Assessment of PC12 cell differentiation and neurite growth: a comparison of morphological and neurochemical measures

Das, Kaberi

doi:10.1016/j.ntt.2004.02.006

Cited by 292 publications

(250 citation statements)

References 38 publications

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“…Arrows, in A, indicates that the cells were still proliferating (cells with round cell bodies) and not differentiated. Differentiated cells (B) have grown in small aggregates, and they have formed small neuronal nets at 7 th day of seeding (Pittman et al, 1993;Das et al, 2004) Pettus, et al (1994); specifically, the increased membrane permeability to macromolecules found in moderate to severe injury. Based on the previously demonstrated loading-rate dependence of cell injury, we varied loading rate over a wide range.…”

Section: Injury Protocolmentioning

confidence: 99%

The Effect of Poloxamer-188 on Neuronal Cell Recovery from Mechanical Injury

Serbest

Horwitz

Barbee

2005

Journal of Neurotrauma

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Neuronal injury resulting from mechanical deformation is poorly characterized at the cellular level. The immediate structural consequences of the mechanical loading lead to a variety of inter-and intra-cellular signaling events that interact on multiple time and length scales. Thus, it is often difficult to establish cause-and-effect relationships such that appropriate treatment strategies can be devised. In this report, we showed that treating mechanically injured neuronal cells with an agent that promotes the resealing of disrupted plasma membranes rescues them from death at 24 h post-injury. A new in vitro model was developed to allow uniform mechanical loading conditions with precisely controlled magnitude and onset rate of loading. Injury severity increased monotonically with increasing peak shear stress and was strongly dependent on the rate of loading as assessed with the MTT cell viability assay, 24 h post-injury. Mechanical injury produced an immediate disruption of membrane integrity as indicated by a rapid and transient release of LDH. For the most severe injury, cell viability decreased approximately 40% with mechanical trauma compared to sham controls. Treatment of cells with Poloxamer 188 at 15 min post-injury restored long-term viability to control values. These data establish membrane integrity as a novel therapeutic target in the treatment of neuronal injury.

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Section: Injury Protocolmentioning

confidence: 99%

The Effect of Poloxamer-188 on Neuronal Cell Recovery from Mechanical Injury

Serbest

Horwitz

Barbee

2005

Journal of Neurotrauma

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“…21,39 Growthassociated protein 43 (GAP-43) is a well-established marker of neuronal plasticity with increased expression during neuronal recovery. 40,41 Importantly, phosphorylation at Ser41 regulates GAP-43 interaction with the cytoskeleton, promoting neurite outgrowth 42 and dephosphorylation results in cytoskeleton destruction and growth cone collapse. 43,44 The transcription factor cAMP-responsive element-binding protein (CREB) has been implicated in neuronal development, synaptic plasticity and in cell survival in response to ischemia.…”

mentioning

confidence: 99%

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

et al. 2015

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A synthetic peptide (sPIF) analogous to the mammalian embryo-derived PreImplantation Factor (PIF) enables neuroprotection in rodent models of experimental autoimmune encephalomyelitis and perinatal brain injury. The protective effects have been attributed, in part, to sPIF's ability to inhibit the biogenesis of microRNA let-7, which is released from injured cells during central nervous system (CNS) damage and induces neuronal death. Here, we uncover another novel mechanism of sPIF-mediated neuroprotection. Using a clinically relevant rat newborn brain injury model, we demonstrate that sPIF, when subcutaneously administrated, is able to reduce cell death, reverse neuronal loss and restore proper cortical architecture. We show, both in vivo and in vitro, that sPIF activates cyclic AMP dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) signaling, leading to increased phosphorylation of major neuroprotective substrates GAP-43, BAD and CREB. Phosphorylated CREB in turn facilitates expression of Gap43, Bdnf and Bcl2 known to have important roles in regulating neuronal growth, survival and remodeling. As is the case in sPIF-mediated let-7 repression, we provide evidence that sPIF-mediated PKA/PKC activation is dependent on TLR4 expression. Thus, we propose that sPIF imparts neuroprotection via multiple mechanisms at multiple levels downstream of TLR4. Given the recent FDA fast-track approval of sPIF for clinical trials, its potential clinical application for treating other CNS diseases can be envisioned.

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“…In general, when at least one neurite of a cell reaches a length equal to or greater than the diameter of the cell body, the cell is classified as differentiated. 19 After division of inclusion body-containing cells, the daughter cells that received the inclusion body developed significantly longer neurites (average neurite length 109.3 ± 19.9 μm) than the daughter cells without an inclusion body (average neurite length 57.6 ± 11.0 μm) during imaging (P < 0.05 by paired 2-tailed Student t test; example Fig. 3B).…”

Section: Live-imaging Reveals That Asymmetric Inheritance Of Inclusiomentioning

confidence: 93%

“…Neurite length is often used to measure the differentiation status of PC12 cells, 19 and only 0.8 ± 0.4% of cells induced for 2 d had at least 1 neurite greater than 100 μm in length, whereas 2.6 ± 1.4% of cells exposed to the induced +2-BP condition for 2 d consisted of these differentiated cells 1-2 d after plating. Live imaging was used to determine if the presence of an inclusion body influenced cell differentiation.…”

Section: Live-imaging Reveals That Asymmetric Inheritance Of Inclusiomentioning

confidence: 99%

The aggregation and inheritance of damaged proteins determines cell fate during mitosis

Bufalino

Kooy

2014

Cell Cycle

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Assessment of PC12 cell differentiation and neurite growth: a comparison of morphological and neurochemical measures

Cited by 292 publications

References 38 publications

The Effect of Poloxamer-188 on Neuronal Cell Recovery from Mechanical Injury

The Effect of Poloxamer-188 on Neuronal Cell Recovery from Mechanical Injury

PreImplantation Factor bolsters neuroprotection via modulating Protein Kinase A and Protein Kinase C signaling

The aggregation and inheritance of damaged proteins determines cell fate during mitosis

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