2009
DOI: 10.1089/ars.2009.2445
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Mitochondria Targeted Peptides Protect Against 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Neurotoxicity

Abstract: A large body of evidence suggests that mitochondrial dysfunction and oxidative damage play a role in the pathogenesis of Parkinson's disease (PD). A number of antioxidants have been effective in animal models of PD. We have developed a family of mitochondria-targeted peptides that can protect against mitochondrial swelling and apoptosis (SS peptides). In this study, we examined the ability of two peptides, SS-31 and SS-20, to protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in … Show more

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Cited by 158 publications
(143 citation statements)
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“…In vivo, SS peptides are protective in a mouse model of ALS, increasing survival and motor performance, and decreasing cell loss [105]. SS peptides also protect dopaminergic neurons against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity both in cell cultures and in the PD animal model [106].…”
Section: Mitochondrial Antioxidantsmentioning
confidence: 99%
“…In vivo, SS peptides are protective in a mouse model of ALS, increasing survival and motor performance, and decreasing cell loss [105]. SS peptides also protect dopaminergic neurons against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity both in cell cultures and in the PD animal model [106].…”
Section: Mitochondrial Antioxidantsmentioning
confidence: 99%
“…SS-31 has been found to protect cells from mitochondrial toxicity in rodent models of human diseases, including ischemic brain injury (47), myocardial infarction (46), and ALS (237). Other animal studies have confirmed the efficacy of SS peptides aimed at PD (366), AD (187), obesity (11), and unilateral urethral obstruction (202) and those employed for cell and organ transplantation (316), although their exact mechanism of action and whether it unequivocally includes an antioxidant activity is not always clear. This antioxidant tetrapeptide has also proved to be beneficial in a mouse model of oxaliplatin-induced neuropathy (328).…”
mentioning
confidence: 94%
“…In vitro: Various cell culture models have been used to study the effects of MPP+ on cells, particularly dopaminergic-based cell lines such as human CNS progenitor cell cultures (Karunakaran et al, 2008), adult neural stem/precursor cells (NPCs) (L'Episcopo et al, 2011), cerebellar granule neurons (CGN) primary cultures (Shang et al, 2004), human SH-SY5Y (Xia et al, 2001) or SK-N-MC cells, mouse MN9D, rat pheochromocytoma PC12 cell line as well as primary rodent ventral mesencephalic neurons (Dauer et al, 2002;Kim-Han et al, 2011;Kinugawa et al, 2013;Wang et al, 2005b), dopaminergic SN4741 cell line (Mudo et al, 2012;Yang et al, 2009), SN crude homogenate (Muralikrishnan & Mohanakumar, 1998) or cortical neurons (Aleyasin et al, 2010).…”
Section: Supporting Publications 2016: En-955 61mentioning
confidence: 99%
“…One of the earliest and most studied key events observed from MPP+ on cells is mitochondrial damage (Yang et al, 2009), documented by rapid reduction in overall mitochondrial motility, slowed anterograde and increased retrograde transport and decreased mitochondrial trafficking accompanied by bioenergetic declines (Kim-Han et al, 2011), oxidative stress and dopaminergic cell loss. MPTP/MPP+ activates the JNK/c-Jun pathway in vivo and in vitro Xia et al, 2001).…”
Section: Supporting Publications 2016: En-955 62mentioning
confidence: 99%