Myocilin is associated with mitochondria in human trabecular meshwork cells

Wentz‐Hunter, Kelly; Ueda, Jun; Shimizu, Nibuyoshi; Yue, Beatrice Y.J.T.

doi:10.1002/jcp.10032

Cited by 45 publications

(33 citation statements)

References 46 publications

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“…70,71 On the basis of this finding, He et al 72 reported that TM cells overexpressing Pro370Leu mutant MYOC demonstrate features of mitochondrial dysfunction and, thus, Pro370Leu mutant MYOC may increase vulnerability of TM cells to cellular insults and cause impaired function and even cell death. The investigators above showed that MYOC causes disregulation of calcium channels causing mitochondrial membrane depolarization in TM cells, TM contraction, and subsequently leading to reduced outflow and IOP elevation.…”

Section: Myoc Protein and Glaucoma Pathogenesismentioning

confidence: 99%

Current concepts on primary open-angle glaucoma genetics: a contribution to disease pathophysiology and future treatment

Gemenetzi

Yang

Lotery

2011

Eye

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Section: Myoc Protein and Glaucoma Pathogenesismentioning

confidence: 99%

Current concepts on primary open-angle glaucoma genetics: a contribution to disease pathophysiology and future treatment

Gemenetzi

Yang

Lotery

2011

Eye

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“…31 Normal human eyes from 22-to 55-year-old donors were obtained from the Illinois Eye Bank (Chicago, IL). Human TM cells were cultured as described previously 33,34 on Falcon Primaria flasks in complete media containing Dulbecco's modified Eagle's medium, 10% FBS, 5% calf serum, and antibiotics. Dexamethasone (10 nmol/L) treatment was performed for 10 days as previously described.…”

Section: Cell Culturesmentioning

confidence: 99%

Differential Effects of Myocilin and Optineurin, Two Glaucoma Genes, on Neurite Outgrowth

Koga

Shen

Park

et al. 2010

The American Journal of Pathology

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Myocilin and optineurin are two genes linked to glaucoma , a major blinding disease characterized by progressive loss of retinal ganglion cells (RGCs) and their axons. To investigate the effects of force-expressed wild-type and mutant myocilin and optineurin on neurite outgrowth in neuronal cells , we transiently transfected cells with pEGFP-N1 (mock control) as well as myocilin and optineurin plasmids including pMYOC WT -EGFP, pMYOC P370L -EGFP, pMYOC 1-367 -EGFP, pOPTN WT -EGFP , and pOPTN E50K -EGFP. PC12 cells transfected with pEGFP-N1 produced , as anticipated, long and extensive neuritis on nerve growth factor induction. The neurite length in those cells transfected with myocilin constructs was shortened and the number of neurites was also reduced. A similar inhibitory effect on neurite outgrowth was also elicited by myocilin transfection in RGC5 cells. In contrast , neither transfection of the optineurin constructs pOPTN WT -EGFP and pOPTN E50K -EGFP nor the myocilin and optineurin small-interfering RNA treatments induced significant alterations in neurite outgrowth. Transfection with the wild-type optineurin construct , but not with that of the wild-type myocilin, increased the apoptotic activity in cells. These results demonstrated that the two glaucoma genes , myocilin and optineurin, exhibited differential effects on neurite outgrowth. They may contribute to the development of neurodegenerative glaucoma via distinct mechanisms.

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“…From the localization data acquired, some of the POAG proteins and the primary interactors were found to be co-localized. For example, MYOC (Uniprot ID:Q99972) and HRAS (UniProt ID:P01112) are co-localised in mitochondria [13,14] . Studies also show that both MYOC and HRAS play a role in cell proliferation and survival [15,16] .…”

Section: Validation Of the Toolmentioning

confidence: 99%

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P.J¹,

S²,

Pj³

et al. 2015

JBPR

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A growing number of diseases seem to be associated with protein aggregation and each disease has several proteins involved in it. To obtain a better understanding of the diseases, the proteins involved in them and their primary interaction partners were collected and clustered. A tool is developed to aid in clustering these proteins and all their primary interactors. The tool is used to cluster proteins involved in Primary Open Angle Glaucoma and their primary interactors. A cluster was selected for analysis based on the availability of experimental analysis in literature. The localization of the proteins in the chosen cluster was collected. On analyzing, four of the proteins in the cluster was found to be associated with heparin binding. Primary open angle glaucoma is known to be associated with loss of retinal vasculature. The tool has helped in finding a cluster of protein interactions with more experimental data. Also it has helped in finding out the 4 proteins associated with the disease that are involved in heparin binding from 10500 proteins. This would not have been possible to do manually. Further studying the role of these four proteins based on heparin binding and loss of vasculature in primary open angle glaucoma would give a better understanding of the disease and the molecular mechanism involved in it.

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Myocilin is associated with mitochondria in human trabecular meshwork cells

Cited by 45 publications

References 46 publications

Current concepts on primary open-angle glaucoma genetics: a contribution to disease pathophysiology and future treatment

Current concepts on primary open-angle glaucoma genetics: a contribution to disease pathophysiology and future treatment

Differential Effects of Myocilin and Optineurin, Two Glaucoma Genes, on Neurite Outgrowth

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