Thrombospondin-1 Differentially Regulates Release of IL-6 and IL-10 by Human Monocytic Cell Line U937

Yamauchi, Yasushi; Imakiire, Takanori; Abe, Hironori; Uchida, Hiroko; Beppu, Richiko; Yamashita, Yuichi; Kuroki, Masahide; Shirakusa, Takayuki

doi:10.1006/bbrc.2002.6386

Cited by 32 publications

(22 citation statements)

References 31 publications

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“…Accordingly, decreased inflammation and increased white matter sparing following spinal cord injury were seen when the TSP-1 receptor CD47 was knocked out, though curiously this protection did not extend to TSP-1 knockout mice (Myers et al, 2011). In addition, TSP-1 enhances the release of the inflammatory cytokines IL-6 and IL-10 via CD36 (Yamauchi et al, 2002a). There is growing evidence for cytokines playing key roles in synaptic plasticity and neurogenesis (Bilbo and Schwarz, 2009; McAfoose and Baune, 2009), such as IL-6’s importance to the modulation of LTP, a form of synaptic plasticity associated with learning and memory (Balschun et al, 2004).…”

Section: Thrombospondin and The Matricellular Protein Response To mentioning

confidence: 99%

“…There is growing evidence for cytokines playing key roles in synaptic plasticity and neurogenesis (Bilbo and Schwarz, 2009; McAfoose and Baune, 2009), such as IL-6’s importance to the modulation of LTP, a form of synaptic plasticity associated with learning and memory (Balschun et al, 2004). However, TSP-1 can also suppress IL-10 release by interacting with latent transforming growth factor beta-1 (TGF-β1) (Yamauchi et al, 2002a). Indeed, TSP-1 is known to activate latent TGF-β1 (Schultz-Cherry et al, 1994; Schultz-Cherry and Murphy-Ullrich, 1993).…”

Section: Thrombospondin and The Matricellular Protein Response To mentioning

confidence: 99%

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Thrombospondins as key regulators of synaptogenesis in the central nervous system

2012

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Thrombospondins (TSPs) are a family of large, oligomeric multidomain glycoproteins that participate in a variety of biological functions as part of the extracellular matrix (ECM). Through their associations with a number of binding partners, TSPs mediate complex cell-cell and cell-matrix interactions in such diverse processes as angiogenesis, inflammation, osteogenesis, cell proliferation, and apoptosis. It was recently shown in the developing central nervous system (CNS) that TSPs promote the formation of new synapses, which are the unique cell-cell adhesions between neurons in the brain. This increase in synaptogenesis is mediated by the interaction between astrocyte-secreted TSPs and their neuronal receptor, calcium channel subunit α2δ-1. The cellular and molecular mechanisms that underlie induction of synaptogenesis via this interaction are yet to be fully elucidated. This review will focus on what is known about TSP and synapse formation during development, possible roles for TSP following brain injury, and what the previously established actions of TSP in other biological tissues may tell us about the mechanisms underlying TSP’s functions in CNS synaptogenesis.

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Section: Thrombospondin and The Matricellular Protein Response To mentioning

confidence: 99%

Section: Thrombospondin and The Matricellular Protein Response To mentioning

confidence: 99%

Thrombospondins as key regulators of synaptogenesis in the central nervous system

2012

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“…(27) TSP1 also has important functions in inflammation that are dependent of its binding with CD36. (28)…”

Section: The Thrombospondinsmentioning

confidence: 99%

The Role of Thrombospondin 1 on Intestinal Inflammation and Carcinogenesis

Gutierrez

2008

Biomark�Insights

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Crohn’s disease and ulcerative colitis are inflammatory bowel diseases (IBD) quite common in the United States and other Western countries. Patients suffering IBD are at greater risk of developing colorectal adenocarcinoma than the general population. Both, the adenomacarcinoma and the inflammation-carcinogenesis processes are characterized by active angiogenesis. Recent studies also have shown that anti-angiogenesis might be a novel therapeutic approach for IBD. Thrombospondin 1 (TSP1) is an extracellular protein well known for its anti-angiogenic properties. TSP1 also has key functions in inflammation, which is assumed to be the primary cause for carcinogenesis in IBD. This review is focused on the role of TSP1 in colorectal carcinogenesis. The therapeutic effects of TSP derived-peptides on inhibiting the inflammation-carcinogenesis progression are also discussed.

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“…Furthermore, the levels of TSP1 expression in host cells increase during early Trypanosoma cruzi and hepatitis C virus infections and contribute to pathogenesis by promoting cellular invasion [10] and TGF-β1-mediated liver fibrosis [11], respectively. In addition, TSP1 modulates expression of IL-6 and IL-10 by monocytes [12] and activation of latent TGF-β [13]. TSP1 binds to human neutrophils [14] and enhances cytokine-, chemoattractant n-fMLP-, and PMA-mediated respiratory burst in human neutrophils and macrophages through its N-terminal domain [15]–[17].…”

Section: Introductionmentioning

confidence: 99%

Endogenous Thrombospondin-1 Regulates Leukocyte Recruitment and Activation and Accelerates Death from Systemic Candidiasis

et al. 2012

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Disseminated Candida albicans infection results in high morbidity and mortality despite treatment with existing antifungal drugs. Recent studies suggest that modulating the host immune response can improve survival, but specific host targets for accomplishing this goal remain to be identified. The extracellular matrix protein thrombospondin-1 is released at sites of tissue injury and modulates several immune functions, but its role in C. albicans pathogenesis has not been investigated. Here, we show that mice lacking thrombospondin-1 have an advantage in surviving disseminated candidiasis and more efficiently clear the initial colonization from kidneys despite exhibiting fewer infiltrating leukocytes. By examining local and systemic cytokine responses to C. albicans and other standard inflammatory stimuli, we identify a crucial function of phagocytes in this enhanced resistance. Subcutaneous air pouch and systemic candidiasis models demonstrated that endogenous thrombospondin-1 enhances the early innate immune response against C. albicans and promotes activation of inflammatory macrophages (inducible nitric oxide synthase+, IL-6high, TNF-αhigh, IL-10low), release of the chemokines MIP-2, JE, MIP-1α, and RANTES, and CXCR2-driven polymorphonuclear leukocytes recruitment. However, thrombospondin-1 inhibited the phagocytic capacity of inflammatory leukocytes in vivo and in vitro, resulting in increased fungal burden in the kidney and increased mortality in wild type mice. Thus, thrombospondin-1 enhances the pathogenesis of disseminated candidiasis by creating an imbalance in the host immune response that ultimately leads to reduced phagocytic function, impaired fungal clearance, and increased mortality. Conversely, inhibitors of thrombospondin-1 may be useful drugs to improve patient recovery from disseminated candidiasis.

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Thrombospondin-1 Differentially Regulates Release of IL-6 and IL-10 by Human Monocytic Cell Line U937

Cited by 32 publications

References 31 publications

Thrombospondins as key regulators of synaptogenesis in the central nervous system

Thrombospondins as key regulators of synaptogenesis in the central nervous system

The Role of Thrombospondin 1 on Intestinal Inflammation and Carcinogenesis

Endogenous Thrombospondin-1 Regulates Leukocyte Recruitment and Activation and Accelerates Death from Systemic Candidiasis

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