Hyaluronan in the rat with special reference to the skin

Reed, Rolf K.; Lilja, Karin; Laurent, Torvard C.

doi:10.1111/j.1748-1716.1988.tb08508.x

Cited by 161 publications

(92 citation statements)

References 29 publications

(23 reference statements)

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“…A painstaking analysis of the body of the rat by Reed et al [6] should be broadly applicable to other mammals. About half of the HYA was recovered from skin, and a quarter from the skeleton and joints taken together.…”

Section: Distribution Of Hyaluronan In Mammalian Organs and Tissuesmentioning

confidence: 99%

Hyaluronan: its nature, distribution, functions and turnover

Fraser

Laurent²,

Laurent

1997

Journal of Internal Medicine

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Fraser JRE, Laurent TC, Laurent UBG (Monash University, Clayton, Victoria, Australia; and University of Uppsala, Uppsala, Sweden). Hyaluronan: its nature, distribution, functions and turnover (Minisymposium: Hyaluronan). J Intern Med 1997; 242: 27–33. Hyaluronan is a polysaccharide found in all tissues and body fluids of vertebrates as well as in some bacteria. It is a linear polymer of exceptional molecular weight, especially abundant in loose connective tissue. Hyaluronan is synthesized in the cellular plasma membrane. It exists as a pool associated with the cell surface, another bound to other matrix components, and a largely mobile pool. A number of proteins, the hyaladherins, specifically recognize the hyaluronan structure. Interactions of this kind bind hyaluronan with proteoglycans to stabilize the structure of the matrix, and with cell surfaces to modify cell behaviour. Because of the striking physicochemical properties of hyaluronan solutions, various physiological functions have been assigned to it, including lubrication, water homeostasis, filtering effects and regulation of plasma protein distribution. In animals and man, the half‐life of hyaluronan in tissues ranges from less than 1 to several days. It is catabolized by receptor‐mediated endocytosis and lysosomal degradation either locally or after transport by lymph to lymph nodes which degrade much of it. The remainder enters the general circulation and is removed from blood, with a half‐life of 2–5 min, mainly by the endothelial cells of the liver sinuoids.

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Section: Distribution Of Hyaluronan In Mammalian Organs and Tissuesmentioning

confidence: 99%

Hyaluronan: its nature, distribution, functions and turnover

Fraser

Laurent²,

Laurent

1997

Journal of Internal Medicine

Self Cite

1,757

1,315

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“…ϩ RNA was isolated from each transfectant, reverse-transcribed, and amplified by PCR with primers specific for GAPDH (980 bp; lanes 1-3), HAS2 (210 bp; lanes 4 -8), and HAS3 (410 bp; lanes 9 -13). Lanes 1,4, and 9 correspond to GFP control transfectants. Lanes 2, 5, and 10 contain products amplified from HAS2-transfected cells.…”

Section: Has Overexpression and Antisense Inhibitionmentioning

confidence: 99%

“…HA is a ubiquitous polysaccharide component of extracellular and cell-associated matrices (3,4), essential for growth and motility of both normal and transformed cells (3,(5)(6)(7). In some cell types, this requirement entails assembly of a pericellular HA matrix (8,9).…”

mentioning

confidence: 99%

Manipulation of Hyaluronan Synthase Expression in Prostate Adenocarcinoma Cells Alters Pericellular Matrix Retention and Adhesion to Bone Marrow Endothelial Cells

Simpson¹,

Wilson²,

Furcht³

et al. 2002

Journal of Biological Chemistry

104

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Prostate cancer metastasis to bone marrow involves initial adhesion of tumor cells to the bone marrow endothelium, followed by transmigration and proliferation within the marrow. Rapid, specific adhesion of highly metastatic prostate adenocarcinoma cells Prostate cancer mortality is frequently the result of bone metastasis. The preferential homing of circulating prostate tumor cells to bone marrow is thought to involve an initial rapid adhesion to cells of the bone marrow endothelium, followed by transmigration of the endothelium, engagement of specific receptors, and subsequent proliferation within the bone marrow microenvironment. Molecular mechanisms underlying these processes are poorly understood, but there is evidence that tumor cells may exploit existing pathways utilized by circulating blood cell progenitors to gain access to bone marrow.To identify potential cell adhesion molecules involved in prostate tumor bone metastasis, research in our laboratory has focused on the interaction of prostate carcinoma cells with bone marrow endothelial cells (BMECs).1 Highly metastatic PC3M-LN4 cells (1) were found to adhere rapidly to human bone marrow-derived sinusoidal endothelial cell lines, whereas poorly metastatic LNCaP cells were only weakly adherent (2). This adhesion, specific for BMECs relative to other endothelial cells, was subsequently found to depend upon the presence of a pericellular hyaluronan (HA) matrix assembled on the PC3M-LN4 cells. The presence of pericellular HA further correlated with elevated HA synthesis and expression of HA biosynthetic enzymes in the metastatic cells. Collectively, our results may implicate tumor cell-associated HA and up-regulation of HA synthase (HAS) in prostate cancer progression, possibly by facilitating arrest in the bone microvasculature and/or preferential tissue colonization of individual tumor cells.

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“…High levels of this glycosaminoglycan exist in synovial and mesothelial fluids (1), in resilient tissues like dermis (2) and cartilage (3), and in the transparent vitreous body of the eye where it was originally discovered (4). Because of its physicochemical properties, hyaluronan can influence many cellular functions including migration, proliferation, and adhesion, but it may also act as a signaling molecule.…”

mentioning

confidence: 99%