Fibroblast skin fibroblasts

Moy LS, Howe K, Moy RL (1996) Glycolic acid modulation of collagen production in human skin fibroblast cultures in vitro. Dermatol Surg 22(5) 439-441... 

Heparan sulfate GlcN, GlcUA GlcN Xyl-Ser Skin fibroblasts, aortic wall... 

The second methodologic consideration relates to the type of cells which are used as controls for the biochemical determinations. While less a problem now, there was a tendency in some early investigations to use cultured skin fibroblasts or similar cells as controls for the cultured amniotic fluid cells. 

Kaback, M. M. and Howell, R. R. "Infantile Metachromatlc Leukodystrophy. Heterozygote Detection in Skin Fibroblasts and Possible Application to Intrauterine Diagnosis". New Engl. J. Med., (1970), 2S2, 1336-1340. 

In mouse models of skin inflammation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), there is a close association between elevated XO activity in the epidermis and hyperplasia (Pence and Reiners, 1987). This association is also seen in psoriasis patients (Eisen and Seegmiller, 1961 Zimmer and Demis, 1966 Kizaki et al., 1977). In the study by Kizaki etal. (1977), the epidermis was increased about five-fold in comparison to normal. It is not known whether XO-derived ROS have any role in psoriatic epidermal hyperproliferation but low levels of hydrogen peroxide added to the culture medium are well known to induce skin fibroblast proliferation in vitro, an eflfect that is greatest at low passage numbers (Murrell et al., 1990). The generation of... 

Moysan, A., Marquis, I., Gaboriau, F., Santus, R., Dubertret, L. and Morliere, P. (1993). Ultraviolet A-induced lipid peroxidation and antioxidant defence systems in cultured skin fibroblasts. J. Invest. Dermatol. 100, 692-698. 

Adenosine deaminase (ADA) is an amino hydrolase that catalyzes the deamination of adenosine and 2 -deoxyadenosine to inosine and 2 -deoxyinosine, respectively. High activity of ADA is seen in thymus and other lymphoid tissues. ADA has been shown in many different physical forms. A small form of the enzyme predominates in the spleen, stomach, and red blood cells, whereas the large form predominates in the kidney, liver, and skin fibroblasts. The small form of the catalytic subunit can be converted to the large form by complexing with a protein termed binding protein or complexing protein. 

Connexin 43 is one of the cell membrane gap junction proteins that allow for cell to cell communication. Cancer cell transformation is correlated with the loss of Connexin 43 expression (Hussain et al. 1989, Zhang et al. 1992). Lycopene increased Connexin 43 expression in fetal skin fibroblasts (Stahl et al. 2000), oral cancer KB-1 cells grown in organotypic rafts (Livny et al. 2003) and breast cancer cell lines (Chalabi et al. 2007). 

Offord, EA, JC Gautier, O Avanti et al. 2002. Photoprotective potential of lycopene, beta-carotene, vitamin E, vitamin C and camosic acid in UVA-irradiated human skin fibroblasts. Free Radio Biol Med 32(12) 1293-1303. 

Obermuller-Jevic, UC. Schlegel, B. Flaccus, A., and Biesalski, HK. 2001. The effect of beta-carotene on the expression of interleukin-6 and heme oxygenase-1 in UV-irradiated human skin fibroblasts in vitro. FEBS Lett 509 186-190. 

MWNTs were found to be cytotoxic in human skin fibroblasts (HSF42) and human epidermal keratinocytes (HEK) [42-44], whereas SWNTs were toxic in human keratinocyte (HaCaT) cultures [25, 26, 45]. Reduced cell proliferation and oxidative stress were reported also in epithelial (HeLa) cells [45] and murine epidermal cells (JB6 P + ) [46] upon incubation with SWNTs. 

Ding, L. et al. (2005) Molecular characterization of the cytotoxic mechanism of multiwall carbon nanotubes and nano-onions on human skin fibroblast. Nano Letters, 5 (12), 2448-64. 

Defects have been found in these mechanisms that cause various human diseases. For example, patients with the genetic disease xeroderma pigmentosum are especially sensitive to ultraviolet light and develop skin cancer. Skin fibroblasts cultured from these patients have been shown to be defective in DNA repair. 

In contrast to transition metals iron and copper, which are well-known initiators of in vitro and in vivo lipid peroxidation (numerous examples of their prooxidant activities are cited throughout this book), the ability of nontransition metals to catalyze free radical-mediated processes seems to be impossible. Nonetheless, such a possibility is suggested by some authors. For example, it has been suggested that aluminum toxicity in human skin fibroblasts is a consequence of the enhancement of lipid peroxidation [74], In that work MDA formation was inhibited by SOD, catalase, and vitamins E and C. It is possible that in this case aluminum is an indirect prooxidant affecting some stages of free radical formation. 

Patients sustain convulsions and neurological deterioration. The urine contains low levels of the metabolites of serotonin, norepinephrine and dopamine. The reductase also plays a role in the maintenance of tetrahydrofolate levels in brain, and some patients have had low folate levels in the serum and CNS. Treatment has been attempted with tryptophan and carbidopa to improve serotonin homeostasis and with folinic acid to replete diminished stores of reduced folic acid. This therapy is sometimes effective. Diagnosis involves assay of DHPR in skin fibroblasts or amniotic cells. Phenylalanine hydroxylase activity is normal. 

Homocystinuria can be treated in some cases by the administration of pyridoxine (vitamin Bs), which is a cofactor for the cystathionine synthase reaction. Some patients respond to the administration of pharmacological doses of pyridoxine (25-100 mg daily) with a reduction of plasma homocysteine and methionine. Pyridoxine responsiveness appears to be hereditary, with sibs tending to show a concordant pattern and a milder clinical syndrome. Pyridoxine sensitivity can be documented by enzyme assay in skin fibroblasts. The precise biochemical mechanism of the pyridoxine effect is not well understood but it may not reflect a mutation resulting in diminished affinity of the enzyme for cofactor, because even high concentrations of pyridoxal phosphate do not restore mutant enzyme activity to a control level. 

Urinary excretion of N-acetylaspartate is elevated and the cerebrospinal fluid concentration may be 50 times control values. The cause is a deficiency of aspartoacylase, which cleaves N-acetylaspartate to form aspartate and acetyl-CoA. The enzyme occurs primarily in the white matter, but N-acetylaspartate is most abundant in gray matter. The defect is expressed in skin fibroblasts. 

The diagnosis of lysosomal disorders is usually based on enzymatic assays in white blood cells or cultured skin fibroblasts [ 1 ]. Molecular studies required for identification of carriers. Initial diagnosis of peroxisomal disorders... 

Defects of the Krebs cycle. Fumarase deficiency was reported in children with mitochondrial encephalomyop-athy. Usually, there is developmental delay since early infancy, microcephaly, hypotonia and cerebral atrophy, with death in infancy or early childhood. The laboratory hallmark of the disease is the excretion of large amounts of fumaric acid and, to a lesser extent, succinic acid in the urine. The enzyme defect has been found in muscle, liver and cultured skin fibroblasts [16]. 

Gauthier, J.M., H. Dubeau, and E. Rassart. 1998. Mercury-induced micronuclei in skin fibroblasts of beluga whales. Environ. Toxicol. Chem. 17 2487-2493. 

Rosenthal, D.S., et al., Mechanisms of JP-8 jet fuel cell toxicity B. Induction of necrosis in skin fibroblasts and keratinocytes and modulation of levels of Bcl-2 family members, Toxicol. Appl. Pharmacol., 171, 107, 2001. 

Reelfs, O., Tyrrell, R. M., and Pourzand, C., Ultraviolet a radiation-induced immediate iron release is a key modulator of the activation of NF-kappaB in human skin fibroblasts, J. Invest. Dermatol. 122, 1440-1447, 2004. 

Werth, V. P., Bashir, M. M., and Zhang, W., IL-12 Completely Blocks Ultraviolet-Induced Secretion of Tumor Necrosis Factor alpha from Cultured Skin Fibroblasts and Keratino-cytes, J. Invest. Dermatol. 120, 116-122, 2003. 

Figure 7.9. Human skin fibroblasts labeled with dil and illuminated by T1RF at two different angles of incidence, (a) 0=74.3°, d= 105 nm (b) 0 = 67.9°, d=406nm. In this setup, 0C = 67.5°. Notice how more of the cell surface is immersed in the deeper evanescent wave of (b). 

Kano, Y., and J. B. Little. 1989. Efficient immortalization by SV40 T DNA of skin fibroblasts from patients with Wilms tumor associated with chromosome lip deletion. Mol Carcinog 2(6) 314—21. 

Chen, W.W., Moser, A.B., and Moser, H.W., 1981, Role oflysosomal add ceramidase in the metabohsm of ceramide in human skin fibroblasts. Arch. Biochem. Biophys. 208 444-455. 

Van Veldhoven, P.P. and Mannaerts, G.P., 1994, Sphinanine 1-phosphate metabohsm in cultured skin fibroblasts evidence for the existence of a sphingosine phosphatase, Biochem. J. 299 597-601. 

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