Detection and Regulation of Cationic Amino Acid Transporters in Healthy and Diseased Ocular Surface

Jäger, Kristin; Bönisch, Ulrike; Risch, Michaela; Worlitzsch, Dieter; Paulsen, Friedrich

doi:10.1167/iovs.08-2368

Cited by 23 publications

(15 citation statements)

References 61 publications

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“…Interestingly, decreased levels of arginine were found to be correlated with a decrease in methionine as a taurine precursor and taurine levels in tears in the course of ocular surface diseases [31]. The inflammatory decrease of arginine levels fits well with an observed upregulation of human cationic transporters 1 and 2 expression under ocular surface disease conditions leading to an increased arginine transport into epithelial cells of the cornea [83]. Since arginine, methionine and taurine levels cohere under disease condition a correlation of their transport of these amino acids during inflammation can be assumed [31].…”

Section: Discussionsupporting

confidence: 53%

“…In HepG2 cells this effect could be proven as an adaptive regulation activation of a high-affinity taurine transporter system [80,81]. Besides taurine, L-arginine is a well studied amino acid involved in immune response [82,83]. Interestingly, decreased levels of arginine were found to be correlated with a decrease in methionine as a taurine precursor and taurine levels in tears in the course of ocular surface diseases [31].…”

Section: Discussionmentioning

confidence: 99%

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Longitudinal analysis of taurine induced effects on the tear proteome of contact lens wearers and dry eye patients using a RP-RP-Capillary-HPLC–MALDI TOF/TOF MS approach

Funke

Azimi

Wolters

et al. 2012

Journal of Proteomics

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Longitudinal analysis of taurine induced effects on the tear proteome of contact lens wearers and dry eye patients using a RP-RP-Capillary-HPLC–MALDI TOF/TOF MS approach

Funke

Azimi

Wolters

et al. 2012

Journal of Proteomics

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“…CAT2A and CAT2B). The expression of CAT2B is observed in many different cell types under inflammatory conditions, and CAT2A exhibit a 10-fold lower substrate affinity [40]. Although CAT2 is important for the transport of L-arginine through the cell membrane, a recent epidemiologic study reported that the expression of SLC7A1 , not SLC7A2 , was significantly elevated in colorectal cancer tissues among colorectal cancer patients[11].…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in SLC7A2 interacts with calcium and magnesium intakes in modulating the risk of colorectal polyps

Sun

Zhu

Shrubsole

et al. 2017

The Journal of Nutritional Biochemistry

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Solute carrier family 7, member 2 (SLC7A2) gene encodes a protein called cationic amino acid transporter 2, which mediates the transport of arginine, lysine and ornithine. L-arginine is necessary for cancer development and progression, including an important role in colorectal cancer pathogenesis. Furthermore, previous studies found both calcium and magnesium inhibit the transport of arginine. Thus, calcium, magnesium or calcium:magnesium intake ratio may interact with polymorphisms in the SLC7A2 gene in associations with colorectal cancer. We conducted a two-phase case-control study within the Tennessee Colorectal Polyps Study. In the first phase, 23 tagging single-nucleotide polymorphisms (SNPs) in the SLC7A2 gene were included for 725 colorectal adenoma cases and 755 controls. In the second phase conducted in an independent set of 607 cases and 2113 controls, we replicated the significant findings in the first phase. We observed that rs2720574 significantly interacted with calcium:magnesium intake ratio in association with odds of adenoma, particularly multiple/advanced adenoma. In the combined analysis, among those with a calcium:magnesium intake ratio below 2.78, individuals who carried GC/CC genotypes demonstrated higher odds of adenoma OR (95% CI):1.36(1.11–1.68) and multiple/advanced adenoma OR (95% CI):1.68(1.28, 2.20) than those who carried the GG genotype. The P for interactions between calcium:magnesium intake ratio and rs2720574 were 0.002 for all adenoma and <0.001 for multiple/advanced adenoma. Among those with the GG genotype, a high calcium:magnesium ratio was associated with increased odds of colorectal adenoma OR (95%CI): 1.73(1.27–2.36) and advanced/multiple adenomas [1.62(1.05–2.50)]. Whereas, among those with the GC/CC genotypes, high calcium:magnesium ratio was related to reduced odds of colorectal adenoma [0.64(0.42–0.99)] and advanced/multiple adenomas [0.55(0.31–1.00)].

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“…IL‐1β (10 ng/ml; Immunotools, Friesoythe, Germany) and/or TNFα (10 ng/ml; Immunotools), lipopolysaccharide (LPS) (500 ng/ml; Santa Cruz Biotechnology, Heidelberg, Germany), peptidoglycan (10 ng/ml; Santa Cruz Biotechnology), or supernatants of Pseudomonas aeruginosa (1:100) or Staphylococcus aureus (1:15) were added 3 hours later, and incubation was continued for 24 hours. Bacteria were produced as recently described (13).…”

Section: Methodsmentioning

confidence: 99%

Trefoil factor 3 is induced during degenerative and inflammatory joint disease, activates matrix metalloproteinases, and enhances apoptosis of articular cartilage chondrocytes

Rösler¹,

Haase²,

Claassen³

et al. 2010

Arthritis & Rheumatism

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Objective. Trefoil factor 3 (TFF3, also known as intestinal trefoil factor) is a member of a family of protease-resistant peptides containing a highly conserved motif with 6 cysteine residues. Recent studies have shown that TFF3 is expressed in injured cornea, where it plays a role in corneal wound healing, but not in healthy cornea. Since cartilage and cornea have similar matrix properties, we undertook the present study to investigate whether TFF3 could induce anabolic functions in diseased articular cartilage.Methods. We used reverse transcriptasepolymerase chain reaction, Western blot analysis, and immunohistochemistry to measure the expression of TFF3 in healthy articular cartilage, osteoarthritis (OA)-affected articular cartilage, and septic arthritisaffected articular cartilage and to assess the effects of cytokines, bacterial products, and bacterial supernatants on TFF3 production. The effects of TFF3 on matrix metalloproteinase (MMP) production were measured by enzyme-linked immunosorbent assay, and effects on chondrocyte apoptosis were studied by caspase assay and annexin V assay.Results. Trefoil factors were not expressed in healthy human articular cartilage, but expression of TFF3 was highly up-regulated in the cartilage of patients with OA. These findings were confirmed in animal models of OA and septic arthritis, as well as in tumor necrosis factor ␣-and interleukin-1␤-treated primary human articular chondrocytes, revealing induction of Tff3/TFF3 under inflammatory conditions. Application of the recombinant TFF3 protein to cultured chondrocytes resulted in increased production of cartilagedegrading MMPs and increased chondrocyte apoptosis.Conclusion. In this study using articular cartilage as a model, we demonstrated that TFF3 supports catabolic functions in diseased articular cartilage. These findings widen our knowledge of the functional spectrum of TFF peptides and demonstrate that TFF3 is a multifunctional trefoil factor with the ability to link inflammation with tissue remodeling processes in articular cartilage. Moreover, our data suggest that TFF3 is a factor in the pathogenesis of OA and septic arthritis.

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Detection and Regulation of Cationic Amino Acid Transporters in Healthy and Diseased Ocular Surface

Cited by 23 publications

References 61 publications

Longitudinal analysis of taurine induced effects on the tear proteome of contact lens wearers and dry eye patients using a RP-RP-Capillary-HPLC–MALDI TOF/TOF MS approach

Longitudinal analysis of taurine induced effects on the tear proteome of contact lens wearers and dry eye patients using a RP-RP-Capillary-HPLC–MALDI TOF/TOF MS approach

Genetic variation in SLC7A2 interacts with calcium and magnesium intakes in modulating the risk of colorectal polyps

Trefoil factor 3 is induced during degenerative and inflammatory joint disease, activates matrix metalloproteinases, and enhances apoptosis of articular cartilage chondrocytes

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