The role of platelet-activating factor in the corneal response to injury

Bazán, Haydee E. P.; Ottino, Paulo

doi:10.1016/s1350-9462(02)00011-3

Cited by 41 publications

(33 citation statements)

References 105 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Platelet activating factor (PAF) is a fundamental mediator of mammalian cell function, which is now thought to play a significant role in a variety of pathophysiological states, inducing acute allergy, inflammation, asthema, gastrointestinal ulceration and toxic shock (Braquet et al, 1987;Bazan and Ottino, 2002). Several PAF antagonists such as ginkgolides, benzofuranoid neolignan and gliotoxin have been reported (Bazan and Ottino, 2002;Shen et al, 1985;Eilertsen and Osterud, 2002;Coyle et al, 1988;Ekimoto et al, 1991) and studies of their biological activities and mechanisms have also been described.…”

Section: Introductionmentioning

confidence: 99%

“…Several PAF antagonists such as ginkgolides, benzofuranoid neolignan and gliotoxin have been reported (Bazan and Ottino, 2002;Shen et al, 1985;Eilertsen and Osterud, 2002;Coyle et al, 1988;Ekimoto et al, 1991) and studies of their biological activities and mechanisms have also been described. In the course of PAF antagonists from medicinal plants, we reported that a water extract of the DJW inhibits the platelet aggregation induced by PAF.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibitory effect of the Korean herbal medicine, Dae-Jo-Whan, on platelet-activating factor-induced platelet aggregation

Chang¹,

Kang²,

Kim³

et al. 2005

Journal of Ethnopharmacology

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of the Korean herbal medicine, Dae-Jo-Whan, on platelet-activating factor-induced platelet aggregation

Chang¹,

Kang²,

Kim³

et al. 2005

Journal of Ethnopharmacology

View full text Add to dashboard Cite

“…The outermost layers of these cells produce numerous microvilli which are in constant contact with the tear film, a key factor in maintaining a smooth outer surface and the optical characteristics of the epithelium. Moreover, the epithelium is continuously shed into the tear film, allowing for its regeneration and turnover almost every 7 days [34]. The corneal epithelium is also an important source of anti-angiogenic molecules [35,36].…”

Section: Corneal Epitheliummentioning

confidence: 99%

“…A thin acellular layer secreted by the corneal endothelium that functions to protect the stroma from infiltration of cells arriving at the cornea [34]. Descemet's membrane lies between the corneal stroma and endothelium.…”

Section: Descemet's (Posterior Limiting) Membranementioning

confidence: 99%

Emerging Roles for the CD36 Scavenger Receptor as a Potential Therapeutic Target for Corneal Neovascularization

Yang¹,

Ong²,

Chemtob³

et al. 2008

EMIDDT

View full text Add to dashboard Cite

Neovascularization (NV) of the normally avascular cornea arises from various causes including inflammation, infection, trauma, and contact lens wear. Corneal NV, whatever the cause, impairs vision and threatens the survival of corneal allografts, thus representing a serious clinical problem for which treatment is limited. Recent interest has focused on vascular endothelial growth factor (VEGF), a key angiogenic factor whose role in corneal NV is amply documented. While experimental studies underscore the efficacy of anti-VEGF targeted agents, there exists no clear consensus on the ideal treatment for this multifaceted pathology. This review discusses the therapeutic potential of CD36, a well established anti-angiogenic receptor. We present evidence that CD36 contributes significantly to the maintenance of corneal avascularity wherein its deficiency leads to age-related corneal NV. Data further reveal that activation of CD36 substantially attenuates and induces regression of inflammatory corneal NV via concerted inhibition of VEGFA, c-Jun N terminal kinase-1, and c-Jun. In parallel studies, we demonstrate that hypoxia, a fundamental stimulus of NV, markedly elevates CD36 corneal expression in a hypoxia-inducible factor-1 and reactive oxygen species dependent manner. Collectively, our findings unveil interesting avenues for future research on the involvement of CD36 in neovascular eye disease and suggest CD36 agonists as potential therapeutic agents for the management of corneal NV, possibly in combination with anti-VEGF therapies.

show abstract

“…[1][2][3][4] Transient amplifying cells undergo additional cell division before undergoing cell differentiation to produce mature cells. [5][6][7][8][9] Identifying the mechanisms that regulate gene expression during the transition from stem cells to transient amplifying cells to terminally differentiated cells is an area of active investigation. Several genes are known to be regulated during this transition.…”

mentioning

confidence: 99%

An Involucrin Promoter AP1 Transcription Factor Binding Site Is Required for Expression of Involucrin in the Corneal Epithelium In Vivo

Adhikary¹,

Crish²,

Bone³

et al. 2005

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

PURPOSE. Cell division of corneal limbal stem cells gives rise to transient amplifying cells that ultimately differentiate to form the multilayered corneal epithelium. The mechanisms that regulate changes in gene expression during this process are not well understood. In the present study, the involucrin gene was used as a model to study this regulation. METHODS. Regulation of human involucrin gene expression and promoter activity was assessed using in vivo transgenic mouse models and cultured primary human corneal epithelial cells. RESULTS. Human involucrin (hINV) is a structural protein that is selectively expressed in differentiating corneal epithelial cells. The results reveal that an activator protein one (AP1) DNAbinding site is essential for appropriate basal and stimulusdependent hINV promoter activity. Mutation of this site, AP1-5, results in a loss of hINV gene expression in the corneal epithelium in vivo and in cultured corneal epithelial cells. A gel mobility supershift analysis revealed interaction of the AP1 factors, Fra-1 and JunB, with this element. Inhibition of AP1 function with a dominant-negative form of AP1 also inhibited expression. Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. CONCLUSIONS. These findings point to an essential role for AP1 transcription factors, acting through a distal regulatory region AP1-5 element, in the regulation of involucrin gene expression during corneal epithelial cell differentiation. (Invest Ophthalmol Vis Sci.

show abstract

The role of platelet-activating factor in the corneal response to injury

Cited by 41 publications

References 105 publications

Inhibitory effect of the Korean herbal medicine, Dae-Jo-Whan, on platelet-activating factor-induced platelet aggregation

Inhibitory effect of the Korean herbal medicine, Dae-Jo-Whan, on platelet-activating factor-induced platelet aggregation

Emerging Roles for the CD36 Scavenger Receptor as a Potential Therapeutic Target for Corneal Neovascularization

An Involucrin Promoter AP1 Transcription Factor Binding Site Is Required for Expression of Involucrin in the Corneal Epithelium In Vivo

Contact Info

Product

Resources

About