estradiol-primed diarthrodial joint fibrocartilaginous cells but not in synoviocytes. Lab. Invest. 78: 925 – 938.en_US
dc.identifier.citedreferenceKapila, S. 2003. Does the relaxin, estrogen and matrix metalloproteinase axis contribute to degradation of TMJ fibrocartilage? J. Musculoskelet. Neuronal Interact. 3: 401 – 405..en_US
dc.identifier.citedreferenceNaqvi, T., T.T. Duong, G. Hashem, et al. 2005. Relaxin's induction of metalloproteinases is associated with the loss of collagen and glycosaminoglycans in synovial joint fibrocartilaginous explants. Arthritis Res. Ther. 7: R1 – R11.en_US
dc.identifier.citedreferenceHashem, G., Q. Zhang, T. Hayami, et al. 2006. Relaxin and beta-estradiol modulate targeted matrix degradation in specific synovial joint fibrocartilages: Progesterone prevents matrix loss. Arthritis Res. Ther. 8: R98.en_US
dc.identifier.citedreferenceSamuel, C.S., L.J. Parry & R.J. Summers. 2003. Physiological or pathological: A role for relaxin in the cardiovascular system? Curr. Opin. Pharmacol. 3: 152 – 158.en_US
dc.identifier.citedreferenceHwang, J.J., D. Macinga & E.A. Rorke. 1996. Relaxin modulates human cervical stromal cell activity. J. Clin. Endocrinol. Metab. 81: 3379 – 3384.en_US
dc.identifier.citedreferenceMushayandebvu, T.I. & M.R. Rajabi. 1995. Relaxin stimulates interstitial collagenase activity in cultured uterine cervical cells from nonpregnant and pregnant but not immature guinea pigs; estradiol-17 beta restores relaxin's effect in immature cervical cells. Biol. Reprod. 53: 1030 – 1037.en_US
dc.identifier.citedreferenceSamuel, C.S., A. Butkus, J.P. Coghlan, et al. 1996. The effect of relaxin on collagen metabolism in the nonpregnant rat pubic symphysis: The influence of estrogen and progesterone in regulating relaxin activity. Endocrinology 137: 3884 – 3890.en_US
dc.identifier.citedreferenceSamuel, C.S., J.P. Coghlan & J.F. Bateman. 1998. Effects of relaxin, pregnancy and parturition on collagen metabolism in the rat pubic symphysis. J. Endocrinol. 159: 117 – 125.en_US
dc.identifier.citedreferencePalejwala, S., D.E. Stein, G. Weiss, et al. 2001. Relaxin positively regulates matrix metalloproteinase expression in human lower uterine segment fibroblasts using a tyrosine kinase signaling pathway. Endocrinology 142: 3405 – 3413.en_US
dc.identifier.citedreferenceUnemori, E.N. & E.P. Amento. 1990. Relaxin modulates synthesis and secretion of procollagenase and collagen by human dermal fibroblasts. J. Biol. Chem. 265: 10681 – 10685.en_US
dc.identifier.citedreferenceUnemori, E.N., L.B. Pickford, A.L. Salles, et al. 1996. Relaxin induces an extracellular matrix-degrading phenotype in human lung fibroblasts in vitro and inhibits lung fibrosis in a murine model in vivo. J. Clin. Invest. 98: 2739 – 2745.en_US
dc.identifier.citedreferencePotier, M., S.J. Elliott, I. Tack, et al. 2001. Expression and regulation of estrogen receptors in mesangial cells: influence on matrix metalloproteinase-9. J. Am. Soc. Nephrol. 12: 241 – 251.en_US
dc.identifier.citedreferenceMarin-Castano, M.E., S.J. Elliott, M. Potier, et al. 2003. Regulation of estrogen receptors and MMP-2 expression by estrogens in human retinal pigment epithelium. Invest. Ophthalmol. Vis. Sci. 44: 50 – 59.en_US
dc.identifier.citedreferenceDi Nezza, L.A., T. Jobling & L.A. Salamonsen. 2003. Progestin suppresses matrix metalloproteinase production in endometrial cancer. Gynecol. Oncol. 89: 325 – 333.en_US
dc.identifier.citedreferenceShimonovitz, S., A. Hurwitz, D. Hochner-Celnikier, et al. 1998. Expression of gelatinase B by trophoblast cells: Down-regulation by progesterone. Am. J. Obstet. Gynecol. 178: 457 – 461.en_US
dc.identifier.citedreferenceKeller, N.R., E. Sierra-Rivera, E. Eisenberg, et al. 2000. Progesterone exposure prevents matrix metalloproteinase-3 (MMP-3) stimulation by interleukin-1Α in human endometrial stromal cells. J. Clin. Endocrinol. Metab. 85: 1611 – 1619.en_US
dc.identifier.citedreferenceSalamonsen, L.A. & D.E. Woolley. 1999. Menstruation: Induction by matrix metalloproteinases and inflammatory cells. J. Reprod. Immunol. 44: 1 – 27.en_US
dc.identifier.citedreferenceZhao, L., C.S. Samuel, G.W. Tregear, et al. 2000. Collagen studies in late pregnant relaxin null mice. Biol. Reprod. 63: 697 – 703.en_US
dc.identifier.citedreferenceHsu, S.Y., K. Nakabayashi, S. Nishi, et al. 2002. Activation of orphan receptors by the hormone relaxin. Science 295: 671 – 674.en_US
dc.identifier.citedreferenceKumagai, J., S.Y. Hsu, H. Matsumi, et al. 2002. INSL3/Leydig insulin-like peptide activates the LGR8 receptor important in testis descent. J. Biol. Chem. 277: 31283 – 31286.en_US
dc.identifier.citedreferenceKrajnc-Franken, M.A., A.J. van Disseldorp, J.E. Koenders, et al. 2004. Impaired nipple development and parturition in LGR7 knockout mice. Mol. Cell. Biol. 24: 687 – 696.en_US
dc.identifier.citedreferenceGrant-Tschudy, K.S. & C.R. Wira. 2004. Effect of estradiol on mouse uterine epithelial cell transepithelial resistance (TER). Am. J. Reprod. Immunol. 52: 252 – 262.en_US
dc.identifier.citedreferenceLu, T., Y. Achari, P. Sciore, et al. 2006. Estrogen receptor alpha regulates matrix metalloproteinase-13 promoter activity primarily through the AP-1 transcriptional regulatory site. Biochim. Biophys. Acta 1762: 719 – 731.en_US
dc.identifier.citedreferenceStevens, T.A. & R. Meech. 2006. BARX2 and estrogen receptor-alpha (ESR1) coordinately regulate the production of alternatively spliced ESR1 isoforms and control breast cancer cell growth and invasion. Oncogene 25: 5426 – 5435.en_US
dc.identifier.citedreferenceMizumoto, H., T. Saito, K. Ashikara, et al. 2002. Acceleration of invasive activity via matrix metalloproteinases by transfection of the estrogen receptor-alpha gene in endometrial carcinoma cells. Int. J. Cancer 100: 401 – 406.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.