Ascorbic acid modulates the production of fibronectin and laminin by cells from an eye tissue-trabecular meshwork

Yue, Beatrice Y.J.T.; Higginbotham, Eve J.; Chang, Isabel

doi:10.1016/0014-4827(90)90117-s

Cited by 40 publications

(19 citation statements)

References 27 publications

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“…The procurement of tissues was in accordance with the Declaration of Helsinki. As previously described (70), CF were grown in L-glutamine-containing DMEM (Invitrogen) supplemented with 15% FBS. Cells were trypsinized and passaged after reaching confluence.…”

Section: Methodsmentioning

confidence: 99%

Role for 3- O -Sulfated Heparan Sulfate as the Receptor for Herpes Simplex Virus Type 1 Entry into Primary Human Corneal Fibroblasts

Tiwari

Clément

Xu³

et al. 2006

J Virol

116

133

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Herpes simplex virus type 1 (HSV-1) infection is the most common cause of infectious blindness in developed countries (33,34,49,62). Following initial infection of epithelial cells, HSV establishes latency in the sensory nerve ganglia of the host (26, 58). The virus emerges sporadically from latency and causes lesions on mucosal epithelium, skin, and the cornea. Prolonged or multiple recurrent episodes of corneal infections can result in vision impairment or blindness due to the development of herpetic stromal keratitis (HSK) (8,23,28,42,44,71). The HSK condition is typically characterized by inflammation leading to scarring, thinning, and vascularization of the corneal stroma (12,15,19,24,33,34). It accounts for 20 to 48% of all recurrent ocular HSV infection cases (33).Primary infection begins with the entry of HSV into host cells. It is a complex process initiated by specific interaction of viral envelope glycoproteins and host cell surface receptors (10,18,52,(58)(59)(60). Both HSV-1 and HSV-2 use glycoproteins B and C (gB and gC, respectively) to mediate their initial attachment to cell surface heparan sulfate (HS) proteoglycans (25,53,67). Binding of herpesviruses to HS proteoglycans likely precedes a conformational change that brings viral gD to the binding domain of host cell surface gD receptors (29-31). Thereafter, a concerted action involving gD, its receptor, three additional HSV glycoproteins (gB, gH, and gL), and possibly an additional gH coreceptor triggers fusion of the viral envelope with the plasma membrane of host cells (43,45,50). Subsequently, viral capsids and tegument proteins are released into the cytoplasm of the host cell.The gD receptors include cell surface molecules derived from three structurally unrelated families. These include a member of the tumor necrosis factor receptor family (40), two members of the nectin family of receptors (21), and the product of certain 3-O-sulfated (3-OS) sulfotransferases (3-OSTs), 3-OS HS (41,55,(57)(58)(59)(60). Herpesvirus entry mediator (HVEM or TNFRSF14) principally mediates entry of HSV-1 and HSV-2 (40, 66) into human T lymphocytes and trabecular meshwork cells and is expressed in many fetal and adult human tissues, including the lung, liver, kidney, and lymphoid tissues (27,32,37,40,62). Nectin-1 and nectin-2, also known as herpesvirus entry proteins C B, respectively, belong to the immunoglobulin superfamily (7,13,21). Both nectin-1 and nectin-2 mediate entry of HSV-1 and HSV-2, but only nectin-1 mediates bovine herpesvirus type 1 entry (9,21,36,38,39,65). The HSV-1 entry-mediating activity of nectin-2 is limited to some mutant strains only (65). Nectin-1 is extensively expressed in human cells of epithelial and neuronal origin (22,48,56,58), while nectin-2 is widely expressed in many human tissues, but with only limited expression in neuronal cells and

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Section: Methodsmentioning

confidence: 99%

Role for 3- O -Sulfated Heparan Sulfate as the Receptor for Herpes Simplex Virus Type 1 Entry into Primary Human Corneal Fibroblasts

Tiwari

Clément

Xu³

et al. 2006

J Virol

116

133

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“…AA plays a major role in the deposition of matrix collagen through its function as a co-factor for proline hydroxylase [8]. Similarly, synthesis of matrix PG and matrix glycoproteins, such as fibronectin and laminin, is enhanced when the medium is supplemented with AA [10, 11, 12, 24]. The anti-oxidant action of AA also has important physiological functions.…”

Section: Discussionmentioning

confidence: 99%

Administration of Ascorbic Acid and an Aldose Reductase Inhibitor (Tolrestat) in Diabetes: Effect on Urinary Albumin Excretion

McAuliffe

Brooks

Fisher

et al. 1998

Nephron

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The important role of ascorbic acid (AA) as an anti-oxidant is particularly relevant in diabetes mellitus where plasma concentrations of AA are reduced. This study was conducted to evaluate the effects of treatment with AA or an aldose reductase inhibitor, tolrestat, on AA metabolism and urinary albumin excretion in diabetes. Blood and urine samples were collected at 0, 3, 6, 9, and 12 months from 20 diabetic subjects who were randomized into two groups to receive either oral AA 500 mg twice daily or placebo. Systolic and diastolic blood pressures, HbA_1c, plasma lipids, urinary albumin, and total glycosaminoglycan excretion were measured at all time points, and heparan sulphate (glycosaminoglycan) was measured at 0 and 12 months. The same parameters, as well as urinary AA excretion, were determined at 0 and 3 months for 16 diabetes subjects receiving 200 mg tolrestat/day. AA treatment increased plasma AA (ANOVA, F ratio = 12.1, p = 0.004) and reduced albumin excretion rate (AER) after 9 months (ANOVA, F ratio = 3.2, p = 0.03), but did not change the other parameters measured. Tolrestat lowered plasma AA (Wilcoxon’s signed-rank test, p < 0.05), but did not change AER or the other parameters measured. The ability of AA treatment to decrease AER may be related to changes in extracellular matrix or improvement in oxidative defence mechanism. Unlike the rat model of diabetes, inhibition of aldose reductase did not normalize plasma AA or AER in humans. In fact, tolrestat reduced the plasma AA concentration, a phenomenon which may be due to increased utilization of AA. Dietary supplementation of AA in diabetic subjects may have long-term benefits in attenuating the progression of diabetic complications.

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“…The TM cultures were prepared, in accordance with federal guidelines and the Declaration of Helsinki, from explanted human tissues (provided by the Illinois Eye Bank, Chicago, IL) as previously described (39). To determine HSV-1 entry, a confluent monolayer of cultured TM cells was plated in 96-well tissue culture dishes and infected with serial dilutions of recombinant HSV-1 (KOS) gL86, which expresses ␤-galactosidase upon entry into cells (20).…”

mentioning

confidence: 99%

A Role for Herpesvirus Entry Mediator as the Receptor for Herpes Simplex Virus 1 Entry into Primary Human Trabecular Meshwork Cells

Tiwari¹,

Clément

Scanlan

et al. 2005

J Virol

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The human eye is an important target for infection with herpes simplex virus 1 (HSV-1). Damage to cells forming the trabeculum of the eye by HSV-1 infection could contribute to the development of glaucoma, a major blinding disease. Primary cultures of human trabecular meshwork cells were used as an in vitro model to demonstrate the ability of HSV-1 to enter into and establish a productive infection of the trabeculum. Blocking of entry by anti-herpesvirus entry mediator (HVEM) antibody implicated HVEM as the major receptor for HSV-1 infection.The trabecular meshwork (TM), a specialized eye tissue, is the major site for regulation of the aqueous humor outflow. Inflammation of cells in the TM (trabeculitis) due to herpes simplex virus 1 (HSV-1) infection during corneal endotheliitis and uveitis leads to elevated intraocular pressure, which is a major risk factor for glaucoma, a major blinding disease (1,19,21,25,32). Recently, immunoreactivity for HSV-1 in the trabeculum of the human eye was demonstrated during corneal endotheliitis (1, 19). HSV-1-induced inflammation of human TM cells impedes aqueous outflow and increases intraocular pressure, as has also been reported with Posner Schlossman syndrome (11, 38). The virus has been detected in aqueous humor (40), tears (14), and ciliary ganglia (2) that innervate the cells of the trabeculum. It is, however, ironic that the ability of the virus to invade and productively infect TM cells remains poorly understood and that several aspects of the virus, including the identity of the mediators of the virus entry into these cells, remain unknown. Since HSV-1 infection of TM cells is a risk factor for glaucoma and uveitis, understanding HSV-1 entry and major entry mediators in TM cells becomes important for designing novel strategies to prevent blindness. Therefore, using primary cultures of human TM cells as a model, the present study was undertaken to determine the susceptibility and the mediator(s) of productive HSV-1 entry into TM cells.HSV entry into cells is a complex process that is initiated by specific interaction of viral envelope glycoproteins and host cell surface receptors (31). The virus uses glycoproteins B and C (gB and gC, respectively) to mediate the initial attachment to cell surface heparan sulfate proteoglycans (12,27). Binding of herpesviruses to heparan sulfate proteoglycans likely precedes a conformational change that brings viral glycoprotein D (gD) to the binding domain of host cell surface gD receptors (7,8,15). Thereafter, a concerted action involving gD, its receptor, three additional HSV glycoproteins (gB, gH, and gL), and possibly an additional gH coreceptor triggers fusion of the viral envelope with the plasma membrane of host cells (22,23,26). To date, three classes of HSV entry receptors have been identified (30, 31). They include herpesvirus entry mediator (HVEM) (20), a member of the tumor necrosis factor receptor family (17); nectin-1 and nectin-2 (3, 5, 10), two members of the immunoglobulin superfamily; and specific sites in heparan su...

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Ascorbic acid modulates the production of fibronectin and laminin by cells from an eye tissue-trabecular meshwork

Cited by 40 publications

References 27 publications

Role for 3- O -Sulfated Heparan Sulfate as the Receptor for Herpes Simplex Virus Type 1 Entry into Primary Human Corneal Fibroblasts

Role for 3- O -Sulfated Heparan Sulfate as the Receptor for Herpes Simplex Virus Type 1 Entry into Primary Human Corneal Fibroblasts

Administration of Ascorbic Acid and an Aldose Reductase Inhibitor (Tolrestat) in Diabetes: Effect on Urinary Albumin Excretion

A Role for Herpesvirus Entry Mediator as the Receptor for Herpes Simplex Virus 1 Entry into Primary Human Trabecular Meshwork Cells

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