Microarray Analysis of the Failure of Filtering Blebs in a Rat Model of Glaucoma Filtering Surgery

Esson, Douglas W.; Popp, Michael P.; Liu, Li; Schultz, Gregory S.; Sherwood, Mark B.

doi:10.1167/iovs.04-0375

Cited by 33 publications

(22 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The first large-scale gene expression analysis after glaucoma filtration surgery in Sprague Dawley rats has confirmed the dynamics of wound healing and an increase in various mediators of scarring (an increase in the expression levels of TGF-β, connective tissue growth factor, and matrix metalloproteinases) and also indicated that RGC-32 expression levels begin to rise on day 0, reach a peak on day 5, and are still elevated on day 12. This pattern of expression for RGC-32 resembled those of TGF-β and connective tissue growth factor, which also peaked on day 5 and were still above baseline on day 12 [14].…”

Section: Rgc−32 and Fibrosismentioning

confidence: 66%

“…Studies investigating the development of excess fibrous connective tissue and the repair process in various organs have reported a consistent pattern of RGC--32 up-regulation [14,18]. The first large-scale gene expression analysis after glaucoma filtration surgery in Sprague Dawley rats has confirmed the dynamics of wound healing and an increase in various mediators of scarring (an increase in the expression levels of TGF-β, connective tissue growth factor, and matrix metalloproteinases) and also indicated that RGC-32 expression levels begin to rise on day 0, reach a peak on day 5, and are still elevated on day 12.…”

Section: Rgc−32 and Fibrosismentioning

confidence: 85%

See 1 more Smart Citation

Role of response gene to complement 32 in diseases

Vlaicu

Cudrici

Ito

et al. 2008

Arch. Immunol. Ther. Exp.

View full text Add to dashboard Cite

The role of response gene to complement (RGC)-32 as a cell cycle regulator has been attributed to its ability to activate cdc2 kinases and to induce S-phase entry and mitosis. However, recent studies revealed novel functions for RGC-32 in diverse processes such as cellular differentiation, inflammation, and fibrosis. Besides responding to C5b-9 stimulation, RGC-32 expression is also induced by growth factors, hormones, and cytokines. Transforming growth factor beta activates RGC-32 through Smad and RhoA signaling, thus initiating smooth muscle cell differentiation. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human malignancies, hyper-immunoglobulin E syndrome, and fibrosis. RCG-32 expression is up-regulated in cutaneous T cell lymphoma and colon, ovarian, and breast cancer, but down-regulated in invasive prostate cancer, multiple myeloma, and drug-resistant glioblastoma. A better understanding of the mechanism by which RGC-32 contributes to the pathogenesis of these diseases will provide new insights into its therapeutic potential. In this review we provide an overview of this field and discuss the most recent research on RGC-32.

show abstract

Section: Rgc−32 and Fibrosismentioning

confidence: 66%

Section: Rgc−32 and Fibrosismentioning

confidence: 85%

Role of response gene to complement 32 in diseases

Vlaicu

Cudrici

Ito

et al. 2008

Arch. Immunol. Ther. Exp.

View full text Add to dashboard Cite

show abstract

“…Trabeculectomy was performed by the same surgeon, mainly the protocol followed the published method with minor modification [10]. Eyelids were retracted by 5-0 traction suture.…”

Section: Rat Model For Filtering Surgerymentioning

confidence: 99%

Bevacizumab Inhibits Angiogenesis and Inflammation in Rat Filtration Surgery Model

Cheng

Xiang

Yang

et al. 2015

Cell Biochem Biophys

View full text Add to dashboard Cite

Bevacizumab can be potentially applied in filtration surgery in glaucoma patients. However, its mechanism remains unclear. In order to explore it, here, we established rat filtration surgery model and treat rat with Bevacizumab. At different time points after surgery, filtering blebs were collected and subjected to angiogenesis and inflammation genes analysis. Our results found that Bevacizumab significantly improved the outcome of filtration surgery and reduced complications (P < 0.05). Furthermore, angiogenesis factor, VEGF, and inflammation factors, TGFβ1 and TGFβ2, were dramatically inhibited by Bevacizumab treatment according to analysis of real-time PCR and western blot. Altogether, our findings suggested that Bevacizumab's beneficial effects on filtration surgery were not limited to antiangiogenesis effect and anti-inflammation effects may be also involved.

show abstract

“…The initial elevation of IOP could be due to postoperative inflammation, whose peak occurs in the first week. 35 The subsequent IOP reduction could be caused by the maximum effect of the drug in this experimental model. We found no evidence of corneal complications (opacity and neovascularization), hypotony, or endophthalmitis, in contrast to that reported by other authors.…”

Section: Discussionmentioning

confidence: 76%