Tissue inhibitor of metalloproteinases 1 regulation of interleukin-10 in B-cell differentiation and lymphomagenesis

Guédez, Liliana; Mansoor, Adnan; Birkedal-Hansen, B; Lim, Megan S.; Fukushima, Paula; Venzon, David; Stetler‐Stevenson, William G.; Stetler‐Stevenson, Maryalice

doi:10.1182/blood.v97.6.1796

Cited by 42 publications

(36 citation statements)

References 36 publications

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“…TIMP-1, identified originally for its erythroid-potentiating activity (5), induces proliferation in a wide range of cell types (6 -8) by mechanisms that are apparently independent of MMPs (9). In addition, TIMP-1 is known to promote activation of angiogenesis (4,10,11), regulate apoptosis (12), amplify inflammation (13), and regulate metastasis formation (14). Similar pleiotropic activities have also been demonstrated for TIMP-2 (15), TIMP-3 (16), and TIMP-4 (17).…”

Section: Introductionmentioning

confidence: 75%

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TIMP-1 Alters Susceptibility to Carcinogenesis

Rhee¹,

Diaz²,

Korets³

et al. 2004

Cancer Research

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Tissue inhibitors of metalloproteinases (TIMPs) are a family of multifunctional proteins known to possess a broad range of biological activities, including inhibition of metalloproteinase activity, regulation of proliferation and apoptosis of a variety of cell types, and, depending on the context, differential regulation of angiogenic and inflammatory responses. Elevated mRNA expression of TIMP family members correlates with malignancy and clinical outcome in many human cancer types; however, a protective role for TIMPs also has been observed in various mouse models of human cancer. In the current study, we found distinct spatial-temporal expression patterns for the mRNA of TIMP family members in a mouse model of epithelial carcinogenesis [i.e., keratin 14-human papillomavirus 16 (K14-HPV16) transgenic mice]. To test the hypothesis that elevated expression of TIMP-1 functionally regulates epithelial carcinogenesis, we introduced a human TIMP-1 transgene into K14-HPV16 transgenic mice and assessed neoplastic progression. Results from these studies suggest that TIMP-1 enhances tumorgenicity by potentiating keratinocyte hyperproliferation and appearance of chromosomal aberrations in premalignant cells, thereby increasing their risk to undergo malignant conversion. In addition, TIMP-1 inhibits tissue gelatinolytic activity in tumor stroma, affects stabilization of collagen fibrils, but does not inhibit malignant conversion of dysplasias into carcinomas or development of metastases. The combined implications of these studies suggest that TIMP-1 is an important contributor to epithelial neoplastic progression and supports the concept that TIMP-1 exerts differential regulation on tissues in a stage-dependent manner.

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Section: Introductionmentioning

confidence: 75%

“…64) and inhibited SV40 large T antigen-induced liver (65) and MMP-3/stromelysin-induced mammary carcinogenesis (20,66). However, paradoxically elevated TIMP-1 mRNA expression also was reported to correlate with malignant progression and poor clinical prognosis of several human cancers (12,67,68).…”

Section: Discussionmentioning

confidence: 99%

TIMP-1 Alters Susceptibility to Carcinogenesis

Rhee¹,

Diaz²,

Korets³

et al. 2004

Cancer Research

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“…10 Regulation of TIMP1 expression is incompletely understood, but previous studies have shown that interleukin (IL)-6 and IL-10 up-regulate TIMP1 expression. [11][12][13][14][15] Recent data also suggest that TIMP1 expression may be regulated by STAT3 because the binding site for STAT3 has been found in the promoter region of the TIMP1 gene in rat cells. 16 Nevertheless, the exact role of STAT3 in regulating TIMP1 expression in human neoplasms has not been examined.…”

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confidence: 99%

Signal Transducer and Activator of Transcription-3 Activation Contributes to High Tissue Inhibitor of Metalloproteinase-1 Expression in Anaplastic Lymphoma Kinase-Positive Anaplastic Large Cell Lymphoma

Lai

Rassidakis

Medeiros

et al. 2004

The American Journal of Pathology

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The tissue inhibitor of metalloproteinase-1 (TIMP1) is expressed in a subset of malignant lymphomas and can inhibit tumor spread and promote cell survival. Recent data suggest that TIMP1 expression may be regulated by signal transducer and activator of transcription (STAT)-3. Thus, we tested the hypothesis that TIMP1 expression is related to STAT3 activation in lymphomas, with a focus on anaplastic large cell lymphomas (ALCLs), which are known to express high levels of phosphorylated/active STAT3 (pSTAT3). The tissue inhibitors of metalloproteinases (TIMPs) constitute a family of secreted proteins, of which their known primary function is inhibition of the degradative action of matrix metalloproteinases. In pathological states, TIMPs have been shown to inhibit tumor invasion and metastasis through regulation of extracellular homeostasis.

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“…31 Both of these features may be influenced by TIMP-1, since it has been shown to regulate B-cell differentiation and induce expression of interleukin-10. 16,32 Moreover, TIMP-1 serum levels have been correlated with hypergammaglobulinemia in patients with eosinophilic fasciitis. 33 However, we did not detect any significant correlation between TIMP-1 and interleukin-10 levels or hypergammaglobulinemia in our patients (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

Boggio¹,

Indelicato²,

Orilieri³

et al. 2010

Haematologica

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BackgroundInherited defects decreasing function of the Fas death receptor cause autoimmune lymphoproliferative syndrome and its variant Dianzani's autoimmune lymphoproliferative disease. Analysis of the lymphocyte transcriptome from a patient with this latter condition detected striking over-expression of osteopontin and tissue inhibitor of metalloproteinases-1. Since previous work on osteopontin had detected increased serum levels in these patients, associated with variations of its gene, the aim of this work was to extend the analysis to tissue inhibitor of metalloproteinases-1. Design and MethodsTissue inhibitor of metalloproteinases-1 levels were evaluated in sera and culture supernatants from patients and controls by enzyme-linked immunosorbent assay. Activation-and Fasinduced cell death were induced, in vitro, using anti-CD3 and anti-Fas antibodies, respectively. ResultsTissue inhibitor of metalloproteinases-1 levels were higher in sera from 32 patients (11 with autoimmune lymphoproliferative syndrome and 21 with Dianzani's autoimmune lymphoproliferative disease) than in 50 healthy controls (P<0.0001), unassociated with variations of the tissue inhibitor of metalloproteinases-1 gene. Both groups of patients also had increased serum levels of osteopontin. In vitro experiments showed that osteopontin increased tissue inhibitor of metalloproteinases-1 secretion by peripheral blood monocytes. Moreover, tissue inhibitor of metalloproteinases-1 significantly inhibited both Fas-and activation-induced cell death of lymphocytes. ConclusionsThese data suggest that high osteopontin levels may support high tissue inhibitor of metalloproteinases-1 levels in autoimmune lymphoproliferative syndrome and Dianzani's autoimmune lymphoproliferative disease, and hence worsen the apoptotic defect in these diseases.Key words: osteopontin, tissue inhibitor of metalloproteinases-1, lymphoproliferation, apoptosis, autoimmunity. Haematologica 2010;95(11):1897-1904 doi:10.3324/haematol.2010 This is an open-access paper. Citation: Boggio E, Indelicato M, Orilieri E, Mesturini R, Mazzarino MC, Campagnoli MF, Ramenghi U, Dianzani U, and Chiocchetti A.Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation. Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

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Tissue inhibitor of metalloproteinases 1 regulation of interleukin-10 in B-cell differentiation and lymphomagenesis

Cited by 42 publications

References 36 publications

TIMP-1 Alters Susceptibility to Carcinogenesis

TIMP-1 Alters Susceptibility to Carcinogenesis

Signal Transducer and Activator of Transcription-3 Activation Contributes to High Tissue Inhibitor of Metalloproteinase-1 Expression in Anaplastic Lymphoma Kinase-Positive Anaplastic Large Cell Lymphoma

Role of tissue inhibitor of metalloproteinases-1 in the development of autoimmune lymphoproliferation

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