Disease relevance of CFHR1

• Corrigendum: A common CFH haplotype, with deletion of CFHR1 and CFHR3, is associated with lower risk of age-related macular degeneration [1].
• Furthermore, it could be concluded that fibroblasts cultures from patients with asthma were surrounded by more extracellular matrix molecules compared to the primary cell line HFL-1, which may mimic the in vivo situation during formation of fibrosis [2].
• Antibody H36/71 was positive in only 4 of 24 (17%) cases of acute myeloid leukemia [3].
• HTLV-I+ sera induced lysis of H36 and of lines expressing HTLV-I antigens in the presence of rabbit complement, but did not lyse cells in presence of human complement [4].
• Quantitative detection of human complement factor H-related protein in transitional cell carcinoma of the urinary bladder [5].

High impact information on CFHR1

• In contrast to the wild-type protein, disease-associated epsilon-sarcoglycan missense mutations (H36P, H36R and L172R) produce proteins that are undetectable at the cell surface and are retained intracellularly [6].
• This adherence of eosinophils to HFL-1 cells was inhibited by both lactose and anti-galectin-9 Ab [7].
• RT-PCR, real-time PCR, and Western blot analyses revealed that both galectin-9 mRNA and protein in HFL-1 cells were up-regulated by IFN-gamma stimulation [7].
• In the present study a role of galectin-9 in the interaction between eosinophils and fibroblasts was investigated using a human lung fibroblast cell line, HFL-1 [7].
• In parallel we identified the cDNA encoding a new complement factor H-related protein, termed FHR-4 [8].

Biological context of CFHR1

• Two cDNA clones termed H36-1 and H36-2 were isolated from a human liver cDNA library [9].
• In contrast, the 3'-end of the H36-1 clone shows sequence homology to the 3'-end of human complement factor H. The second clone, H36-2, is nearly identical to H36-1 [9].
• Some have arisen as a result of gene conversion between CFH and CFHL1 [10].
• The production of procollagen molecules by human diploid fetal lung fibroblasts (HFL-1 cells) remains constant in both rapid and stationary growth phases [11].
• To evaluate the control soft tissue fibroblasts have over collagen production, HFL-1, a diploid human lung cell strain, was studied during periods of rapid cell growth and relatively slow growth over 25 population doublings [12].

Anatomical context of CFHR1

• The expression of the T cell receptor (Ti)-alpha and -beta subunits in human thymocytes was studied with the use of two rabbit antisera directed at constant regions of human Ti-alpha- and Ti-beta-chains (H36 and H38, respectively) [13].
• Stimulation of HFL-1 cells with IFN-gamma up-regulated adhesion of eosinophils, but not neutrophils, to HFL-1 cells [7].
• Collagen degradation in two other lung cell lines, Wl-38 and lMR-90, did not differ from the level in HFL-1 [14].
• A novel, complement factor H-related regulatory protein expressed on the surface of human B cell lines [15].
• Coculture of nonleukemic stromal cells and AML blasts separated by a semipermeable membrane decreased proliferation of the fibroblast line HFL1, and the inhibition was maintained when HFL1 and AML cells were cultured in direct contact [16].

Associations of CFHR1 with chemical compounds

• This group includes the complement and immune regulators Factor H, the Factor H-like protein 1 (FHL-1) and five Factor H-related proteins proteins (FHR-1, -2, -3, -4 and -5) [17].
• Although the specific activity of intracellular free proline and the per cent hydroxylation of proline in collagen varied considerably depending on the growth rates of the cells, collagen production by HFL-1 was constant, even during periods of rapid cell growth [12].
• Lung epithelial cells (A549), fibroblasts (HFL1), and blood lymphocytes had increased glutathione (GSH) levels after 8 h incubation with HSA [18].
• To test the hypothesis, we evaluated the potential of erythromycin to modulate the release of eosinophil chemoattractants from the human lung fibroblast cell line HFL-1 [19].
• Histamine or serotonin treatment of HFL-1 augmented the expression of eotaxin mRNA [20].

Regulatory relationships of CFHR1

• Eosinophil chemotactic activity by HFL-1 supernatant fluids was inhibited by anti-human eotaxin-neutralizing antibody [20].

Other interactions of CFHR1

• The function of the factor H-related proteins (FHR-1 to FHR-4) is currently under investigation [21].
• Erythromycin attenuated the release of these cytokines and eosinophil chemotactic activity by the HFL-1 [19].
• The present study investigates the role of mitogen-activated protein (MAP) kinase in the expression of CTGF mRNA in the human lung fibroblast line, HFL-1 [22].
• We observed that a human lung fibroblast, HFL-1 produces eotaxin-1 and -3 in response to TNF-alpha plus IL-4 stimulation, accompanied with NF-kappaB and STAT6 activation [23].
• On the one hand, IL-4, known as a Th2 cytokine, did not affect the galectin-9 expression in HFL-1 cells [7].

Analytical, diagnostic and therapeutic context of CFHR1

• METHODS: Western blot analyses of purified FH, recombinant factor H-related protein 1 (FHR-1), and serum and urine samples were used to identify the ligands of X13.2 and X52 [24].
• Sequence analysis shows that all four of these changes could have arisen as a result of gene conversion between CFH and CFHL1 [25].
• To verify this hypothesis, we examined the ability of GSH to suppress human lung fibroblast (ATCC; HFL-1) proliferation in vitro in the presence of either IPF bronchoalveolar lavage fluid (BAL) or calf serum (CS) [26].
• Effect of intravesical instillations on the human complement factor H related protein (BTA stat) Test [27].
• Postoperative pain was evaluated using a visual analog scale or the Children and Infants Postoperative Pain Score at hour H1, H6, H12, H18, H24, H36, and H48, and in terms of rescue analgesia, adverse events, and motor blocks [28].

References