Subretinal Fluid Levels of Signal-Transduction Proteins and Apoptosis Molecules in Macula-Off Retinal Detachment Undergoing Scleral Buckle Surgery

Carpineto, Paolo; Aharrh-Gnama, Agbéanda; Ciciarelli, Vincenzo; Borrelli, Enrico; Petti, Francesco; Aloia, Raffaella; Lamolinara, Alessia; Nicola, Marta Di; Mastropasqua, Leonardo

doi:10.1167/iovs.16-20372

Cited by 5 publications

(5 citation statements)

References 34 publications

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“…This indicates that the stress following RD could induce an increase in the concentration of p53, which appears to be protective for photoreceptors, until surgery is performed. Finally, it was demonstrated that higher subretinal ERK1/2 protein concentrations are related to better visual acuities 6 months after surgery, suggesting the functional importance of this protein [ 57 ].…”

Section: Physiopathology: “Epr Dysfunction”mentioning

confidence: 99%

“…Cell death pathways can influence the development of intraretinal fibrosis. While some authors support the protective role of apoptosis [ 57 ], others consider it is a mechanism involved in the development of PVR [ 14 , 70 , 71 ]. Apoptosis has two main signaling cascades that lead to DNA fragmentation and cell death, which are both mediated by caspase [ 72 , 73 , 74 , 75 ].…”

Section: Physiopathology: “Epr Dysfunction”mentioning

confidence: 99%

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Proliferative Vitreoretinopathy: A Reappraisal

Carpineto

Licata

Ciancaglini

2023

JCM

Self Cite

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Proliferative vitreoretinopathy (PVR) remains the main cause of failure after retinal detachment (RD) surgery. Despite the development of modern technologies and sophisticated techniques for the management of RD, the growth of fibrocellular membranes within the vitreous cavity and on both sides of the retinal surface, as well as intraretinal fibrosis, can compromise surgical outcomes. Since 1983, when the term PVR was coined by the Retina Society, a lot of knowledge has been obtained about the physiopathology and risk factors of PVR, but, despite the proposal of a lot of therapeutic challenges, surgical skills seem to be the only effective way to manage PVR complications.

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Section: Physiopathology: “Epr Dysfunction”mentioning

confidence: 99%

Section: Physiopathology: “Epr Dysfunction”mentioning

confidence: 99%

Proliferative Vitreoretinopathy: A Reappraisal

Carpineto

Licata

Ciancaglini

2023

JCM

Self Cite

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“…Carpineto et al (Carpineto et al, 2016) detected D315 cl-caspase-9, and other apoptotic signaling proteins, in subretinal fluid from patients with rhegmatogenous retinal detachment (RRD). Rhegmatogenous detachments are caused by a hole or tear in the retina, which allows fluid to accumulate in the subretinal space, requiring emergency treatment by intraocular surgery.…”

Section: Caspase-9 In Retinal Neuropathymentioning

confidence: 99%

Caspase-9: A Multimodal Therapeutic Target With Diverse Cellular Expression in Human Disease

Avrutsky

Troy

2021

Front. Pharmacol.

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Caspase-9, a cysteine-aspartic protease known for its role as an initiator of intrinsic apoptosis, regulates physiological cell death and pathological tissue degeneration. Its nonapoptotic functions, including regulation of cellular differentiation/maturation, innate immunity, mitochondrial homeostasis, and autophagy, reveal a multimodal landscape of caspase-9 functions in health and disease. Recent work has demonstrated that caspase-9 can drive neurovascular injury through nonapoptotic endothelial cell dysfunction. CASP9 polymorphisms have been linked with various cancers, neurological disorders, autoimmune pathologies and lumbar disc disease. Clinical reports suggest alterations in caspase-9 expression, activity or function may be associated with acute and chronic neurodegeneration, retinal neuropathy, slow-channel myasthenic syndrome, lumbar disc disease, cardiomyopathies, atherosclerosis and autoimmune disease. Healthy tissues maintain caspase-9 activity at low basal levels, rendering supraphysiological caspase-9 activation a tractable target for therapeutic interventions. Strategies for selective inhibition of caspase-9 include dominant negative caspase-9 mutants and pharmacological inhibitors derived from the XIAP protein, whose Bir3 domain is an endogenous highly selective caspase-9 inhibitor. However, the mechanistic implications of caspase-9 expression and activation remain indeterminate in many pathologies. By assembling clinical reports of caspase-9 genetics, signaling and cellular localization in human tissues, this review identifies gaps between experimental and clinical studies on caspase-9, and presents opportunities for further investigations to examine the consequences of caspase activity in human disease.

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“…The master process then analyzes the level of pro-death signal P in each (living) cell and updates the cell's k death according to the rule. Note that cell death could be linked to a variety of pro-death (apoptotic) signals, such as an external cue [11][12][13] or intracellular expression of a death-inducing protein [14,15]. In this example model, P represents such an intracellular signal.…”

Section: Model Imentioning

confidence: 99%

Multicellular Models Bridging Intracellular Signaling and Gene Transcription to Population Dynamics

et al. 2018

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Cell signaling and gene transcription occur at faster time scales compared to cellular death, division, and evolution. Bridging these multiscale events in a model is computationally challenging. We introduce a framework for the systematic development of multiscale cell population models. Using message passing interface (MPI) parallelism, the framework creates a population model from a single-cell biochemical network model. It launches parallel simulations on a single-cell model and treats each stand-alone parallel process as a cell object. MPI mediates cell-to-cell and cell-to-environment communications in a server-client fashion. In the framework, model-specific higher level rules link the intracellular molecular events to cellular functions, such as death, division, or phenotype change. Cell death is implemented by terminating a parallel process, while cell division is carried out by creating a new process (daughter cell) from an existing one (mother cell). We first demonstrate these capabilities by creating two simple example models. In one model, we consider a relatively simple scenario where cells can evolve independently. In the other model, we consider interdependency among the cells, where cellular communication determines their collective behavior and evolution under a temporally evolving growth condition. We then demonstrate the framework’s capability by simulating a full-scale model of bacterial quorum sensing, where the dynamics of a population of bacterial cells is dictated by the intercellular communications in a time-evolving growth environment.

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Subretinal Fluid Levels of Signal-Transduction Proteins and Apoptosis Molecules in Macula-Off Retinal Detachment Undergoing Scleral Buckle Surgery

Abstract: Signal-transduction proteins and early apoptosis proteins are associated with different clinical features and postsurgery outcomes.

Cited by 5 publications

References 34 publications

Proliferative Vitreoretinopathy: A Reappraisal

Proliferative Vitreoretinopathy: A Reappraisal

Caspase-9: A Multimodal Therapeutic Target With Diverse Cellular Expression in Human Disease

Multicellular Models Bridging Intracellular Signaling and Gene Transcription to Population Dynamics

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