Guest guest Posted March 16, 2004 Report Share Posted March 16, 2004 Smooth Muscle Cells. More than just fibroids...as I've said for some time now...wouldn't it be nice if this whole puzzle of fibroids was a tumbler lock that just rolled open with a bit more effort in research...Check out all of the following research links for exciting info/progress made in work published during the past few months. I feel so, so, well, er uh, " vindicated " for thinking there might be " something " which links artheriosclerosis and fibroids...and also happen to think there's a link to alzheimer's too...but that's another story...my money is on a little known or understood bacteria that potentially has been a devilish culprit all along...can't wait to read what the researchers discover next! Even if they prove my next line of thinking completely wrong, I won't even give a rip -- as long as progress continues to be made which might give us ANSWERS!!!!!! ***************************** A link between clogged arteries and uterine fibroids? by C.W. Wolff Tuesday, March 16, 2004 Tufts Journal Uterine fibroids affect more than one in five American women, and more than 200,000 will have hysterectomies each year because of this painful, chronic condition. Another one million Americans die because of heart and blood vessel diseases, and nearly two million will undergo surgical procedures to widen blocked arteries. Re-clogging of the arteries will occur in several hundred thousand of these patients. read the rest here: http://tuftsjournal.tufts.edu/archive/2003/february/features/genetic_explorers.s\ html ***************************** Research Description Tufts University 2/6/2004 The goal of our laboratory is to elucidate the mechanisms regulating proliferation of smooth muscle cells (SMC), using a concerted biochemical, molecular, and cell biological approach. Hyperproliferation of vascular SMC [Fig. 1] can lead to a wide variety of pathologies, including hypertension and atherosclerosis. SMC hyperproliferation is responsible for the 20-30% failure rates following vascular procedures such as angioplasty and coronary artery bypass grafts. read the rest here: http://www.tufts.edu/sackler/cmdb/castellot-lab.htm ******************************** The growth arrest-specific gene CCN5 is deficient in human leiomyomas and inhibits the proliferation and motility of cultured human uterine smooth muscle cells. Mason HR, Lake AC, Wubben JE, Nowak RA, Castellot JJ Jr. Mol Hum Reprod. 2004 Mar;10(3):181-7. Epub 2004 Jan 29. " ...our data strongly suggest that CCN5 may exert an important function in maintaining the normal uterine phenotype and that loss of the anti-proliferative protein CCN5 from normal myometrium may account, at least in part, for tumorigenesis... " read the abstract here (or order the full paper): http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra\ ct&list_uids=14981145 ********************************** CCN5 modulates the antiproliferative effect of heparin and regulates cell motility in vascular smooth muscle cells. Lake AC, Castellot JJ Jr. Cell Communication and Signaling 2003, 1:5 © 2003 Lake and Castellot; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. ABSTRACT Background Vascular smooth muscle cell (VSMC) hyperplasia plays an important role in both chronic and acute vascular pathologies including atherosclerosis and restenosis. Considerable work has focused on the mechanisms regulating VSMC proliferation and motility. Earlier work in our lab revealed a novel growth arrest-specific (gas) gene induced in VSMC exposed to the antiproliferative agent heparin. This gene is a member of the CCN family and has been given the name CCN5. The objective of the present study is to elucidate the function of CCN5 protein and to explore its mechanism of action in VSMC. Results Using RNA interference (RNAi), we first demonstrate that CCN5 is required for the antiproliferative effect of heparin in VSMC. We also use this gene knockdown approach to show that CCN5 is an important negative regulator of motility. To explore the mechanism of action of CCN5 on VSMC motility, we use RNAi to demonstrate that knock down of CCN5 up regulates expression of matrix metalloproteinase-2 (MMP-2), an important stimulator of motility in VSMC. In addition, forced expression of CCN5 via adenovirus results in reduced MMP-2 activity, this also corroborates the gene knock down results. Finally, we show that loss of CCN5 expression in VSMC causes changes in VSMC morphology and cytoskeletal organization, including a reduction in the amount and macromolecular assembly of smooth muscle cell α-actin. Conclusions This work provides important new insights into the regulation of smooth muscle cell proliferation and motility by CCN5 and may aid the development of therapies for vascular diseases. read the whole paper here: http://www.biosignaling.com/content/1/1/5 ******************************** Estrogen Induces CCN5 Expression in the Rat Uterus in Vivo Mason HR, Grove-Strawser D, Rubin BS, Nowak RA, Castellot JJ Jr. Endocrinology Vol. 145, No. 2 976-982. read the abstract here: http://endo.endojournals.org/cgi/content/abstract/145/2/976 ******************************** A tutorial review on CCN: COMMENTARY: The CCN family: A new stimulus package Brigstock DR. J Endocrinol. 2003 Aug;178(2):169-75. http://journals.endocrinology.org/joe/178/joe1780169.htm (full free .pdf text available at this link for downloading) ******************************** A stretch of the imagination...but I can't help but think there's a link somewhere in the following paper to the impact of fibroid embolization on myometrium and placental development...it's days/times like this that I truly wished I had paid more attention to science in school... CYR61 (CCN1) Is Essential for Placental Development and Vascular Integrity Mo F, Muntean AG, Chen CC, Stolz DB, Watkins SC, Lau LF. Molecular and Cellular Biology, December 2002, p. 8709-8720, Vol. 22, No. 24. read the full paper here (.pdf): http://mcb.asm.org/cgi/reprint/22/24/8709.pdf ******************************** Expression and Action of Connective Tissue Growth Factor Dissertation, 2003 Amy Rachfal read the entire dissertation here (yes, it's long!): http://www.ohiolink.edu/etd/send-pdf.cgi?osu1069791086 *********************************** Quote Link to comment Share on other sites More sharing options...
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