Pathogenesis of Mesothelial Reactions to Asbestos Fibers

Branchaud, Ruth M.; Garant, Lynn J.; Kane, Agnes B.

doi:10.1159/000163784

Cited by 18 publications

(10 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Upregulation of TLR4 was consistent with the observation that the scaffold could activate macrophages, with or without fibroblasts [17]. In addition, macrophage activations are generally associated with phagocytosis of biomaterials [41][42][43]. Increased expression of TLR4 during scaffold degradation suggested its role in removing the debris of degraded scaffold through receptor-mediated phagocytosis.…”

Section: Receptors Involved In Scaffold Degradationsupporting

confidence: 83%

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

2008

View full text Add to dashboard Cite

Fibroblast and macrophage are two dominant cell types respond cooperatively to degrade implanted biomaterials. Using an electrospun Dextran/Poly-lactide-co-glycolide (PLGA) scaffold as a model, an in vitro fibroblast/macrophage co-culture system was developed to investigate the degradability of implantable biodegradable materials. SEM showed that both fibroblasts and macrophages were able to degrade the scaffold, separately or cooperatively. Under the synergistic coordination of macrophages and fibroblasts, scaffolds showed faster degradation rate than their counterparts incubated with a single type of cells as well as in PBS or cell culture medium. Lysozyme, non-specific esterase (NSE), gelatinase, hyaluronidase-1 and α-glucosidase were upregulated in the presence of the scaffold, suggesting their roles in the cell-mediated scaffold degradation. In addition, the expressions of cell surface receptors CD204 and Toll like receptor 4 (TLR4) were elevated one week after cell seeding, implying that these receptors might be involved in scaffold degradation. The results of in vivo subdermal implantation of the scaffold further confirmed the biodegradability of the Dextran/PLGA scaffold. The fibroblast/macrophage co-culture model adequately mimicked the in vivo environment and could be further developed into an in vitro tool for initial biomaterial evaluation.

show abstract

Section: Receptors Involved In Scaffold Degradationsupporting

confidence: 83%

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

2008

View full text Add to dashboard Cite

show abstract

“…Asbestos fibers can also induce non-genotoxic damages, including the abnormal activation of the AP-1/TNF-α/NF-κB autocrine pathway, which increases cell survival after DNA damage and promotes uncontrolled cell growth [6]. After the fibers’ damage to the mesothelium integrity, macrophages are activated in an attempt to remove the fibers [6–8]. These events trigger a long-lasting inflammation, which can enhance DNA damage for the production of free radicals and inflammatory cytokines [9].…”

Section: Introductionmentioning

confidence: 99%

Curcumin blocks autophagy and activates apoptosis of malignant mesothelioma cell lines and increases the survival of mice intraperitoneally transplanted with a malignant mesothelioma cell line

et al. 2017

View full text Add to dashboard Cite

Malignant mesothelioma (MM) is a primary tumor arising from the serous membranes. The resistance of MM patients to conventional therapies, and the poor patients’ survival, encouraged the identification of molecular targets for MM treatment. Curcumin (CUR) is a “multifunctional drug”. We explored the in vitro effects of CUR on cell proliferation, cell cycle regulation, pro-survival signaling pathways, apoptosis, autophagy of human (MM-B1, H-Meso-1, MM-F1), and mouse (#40a) MM cells. In addition, we evaluated the in vivo anti-tumor activities of CUR in C57BL/6 mice intraperitoneally transplanted with #40a cells forming ascites.CUR in vitro inhibited MM cells survival in a dose- and time-dependent manner and increased reactive oxygen species’intracellular production and induced DNA damage. CUR triggered autophagic flux, but the process was then blocked and was coincident with caspase 8 activation which activates apoptosis. CUR-mediated apoptosis was supported by the increase of Bax/Bcl-2 ratio, increase of p53 expression, activation of caspase 9, cleavage of PARP-1, increase of the percentage of cells in the sub G1 phase which was reduced (MM-F1 and #40a) or abolished (MM-B1 and H-Meso-1) after MM cells incubation with the apoptosis inhibitor Z-VAD-FMK. CUR treatment stimulated the phosphorylation of ERK1/2 and p38 MAPK, inhibited that of p54 JNK and AKT, increased c-Jun expression and phosphorylation and prevented NF-κB nuclear translocation. Intraperitoneal administration of CUR increased the median survival of C57BL/6 mice intraperitoneally transplanted with #40a cells and reduced the risk of developing tumors. Our findings may have important implications for the design of MM treatment using CUR.

show abstract

“…Chronic inflammation is a recognized risk factor of human cancer (Federico, et al, 2007, Kundu & Surh, 2008, Weitzman & Gordon, 1990). Frustrated phagocytosis of long asbestos fibers by alveolar macrophages triggers inflammatory responses and the release of ROS and RNS from the cells (Branchaud et al, 1993; Kane, 1996). Reactive radical species further recruit more macrophage and other inflammatory cells to the lung.…”

Section: Is There a Mutagenic Mode Of Action (Moa) In Fiber Carcinogementioning

confidence: 99%

Role of Mutagenicity in Asbestos Fiber-Induced Carcinogenicity and Other Diseases

Huang

Jaurand

Kamp

et al. 2011

Journal of Toxicology and Environmental Health, Part B

142

149

View full text Add to dashboard Cite

The cellular and molecular mechanisms of how asbestos fibers induce cancers and other diseases are not well understood. Both serpentine and amphibole asbestos fibers have been shown to induce oxidative stress, inflammatory responses, cellular toxicity and tissue injuries, genetic changes, and epigenetic alterations in target cells in vitro and tissues in vivo. Most of these mechanisms are believe to be shared by both fiber-induced cancers and noncancerous diseases. This article summarizes the findings from existing literature with a focus on genetic changes, specifically, mutagenicity of asbestos fibers. Thus far, experimental evidence suggesting the involvement of mutagenesis in asbestos carcinogenicity is more convincing than asbestos-induced fibrotic diseases. The potential contributions of mutagenicity to asbestos-induced diseases, with an emphasis on carcinogenicity, are reviewed from five aspects: (1) whether there is a mutagenic mode of action (MOA) in fiber-induced carcinogenesis; (2) mutagenicity/carcinogenicity at low dose; (3) biological activities that contribute to mutagenicity and impact of target tissue/cell type; (4) health endpoints with or without mutagenicity as a key event; and finally, (5) determinant factors of toxicity in mutagenicity. At the end of this review, a consensus statement of what is known, what is believed to be factual but requires confirmation, and existing data gaps, as well as future research needs and directions, is provided.

show abstract

Pathogenesis of Mesothelial Reactions to Asbestos Fibers

Cited by 18 publications

References 14 publications

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

The biodegradability of electrospun Dextran/PLGA scaffold in a fibroblast/macrophage co-culture

Curcumin blocks autophagy and activates apoptosis of malignant mesothelioma cell lines and increases the survival of mice intraperitoneally transplanted with a malignant mesothelioma cell line

Role of Mutagenicity in Asbestos Fiber-Induced Carcinogenicity and Other Diseases

Contact Info

Product

Resources

About