Parathyroid hormone-related peptide protects cardiomyocytes from oxidative stress-induced cell death: First evidence of a novel endocrine–cardiovascular interaction

Datta, Nabanita S.; Chukkapalli, Sahiti; Vengalil, Nathan; Zhan, Enbo; Przyklenk, Karin; Lasley, Robert D.

doi:10.1016/j.bbrc.2015.10.130

Cited by 8 publications

(6 citation statements)

References 49 publications

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“…In a study conducted on mice, it was found that downregulation of MKP1 provided strong protection against oxidative stress, and PTHrP was cardioprotective most probably via downregulation of MKP-1 and the activation of the MAPK and PI3K/AKT signals. In that study, it was found that a PTHrP application before the mice had been exposed to oxidative damage via H 2 O 2 , reduced cardiomyocyte damage (31). In our study, the negative correlation between the PTH level and the disulfide and disulfide/thiol ratios showed that hypoparathyroidism is a state of oxidative stress.…”

Section: Discussionsupporting

confidence: 58%

Dynamic thiol/disulfide homeostasis and oxidant status in patients with hypoparathyroidism

Dağdeviren

Akkan

et al. 2019

Journal of Medical Biochemistry

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Summary Background In this study, we aimed at determining the dynamic thiol/disulfide homeostasis and oxidant balance, and investigating the relation of these parameters to the severity of the disease and the serum calcium levels. Methods 55 patients with iatrogenic hypoparathyroidism follow-ups and 40 healthy volunteers were included in the study. The blood dynamic thiol/sulfide balance, Total Antioxidant Status (TAS), Total Oxidant Status (TOS), Paraoxonase Enzyme Activity (PON) levels were measured in serum samples. Results In our study, it was found that the disulfide, disulfide/native thiol, disulfide/total thiol levels were higher in the hypoparathyroidism group. A negative correlation was found between 25-hydroxy vitamin D (25-OH vitamin D) and disulfide, disulfide/native thiol and disulfide/total thiol, and a positive correlation was found between native thiol and total thiol ratio; and the corrected calcium levels and PON levels were negatively correlated. Conclusions Consequently, a change in favour of disulfide was found in the dynamic thiol-disulfide homeostasis in the hypoparathyroidism group in our study.

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Section: Discussionsupporting

confidence: 58%

Dynamic thiol/disulfide homeostasis and oxidant status in patients with hypoparathyroidism

Dağdeviren

Akkan

et al. 2019

Journal of Medical Biochemistry

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“…17) Oxidative stress can result in the activation of MAPK cascade in cardiac ischemia/ reperfusion injury. 18) The activation of p38 and ERK during cardiac ischemia/reperfusion injury is associated with mitochondrial dysfunction. 19) The mitochondria are important and central mediators of death.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporin A Protects H9c2 Cells Against Chemical Hypoxia-Induced Injury via Inhibition of MAPK Signaling Pathway

et al. 2016

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This study aimed to investigate the effects and molecular mechanism of cyclosporin A (CsA) on cobalt chloride (CoCl2)-induced injury in H9c2 embryonic rat cardiac cells. The results showed that CsA could protect H9c2 cells against CoCl2-induced hypoxic injury. CsA effectively improved cell viability, and decreased LDH leakage, cell apoptosis, MDA concentration, and ROS generation, and increased SOD activity, GSH production, and CAT activity in a dosedependent manner. In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways. The results also suggested that CsA protected H9c2 cells against CoCl2-induced hypoxic injury, possibly by suppressing the MAPK signaling pathway. Thus, CsA is a potential therapeutic agent for cardiac hypoxic injury.

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“…108 Finally, and most recently, a direct link between exogenous administration of PTHrP, RISK signaling, and cardiomyocyte fate has been established. 109 In isolated adult murine cardiomyocytes subjected to ROS-induced stress (as discussed previously, a pivotal component of lethal ischemia-reperfusion injury), viability was significantly improved in cells pretreated with PTHrP versus untreated controls (75% vs 25%, respectively; Figure 3). The favorable effects of PTHrP treatment were accompanied by a downregulation in the expression of MKP-1 and were abrogated by pharmacologic inhibitors of MAPKs and PI3 kinase/Akt.…”

Section: Cardiovascular Effects Of Pthrp: Is Pthrp a "Conditioning MImentioning

confidence: 61%

“…Further corroboration was provided in experiments utilizing cardiomyocytes harvested from MKP-1 null mice: knockout of MKP-1 had the predicted effect of rendering cardiomyocytes resistant to ROS-induced death, with no significant benefit provided by administration of PTHrP. 109…”

Section: Cardiovascular Effects Of Pthrp: Is Pthrp a "Conditioning MImentioning

confidence: 92%