Hyaluronate activation of CD44 induces insulin-like growth factor-1 expression by a tumor necrosis factor-alpha-dependent mechanism in murine macrophages.

Noble, Paul W.; Lake, Fiona; Henson, Peter M.; Riches, David W. H.

doi:10.1172/jci116469

Cited by 307 publications

(203 citation statements)

References 60 publications

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“…29 Some tumor cells express 24,25 and secrete 7 high amounts of HA. Ligation of CD44 on monocytes by HA induces release of IL-1 and TNF, 30,31 which is in keeping with the present findings that exposure of monocytes to HA induced significant production of ROIs. The latter was inhibited when monocytes were preincubated with anti-CD44 (but not anti-CD18 or anti-CD29) MAbs.…”

Section: Discussionsupporting

confidence: 92%

Cross-talk between human monocytes and cancer cells during reactive oxygen intermediates generation: The essential role of hyaluronan

et al. 2001

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Section: Discussionsupporting

confidence: 92%

Cross-talk between human monocytes and cancer cells during reactive oxygen intermediates generation: The essential role of hyaluronan

et al. 2001

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“…A direct effect of HYA on central mechanisms in cell activation is supported by the observation that soluble HYA stimulates IL 1-␤, TNF-␣, and insulinlike growth factor-1 (IGF-1) mRNA transcript expression as well as IGF-1 protein synthesis, Monoclonal antibodies to the HYA-receptor CD44 blocked the effects of HYA on IL-1-␤, TNF-␣ and IGF-1 expression [50]. There is also evidence that CD44 receptors function as matrix-organizing, matrix-anchoring HYA-binding proteins [51].…”

Section: Discussionmentioning

confidence: 99%

Dynamic role of hyaluronan (HYA) in connective tissue activation and inflammation

Gerdin

Hällgren

1997

Journal of Internal Medicine

124

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Gerdin B, Hällgren R (University Hospital, Uppsala, Sweden). Dynamic role of hyaluronan (HYA) in connective tissue activation and inflammation (Minisymposium: Hyaluronan). J Intern Med 1997; 242: 49–55. An increased tissue accumulation of HYA occurs in several human and experimental inflammatory conditions. Such is the case in sarcoidosis, idiopathic pulmonary fibrosis and farmer's lung in man, and experimental bleomycin‐induced lung damage in rats. Graft rejection in man and rats, experimental myocarditis in mice and myocardial infarction in rats follow the same pattern. Increased amounts of HYA also appear in gut luminal perfusion fluid in human inflammatory bowel disease. A transient accumulation of HYA is seen in wound healing, which is more sustained in fetuses. An increased accumulation of water and presentation of ligands for receptors on inflammatory cells are two consequences of the HYA accumulation.

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“…Several studies strongly suggest that macrophages are a major extrahepatic source of IGF-1. 21,[36][37][38] In an animal injury model, Lu et al 36 found that macrophages of the Ly-6C(-) subtype accumulated in damaged muscle and produced a high level of IGF-1 to promote muscle regeneration. In a human study, IGF-1 has been implicated in the pathogenesis of idiopathic pulmonary fibrosis, and interstitial macrophages were identified as a source of IGF-1.…”

Section: Discussionmentioning

confidence: 99%

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

Klein

Hassounah

et al. 2015

Journal of the American Society of Nephrology

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Effective therapeutic strategies to treat CKD-induced muscle atrophy are urgently needed. Lowfrequency electrical stimulation (LFES) may be effective in preventing muscle atrophy, because LFES is an acupuncture technique that mimics resistance exercise by inducing muscle contraction. To test this hypothesis, we treated 5/6-nephrectomized mice (CKD mice) and control mice with LFES for 15 days. LFES prevented soleus and extensor digitorum longus muscle weight loss and loss of hind-limb muscle grip in CKD mice. LFES countered the CKD-induced decline in the IGF-1 signaling pathway and led to increases in markers of protein synthesis and myogenesis and improvement in muscle protein metabolism. In control mice, we observed an acute response phase immediately after LFES, during which the expression of inflammatory cytokines (IFN-g and IL-6) increased. Expression of the M1 macrophage marker IL-1b also increased acutely, but expression of the M2 marker arginase-1 increased 2 days after initiation of LFES, paralleling the change in IGF-1. In muscle cross-sections of LFES-treated mice, arginase-1 colocalized with IGF-1. Additionally, expression of microRNA-1 and -206, which inhibits IGF-1 translation, decreased in the acute response phase after LFES and increased at a later phase. We conclude that LFES ameliorates CKDinduced skeletal muscle atrophy by upregulation of the IGF-1 signaling pathway, which improves protein metabolism and promotes myogenesis. The upregulation of IGF-1 may be mediated by decreased expression of microRNA-1 and -206 and/or activation of M2 macrophages.

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Hyaluronate activation of CD44 induces insulin-like growth factor-1 expression by a tumor necrosis factor-alpha-dependent mechanism in murine macrophages.

Cited by 307 publications

References 60 publications

Cross-talk between human monocytes and cancer cells during reactive oxygen intermediates generation: The essential role of hyaluronan

Cross-talk between human monocytes and cancer cells during reactive oxygen intermediates generation: The essential role of hyaluronan

Dynamic role of hyaluronan (HYA) in connective tissue activation and inflammation

Low-Frequency Electrical Stimulation Attenuates Muscle Atrophy in CKD—A Potential Treatment Strategy

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