Functional modulation of smooth muscle cells by the inflammatory mediator CAP37

Gonzalez, Melva L.; Ruan, Xin; Kumar, Padmasini; Grammas, Paula; Pereira, H. Anne

doi:10.1016/j.mvr.2003.12.007

Cited by 22 publications

(33 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Low doses of lipopolysaccharide stimulated expression of MCP-1, IL-6 and IL-1α by aortic SMC (Rice et al, 2003). The neutrophil protein CAP-37 induced expression of intercellular adhesion molecule-1 by SMC (Gonzalez et al, 2004). IL-18 and angiotensin II, agents involved in atherosclerosis, activated MAP kinase and NF-κB signaling in vascular SMC, resulting in enhanced expression of IL-6, IL-8 and MCP-1 gene expression and increased functional IL-18 receptor activity (Gerdes et al, 2002;Sahar et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

Human postmortem brain-derived cerebrovascular smooth muscle cells express all genes of the classical complement pathway: A potential mechanism for vascular damage in cerebral amyloid angiopathy and Alzheimer's disease

Walker

Dalsing-Hernandez

Lue

2008

Microvascular Research

View full text Add to dashboard Cite

Deposition of amyloid around blood vessels, known as cerebral amyloid angiopathy (CAA), is a major pathological feature found in the majority of Alzheimer's disease (AD) cases, and activated complement fragments have been detected on CAA deposits in AD brains. In this study, we demonstrate for the first time that human cerebrovascular smooth muscle cells (HCSMC) isolated from cortical vessels derived from postmortem brains can express mRNAs for complement genes C1qB, C1r, C1s, C2, C3, C4, C5, C6, C7, C8 and C9, the components of the classical complement pathway. Secretion of the corresponding complement proteins for these genes was also demonstrated, except for C1q and C5. Of particular significance was the observation that treatment of HCSMC with aggregated amyloid beta (Aβ)1-42 increased expression of complement C3 mRNA and increased release of C3 protein. Aβ treatment of HCSMC also increased expression of C6 mRNA. Interferon-γ induced expression and release of complement C1r, C1s, C2 and C4. As HCSMC are closely associated with Aβ deposits in vessels in the brain, their production of complement proteins could amplify the proinflammatory effects of amyloid in the perivascular environment, further compromising brain vascular integrity.

show abstract

Section: Discussionmentioning

confidence: 98%

Human postmortem brain-derived cerebrovascular smooth muscle cells express all genes of the classical complement pathway: A potential mechanism for vascular damage in cerebral amyloid angiopathy and Alzheimer's disease

Walker

Dalsing-Hernandez

Lue

2008

Microvascular Research

View full text Add to dashboard Cite

show abstract

“…There, Lee et al [30] demonstrate the presence of azurocidin in smooth muscle cells of atherosclerotic vessels. Functionally, azurocidin was found to stimulate proliferation, migration, and expression of E-selectin and ICAM-1 in aortic smooth muscle cells [73].…”

Section: Activation Of Other Cell Typesmentioning

confidence: 95%

Neutrophil-derived azurocidin alarms the immune system

Soehnlein

Lindbom

2008

Journal of Leukocyte Biology

102

100

View full text Add to dashboard Cite

Azurocidin (heparin-binding protein/ cationic antimicrobial protein of 37 kD) is a protein that is mobilized rapidly from emigrating polymorphonuclear leukocytes (PMN). Initially, this inactive serine protease was recognized for its antimicrobial effects. However, it soon became apparent that azurocidin may act to alarm the immune system in different ways and thus serve as an important mediator during the initiation of the immune response. Azurocidin, released from PMN secretory vesicles or primary granules, acts as a chemoattractant and activator of monocyte and macrophages. The functional consequence is enhancement of cytokine release and bacterial phagocytosis, allowing for a more efficient bacterial clearance. Leukocyte activation by azurocidin is mediated via ␤ 2 -integrins, and azurocidin-induced chemotaxis is dependent on formyl-peptide receptors. In addition, azurocidin activates endothelial cells leading to vascular leakage and edema formation. For these reasons, targeting azurocidin release and its actions may have therapeutic potential in inflammatory disease conditions. J. Leukoc. Biol. 85: 344 -351; 2009.

show abstract

“…3,9,10 Furthermore, CAP37 upregulates adhesion molecules on endothelial, smooth muscle, and corneal epithelial cells. 6,8,11 Its ability to upregulate adhesion molecules and to mediate migration and proliferation of human corneal epithelial cells (HCECs) in vitro led us to postulate that CAP37 may have an important role in corneal wound healing. Its induced expression in corneal epithelial cells in response to infection suggests a role in host defense and inflammation.…”

mentioning

confidence: 99%