Enhanced expression of the complement factor H mRNA in proliferating human RPE cells

Kociok, Norbert; Joussen, Antonia M.

doi:10.1007/s00417-010-1371-4

Cited by 4 publications

(4 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Wang et al showed that a component of drusen, amyloid beta, can bind to CFI and consequently reduce its function, potentially leading to chronic low-grade inflammation ). However proliferating RPE cells, also seen in early AMD, demonstrate increased expression of CFI protein (Kociok and Joussen 2010). RPE hypertrophy may be a response to inflammation, and increased CFI levels may be induced as a compensatory response.…”

Section: Complement Factor Imentioning

confidence: 95%

“…In vitro studies show an increase in RPE CFH production by interferon-gamma (Kim et al 2009), and reduction in conditions of oxidative stress ). In addition, CFH secretion is associated with in vitro RPE migration and hypertrophy, suggesting the RPE proliferation seen in AMD may be accompanied by a compensatory increase in complement regulatory factors (Kim et al 2009;Kociok and Joussen 2010).…”

Section: Local Intraocular Cfh and Amdmentioning

confidence: 95%

See 1 more Smart Citation

Age-related macular degeneration and the complement system

et al. 2012

View full text Add to dashboard Cite

Section: Complement Factor Imentioning

confidence: 95%

Section: Local Intraocular Cfh and Amdmentioning

confidence: 95%

Age-related macular degeneration and the complement system

et al. 2012

View full text Add to dashboard Cite

“…Concurrently, this activation stimulates the age-induced response of augmented synthesis of endogenous CRMs, such as CFH [ 21 , 22 ] or CFB [ 20 ]. Moreover, Kociok and Joussen observed that human RPE cells that are stimulated to proliferate in culture conditions express CRMs, such as CFH and CFI, at the mRNA and protein levels [ 23 ]. Interestingly, in cultured human and murine RPE cells, the membrane-bound CRMs, such as CD46, CD55, and CD59, were also shown to be specifically upregulated by inflammatory cytokines, including IFN- γ , TNF- α , and IL-1 β , as well as by repetitive nonlethal exposure to oxidative stress [ 24 ].…”

Section: Biology Of Complement System In Retinamentioning

confidence: 99%

Complement System in Pathogenesis of AMD: Dual Player in Degeneration and Protection of Retinal Tissue

Kawa

Machalińska

Rogińska

et al. 2014

Journal of Immunology Research

View full text Add to dashboard Cite

Age-related macular degeneration (AMD) is the most common cause of blindness among the elderly, especially in Western countries. Although the prevalence, risk factors, and clinical course of the disease are well described, its pathogenesis is not entirely elucidated. AMD is associated with a variety of biochemical abnormalities, including complement components deposition in the retinal pigment epithelium-Bruch's membrane-choriocapillaris complex. Although the complement system (CS) is increasingly recognized as mediating important roles in retinal biology, its particular role in AMD pathogenesis has not been precisely defined. Unrestricted activation of the CS following injury may directly damage retinal tissue and recruit immune cells to the vicinity of active complement cascades, therefore detrimentally causing bystander damage to surrounding cells and tissues. On the other hand, recent evidence supports the notion that an active complement pathway is a necessity for the normal maintenance of the neurosensory retina. In this scenario, complement activation appears to have beneficial effect as it promotes cell survival and tissue remodeling by facilitating the rapid removal of dying cells and resulting cellular debris, thus demonstrating anti-inflammatory and neuroprotective activities. In this review, we discuss both the beneficial and detrimental roles of CS in degenerative retina, focusing on the diverse aspects of CS functions that may promote or inhibit macular disease.

show abstract

“…Non-coding RNA consists of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs). Recent epigenetic and genetic evidence has indicated that miRNAs, such as miR-146A, miRNA-9, miRNA-155 and miRNA-125b are upregulated to modulate a family of potentially pathogenic genes involved in Alzheimer's disease and cancer (17)(18)(19)(20). In 2011, Salmena et al (21) proposed a competing endogenous RNA (ceRNA) hypothesis, which is now supported by further evidence (22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA associated-competing endogenous RNAs are induced by clusterin in retinal pigment epithelial cells

Ye¹,

Li²,

He³

2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Age related macular degeneration is one of the most common causes of vision loss in the elderly. Long noncoding RNAs (lncRNAs) serve important roles in regulating gene expression by acting as competing endogenous RNAs (ceRNAs). However, the roles of specific lncRNAs and their associated ceRNA function induced by clusterin in cultured retinal pigment epithelial (RPE) cells remain to be fully elucidated. Based on high throughput sequencing data from RPE cells treated with or without clusterin, the present study identified differentially expressed mRNAs, lncRNAs and microRNAs (miRNAs). A lncRNA‑mRNA‑microRNA (miRNA) network (ceRNA network) was subsequently constructed based on the bioinformatic database miRanda and miRNA targets database miRTarBase. These results demonstrated the expression pattern of several lncRNAs, and a clear clusterin‑associated ceRNA network in RPE cells, which included 75 lncRNAs and 32 miRNAs in RPE cells induced by clusterin. Collectively, the present study uncovered and characterized via bioinformatics the global properties of the ceRNA network in human RPE cells in response to clusterin. These results may aid in the elucidation of the molecular mechanisms of clusterin in age‑related macular degeneration.

show abstract

Enhanced expression of the complement factor H mRNA in proliferating human RPE cells

Cited by 4 publications

References 31 publications

Age-related macular degeneration and the complement system

Age-related macular degeneration and the complement system

Complement System in Pathogenesis of AMD: Dual Player in Degeneration and Protection of Retinal Tissue

Long non-coding RNA associated-competing endogenous RNAs are induced by clusterin in retinal pigment epithelial cells

Contact Info

Product

Resources

About