Microarray Expression Profiling Identifies Early Signaling Transcripts Associated with 6-OHDA-Induced Dopaminergic Cell Death

Holtz, William A.; Turetzky, Jay M.; O’Malley, Karen L.

doi:10.1089/ars.2005.7.639

Cited by 27 publications

(22 citation statements)

References 33 publications

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“…8B). At this time, many UPR markers have been upregulated as well as showing early signs of apoptosis (13)(14)(15)25). Thus, the apparent shrinkage of neurons and nuclei (Neu N staining) after toxin treatment was consistent with our previous findings that 6-OHDAmediated cell death proceeds via UPR upregulation and downstream apoptosis.…”

Section: -Ohda Also Leads To Erp57 Juxtanuclear Clustering In Primarsupporting

confidence: 90%

“…Prolonged cell stress, however, overwhelms these processes, and apoptosis is initiated (43). Previous results from this laboratory (13)(14)(15), as well as others (e.g., 36), demonstrated a link between PD-associated genetic and environmental factors with the discovery that the widely used parkinsonian mimetic, 6-hydroxydopamine (6-OHDA) induces the upregulation of genes involved in the ER stress response. Mechanistically, 6-OHDA-induced reactive oxygen species (ROS) lead to the rapid formation of oxidized, carbonylated proteins that precede UPR upregulation (14).…”

Section: Introduction Nmentioning

confidence: 89%

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Cell Stress Induced by the Parkinsonian Mimetic, 6-Hydroxydopamine, is Concurrent with Oxidation of the Chaperone, ERp57, and Aggresome Formation

Kim-Han

O’Malley

2007

Antioxidants & Redox Signaling

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Section: -Ohda Also Leads To Erp57 Juxtanuclear Clustering In Primarsupporting

confidence: 90%

Section: Introduction Nmentioning

confidence: 89%

Cell Stress Induced by the Parkinsonian Mimetic, 6-Hydroxydopamine, is Concurrent with Oxidation of the Chaperone, ERp57, and Aggresome Formation

Kim-Han

O’Malley

2007

Antioxidants & Redox Signaling

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“…In in vitro models of PD (6-OHDA treated neuroblastoma cells) or in in vivo models of PD (MPTP mouse or rabbit, 6-OHDA rat) there is a markedly increased expression of CHOP/Gadd153 and/or Bip/ Grp78 (Ghribi et al 2003;Silva et al 2005;Yamamuro et al 2006). Moreover, stress-induced transcription factors such as ATF3, ATF4, and/ or CHOP were up-regulated in 6-OHDA treated cells (Chen et al 2004;Holtz et al 2005). Therefore, the reticular pathway is highly relevant for PD pathology.…”

Section: Er Responsementioning

confidence: 98%

Programmed Cell Death in Parkinson's Disease

Venderová

Park²

2012

Cold Spring Harbor Perspectives in Medicine

210

133

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Parkinson's disease is a debilitating disorder characterized by a progressive loss of dopaminergic neurons caused by programmed cell death. The aim of this review is to provide an upto-date summary of the major programmed cell death pathways as they relate to PD. For a long time, programmed cell death has been synonymous with apoptosis but there now is evidence that other types of programmed cell death exist, such as autophagic cell death or programmed necrosis, and that these types of cell death are relevant to PD. The pathways and signals covered here include namely the death receptors, BCL-2 family, caspases, calpains, cdk5, p53, PARP-1, autophagy, mitophagy, mitochondrial fragmentation, and parthanatos. The review will present evidence from postmortem PD studies, toxin-induced models (especially MPTP/MPPþ, 6-hydroxydopamine and rotenone), and from a-synuclein, LRRK2, Parkin, DJ-1, and PINK1 genetic models of PD, both in vitro and in vivo.

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“…Treatment with 6-hydroxydopamine (6-OHDA), a drug that induces a Parkinson's-like disease (PD), increases expression of several UPR genes, including ATF4, suggesting a potential role for ER stress in PD (Holtz et al 2005). One of contributing factors for PD development is loss of the E3 ubiquitin ligase Parkin in dopaminergic neurons.…”

Section: Atf4mentioning

confidence: 99%

Physiological/pathological ramifications of transcription factors in the unfolded protein response

2017

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Numerous environmental, physiological, and pathological insults disrupt protein-folding homeostasis in the endoplasmic reticulum (ER), referred to as ER stress. Eukaryotic cells evolved a set of intracellular signaling pathways, collectively termed the unfolded protein response (UPR), to maintain a productive ER protein-folding environment through reprogramming gene transcription and mRNA translation. The UPR is largely dependent on transcription factors (TFs) that modulate expression of genes involved in many physiological and pathological conditions, including development, metabolism, inflammation, neurodegenerative diseases, and cancer. Here we summarize the current knowledge about these mechanisms, their impact on physiological/pathological processes, and potential therapeutic applications.

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Microarray Expression Profiling Identifies Early Signaling Transcripts Associated with 6-OHDA-Induced Dopaminergic Cell Death

Cited by 27 publications

References 33 publications

Cell Stress Induced by the Parkinsonian Mimetic, 6-Hydroxydopamine, is Concurrent with Oxidation of the Chaperone, ERp57, and Aggresome Formation

Cell Stress Induced by the Parkinsonian Mimetic, 6-Hydroxydopamine, is Concurrent with Oxidation of the Chaperone, ERp57, and Aggresome Formation

Programmed Cell Death in Parkinson's Disease

Physiological/pathological ramifications of transcription factors in the unfolded protein response

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