Increased Expression of Serum Amyloid A in Glaucoma and Its Effect on Intraocular Pressure

Wang, Wan-Heng; McNatt, Loretta G.; Pang, Iok‐Hou; Hellberg, Peggy E.; Fingert, John H.; McCartney, Mitchell D.; Clark, Abbot F.

doi:10.1167/iovs.07-1104

Cited by 48 publications

(38 citation statements)

References 34 publications

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“…In a mouse model of ocular hypertension that assayed gene expression before the onset of retinal cell apoptosis, serum amyloid A (SAA), too, was found to be up-regulated in retinal microglia (Walsh et al 2009). It is interesting in this context that SAA is also up-regulated in the glaucomatous trabecular meshwork (Wang et al 2008a). Microglial activation may be detrimental to ganglion cell survival.…”

Section: Differential Gene Expression In Glaucomamentioning

confidence: 99%

“…Microarray studies of gene expression have been conducted using isolated trabecular meshwork cells, organ cultures, and fresh tissue from a variety of animal models and humans (Gonzalez et al 2000;Ishibashi et al 2002;Lo et al 2003;Vittitow and Borras 2004;Zhao et al 2004;Diskin et al 2006;Liton et al 2006;Rozsa et al 2006;Fan et al 2008;Wang et al 2008a;Danias et al 2011;Liu et al 2013). The conditions assayed in these studies were primaryopen angle glaucoma, elevated pressure, and treatment of trabecular meshwork cells with steroids or TGFb.…”

Section: Differential Gene Expression In Structures Of the Anterior Eyementioning

confidence: 99%

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Differential Gene Expression in Glaucoma

Jakobs

2014

Cold Spring Harbor Perspectives in Medicine

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In glaucoma, regardless of its etiology, retinal ganglion cells degenerate and eventually die. Although age and elevated intraocular pressure (IOP) are the main risk factors, there are still many mysteries in the pathogenesis of glaucoma. The advent of genome-wide microarray expression screening together with the availability of animal models of the disease has allowed analysis of differential gene expression in all parts of the eye in glaucoma. This review will outline the findings of recent genome-wide expression studies and discuss their commonalities and differences. A common finding was the differential regulation of genes involved in inflammation and immunity, including the complement system and the cytokines transforming growth factor b (TGFb) and tumor necrosis factor a (TNFa). Other genes of interest have roles in the extracellular matrix, cell -matrix interactions and adhesion, the cell cycle, and the endothelin system.

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Section: Differential Gene Expression In Glaucomamentioning

confidence: 99%

Section: Differential Gene Expression In Structures Of the Anterior Eyementioning

confidence: 99%

Differential Gene Expression in Glaucoma

Jakobs

2014

Cold Spring Harbor Perspectives in Medicine

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“…Interestingly, TNFR1b ablation affords robust neuroprotection to RGCs in mouse model of elevated IOP. Geneprofiling studies have also indicated upregulation of serum amyloid A which is an inflammatory marker in the trabecular meshwork and retina in human glaucoma [79]. Reduction in Ab-derived neuro-inflammation through minocycline treatment which leads to microglial inhibition has protective effects in AD as well as on the RGCs in glaucoma [6,80].…”

Section: Association With Inflammatory Pathwaysmentioning

confidence: 99%

One protein, multiple pathologies: multifaceted involvement of amyloid β in neurodegenerative disorders of the brain and retina

Gupta

Chitranshi

et al. 2016

Cell. Mol. Life Sci.

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Accumulation of amyloid β (Aβ) and its aggregates in the ageing central nervous system is regarded synonymous to Alzheimer's disease (AD) pathology. Despite unquestionable advances in mechanistic and diagnostic aspects of the disease understanding, the primary cause of Aβ accumulation as well as its in vivo roles remains elusive; nonetheless, the majority of the efforts to address pathological mechanisms for therapeutic development are focused towards moderating Aβ accumulation in the brain. More recently, Aβ deposition has been identified in the eye and is linked with distinct age-related diseases including age-related macular degeneration, glaucoma as well as AD. Awareness of the Aβ accumulation in these markedly different degenerative disorders has led to an increasing body of work exploring overlapping mechanisms, a prospective biomarker role for Aβ and the potential to use retina as a model for brain related neurodegenerative disorders. Here, we present an integrated view of current understanding of the retinal Aβ deposition discussing the accumulation mechanisms, anticipated impacts and outlining ameliorative approaches that can be extrapolated to the retina for potential therapeutic benefits. Further longitudinal investigations in humans and animal models will determine retinal Aβ association as a potential pathognomonic, diagnostic or prognostic biomarker.

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“…Like other neurodegenerative disorders, deposition of unfolded or misfolded proteins aggregates has been found in RGC of glaucoma patients Janciauskiene and Krakau 2001;Vemuganti and Mandal 2002;Bhattacharya et al 2005;Gupta et al 2008;Wang et al 2008;Wostyn et al 2008;Yin et al 2008). Deposition of cochlin, which is primarily associated with deafness has also been observed in glaucomatous TM cells (Bhattacharya et al 2005).…”

Section: Glaucoma As a Neurodegenerative Disordermentioning

confidence: 99%

Molecular complexity of primary open angle glaucoma: current concepts

Ray

Mookherjee

2009

J Genet

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Glaucoma is a group of heterogeneous optic neuropathies with complex genetic basis. Among the three principle subtypes of glaucoma, primary open angle glaucoma (POAG) occurs most frequently. Till date, 25 loci have been found to be linked to POAG. However, only three underlying genes (Myocilin, Optineurin and WDR36) have been identified. In addition, at least 30 other genes have been reported to be associated with POAG. Despite strong genetic influence in POAG pathogenesis, only a small part of the disease can be explained in terms of genetic aberration. Current concepts of glaucoma pathogenesis suggest it to be a neurodegenerative disorder which is triggered by different factors including mechanical stress due to intra-ocular pressure, reduced blood flow to retina, reperfusion injury, oxidative stress, glutamate excitotoxicity, and aberrant immune response. Here we present a mechanistic overview of potential pathways and crosstalk between them operating in POAG pathogenesis.

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Increased Expression of Serum Amyloid A in Glaucoma and Its Effect on Intraocular Pressure

Abstract: These findings indicate that SAA, which is an acute-phase apolipoprotein that plays important roles in infection, inflammation, and tissue repair, may contribute to the pathogenic changes to the TM in glaucoma.

Cited by 48 publications

References 34 publications

Differential Gene Expression in Glaucoma

Differential Gene Expression in Glaucoma

One protein, multiple pathologies: multifaceted involvement of amyloid β in neurodegenerative disorders of the brain and retina

Molecular complexity of primary open angle glaucoma: current concepts

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