PARP mediates structural alterations in diabetic cardiomyopathy

Chiu, Jane; Farhangkhoee, Hana; Xu, Bing; Chen, Shali; George, Biju; Chakrabarti, Subrata

doi:10.1016/j.yjmcc.2008.06.009

Cited by 63 publications

(61 citation statements)

References 39 publications

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“…At the same time, we detected slightly decreased PARP-1 activity at 16-week post-diabetes induction, which correlates with the undetected development of cardiomyopathy [22,23]. Increased activity of PARP-1 is usually related to the development of cardiomyopathy [24,25]. Overactivation of PARP-1 in response to ROS-induced DNA breaks leads to cell dysfunction and a necrotic-type of cell death.…”

Section: Discussionmentioning

confidence: 53%

The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats

et al. 2010

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The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration. A 150% increase in CAT activity was detected at the end of the 2nd week post-STZ administration, and CAT activity remained 80% above the control level throughout 16 weeks. While total SOD and CuZn-SOD exhibited progressively decreasing activities, those of Mn-SOD and GST were elevated. Neither DNA strand breaks (apoptosis or necrosis) nor changes in PARP-1 activity and in CTGF levels (fibrosis) were observed in the diabetic heart. The absence of cardiomyopathy is accompanied with increased activities of CAT, MnSOD and GST.

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Section: Discussionmentioning

confidence: 53%

The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats

et al. 2010

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“…The mRNA level of GPx3, an antioxidant enzyme which is known to be increased in the diabetic cardiovascular system as a response to enhanced oxidative stress, 36,37 was also significantly elevated in CRP/DM compared with Wt/Con (P<0.01), CRP/Con (P< 0.01), and Wt/DM (P<0.05, Figure 2C). Furthermore, nuclear staining of 8-OHdG, a marker of DNA damage induced by oxidative stress, 38 was significantly increased in CRP/DM compared with Wt/Con, CRP/Con, and Wt/DM (all P<0.01, Figures 2D-a -h).…”

Section: Oxidative Stressmentioning

confidence: 88%

Overexpression of Human C-Reactive Protein Exacerbates Left Ventricular Remodeling in Diabetic Cardiomyopathy

Mano

Anzai

Kaneko

et al. 2011

Circ J

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“…), respectively, 60 min before inducing AUR. This dose was selected because it has been previously demonstrated that pretreatment with a 30 mg/kg dose of 3-AB before I/R injury exerts protective effects and is well-tolerated with no side effects being observed even when this dose was used long-term in rodents [16,17]. In previous experiment, we found that bladder apoptosis and PARP activity reached a peak at 2 h during various periods of reperfusion for 30 min, 1 h, 2 h, 3 days, 1 week and 2 week [15].…”

Section: Animal Modelmentioning

confidence: 99%

PARP inhibition prevents oxidative injury of bladder induced by acute urinary retention and subsequent emptying

2011

Apoptosis

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It has been demonstrated that increases in poly(ADP-ribose) polymerase (PARP) activity causes damage to several organs under ischemia/reperfusion (I/R) conditions. The aims of this study were to investigate whether inhibition of PARP could suppress apoptosis in the bladder following acute urinary retention (AUR) and subsequent bladder emptying. Twelve-week-old male Sprague Dawley rats were divided into a control group, saline treated group, and 3-aminobenzamide (3-AB, a specific PARP inhibitor)-treated group. Sixty minutes after the administration of saline and 3-AB, the saline and 3-AB-treated groups had 60 min of over-distension and followed by 2 h of drainage. The degree of bladder apoptosis, levels of malondialdehyde (MDA), ATP and nicotinamide adenine dinucleotide (NAD+); expression of poly(ADP-ribose) (PAR), phosphorylation of protein kinase B (Akt); and levels of Bcl-2, Bax, and caspase 3 activity in the bladder were determined. Molecular and histological analyses showed that bladder apoptosis was associated with increases in the amount of PAR and decreases in ATP and NAD+ levels in the saline treated group. In addition, phosphorylated Akt and Bcl-2/Bax ratio were significantly decreased. The activity of caspase 3 was significantly increased in the saline treated group. Inhibition of PARP significantly increased the levels of ATP and NAD+, phosphorylation of Akt, and Bcl-2/Bax ratio, and significantly reduced the activation of caspase 3. As a result, apoptosis in the bladder was attenuated. These results indicate that PARP activation may be involved in apoptosis in the bladder induced by AUR and subsequent emptying via energy depletion and suppression of Akt activity.

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PARP mediates structural alterations in diabetic cardiomyopathy

Cited by 63 publications

References 39 publications

The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats

The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats

Overexpression of Human C-Reactive Protein Exacerbates Left Ventricular Remodeling in Diabetic Cardiomyopathy

PARP inhibition prevents oxidative injury of bladder induced by acute urinary retention and subsequent emptying

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