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1.

001-es BibID:BIBFORM051960
Első szerző:Bolisetty, Subhashini
Cím:Mitochondria-targeted heme oxygenase-1 decreases oxidative stress in renal epithelial cells / Subhashini Bolisetty, Amie Traylor, Abolfazl Zarjou, Michelle S. Johnson, Gloria A. Benavides, Karina Ricart, Ravindra Boddu, Ray D. Moore, Aimee Landar, Stephen Barnes, Victor Darley-Usmar, Anupam Agarwal
Dátum:2013
ISSN:1931-857X 1522-1466
Megjegyzések:Mitochondria are both a source and target of the actions of reactive oxygen species and possess a complex system of inter-related antioxidants that control redox signaling and protect against oxidative stress. Interestingly, the antioxidant enzyme heme oxygenase-1 (HO-1) is not present in the mitochondria despite the fact that the organelle is the site of heme synthesis and contains multiple heme proteins. Detoxification of heme is an important protective mechanism since the reaction of heme with hydrogen peroxide generates pro-oxidant ferryl species capable of propagating oxidative stress and ultimately cell death. We therefore hypothesized that a mitochondrially localized HO-1 would be cytoprotective. To test this, we generated a mitochondria-targeted HO-1 cell line by transfecting HEK293 cells with a plasmid construct containing the manganese superoxide dismutase mitochondria leader sequence fused to HO-1 cDNA (Mito-HO-1). Nontargeted HO-1-overexpressing cells were generated by transfecting HO-1 cDNA (HO-1) or empty vector (Vector). Mitochondrial localization of HO-1 with increased HO activity in the mitochondrial fraction of Mito-HO-1 cells was observed, but a significant decrease in the expression of heme-containing proteins occurred in these cells. Both cytosolic HO-1- and Mito-HO-1-expressing cells were protected against hypoxia-dependent cell death and loss of mitochondrial membrane potential, but these effects were more pronounced with Mito-HO-1. Furthermore, decrement in production of tricarboxylic acid cycle intermediates following hypoxia was significantly mitigated in Mito-HO-1 cells. These data suggest that specific mitochondrially targeted HO-1 under acute pathological conditions may have beneficial effects, but the selective advantage of long-term expression is constrained by a negative impact on the synthesis of heme-containing mitochondrial proteins.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Renal Physiology. - 305 : 3 (2013), p. F255-F264. -
További szerzők:Traylor, Amie Zarjou, Abolfazl (1979-) (kutató orvos) Johnson, Michelle S. Benavides, Gloria A. Ricart, Karina Boddu, Ravindra Moore, Ray D. Landar, Aimee Barnes, Stephen Darley-Usmar, Victor Agarwal, Anupam
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2.

001-es BibID:BIBFORM051958
Első szerző:Pegues, Melissa A.
Cím:C-reactive protein exacerbates renal ischemia-reperfusion injury / Melissa A. Pegues, Mark A. McCrory, Abolfazl Zarjou, Alexander J. Szalai
Dátum:2013
ISSN:1931-857X 1522-1466
Megjegyzések:Renal ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI), occurring with hypotension and cardiovascular surgery and inevitably during kidney transplantation. Mortality from AKI is high due to incomplete knowledge of the pathogenesis of IRI and the lack of an effective therapy. Inflammation accompanies IRI and increases the blood level of C-reactive protein (CRP), a biomarker of worsened outcomes in AKI. To test if CRP is causal in AKI we subjected wild-type mice (WT) and human CRP transgenic mice (CRPtg) to bilateral renal IRI (both pedicles clamped for 30 min at 37°C then reperfused for 24 h). Serum human CRP level was increased approximately sixfold after IRI in CRPtg (10.62 ± 1.31 g/ml at baseline vs. 72.01 ± 9.41 g/ml at 24 h) but was not elevated by sham surgery wherein kidneys were manipulated but not clamped. Compared with WT, serum creatinine, urine albumin, and histological evidence of kidney damage were increased after IRI in CRPtg mice. RT-PCR analysis of mRNA isolated from whole kidneys of CRPtg and WT subjected to IRI revealed that in CRPtg kidneys 1) upregulation of markers of macrophage classical activation (M1 markers) was blunted, 2) downregulation of markers of macrophage alternative activation (M2 markers) was more robust, and 3) expression of the activating receptor FcγRI was increased. Our finding that CRP exacerbates IRI-induced AKI, perhaps by shifting the balance of macrophage activation and FcγR expression towards a detrimental portfolio, might make CRP a promising therapeutic target for the treatment of AKI.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Renal Physiology. - 304 : 11 (2013), p. F1358-F1365. -
További szerzők:McCrory, Mark A. Zarjou, Abolfazl (1979-) (kutató orvos) Szalai Alexander J.
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3.

001-es BibID:BIBFORM051971
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Identification of a microRNA signature in renal fibrosis: role of miR-21 / Abolfazl Zarjou, Shanzhong Yang, Edward Abraham, Anupam Agarwal, Gang Liu
Dátum:2011
ISSN:1931-857X 1522-1466
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology-Renal Physiology. - 301 : 4 (2011), p. F793-F801. -
További szerzők:Yang, Shanzhong Abraham, Edward Agarwal, Anupam Liu, Gang
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4.

001-es BibID:BIBFORM051975
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:ATP as a death factor: purinergic signaling in renal epithelial-fibroblast cross talk / Abolfazl Zarjou, Anupam Agarwal
Dátum:2010
ISSN:1931-857X 1522-1466
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology-Renal Physiology. - 300 : 1 (2010), p. F60-F61. -
További szerzők:Agarwal, Anupam
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5.

001-es BibID:BIBFORM051961
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Superoxide in AVF dysfunction : a new target for intervention / Abolfazl Zarjou, Anupam Agarwal
Dátum:2012
ISSN:1931-857X 1522-1466
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Renal Physiology. - 303 : 12 (2012), p. F1599-F1600. -
További szerzők:Agarwal, Anupam
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6.

001-es BibID:BIBFORM035236
Első szerző:Zarjou, Abolfazl (kutató orvos)
Cím:Paracrine effects of mesenchymal stem cells in cisplatin-induced renal injury require heme oxygenase-1 / Zarjou Abolfazl, Kim Junghyun, Traylor Amie M., Sanders Paul W., Balla József, Agarwal Anupam, Curtis Lisa M.
Dátum:2011
ISSN:0363-6127
Megjegyzések:Multipotent mesenchymal stem cells (MSC) have become a popular and promising therapeutic approach in many clinical conditions. MSC are beneficial in animal models of acute kidney injury (AKI), by mediating differentiation-independent paracrine properties, and have prompted ongoing clinical trials to evaluate the safety and efficacy of MSC. Heme oxygenase-1 (HO-1) is induced in response to stress including AKI and has important anti-apoptotic, anti-inflammatory, and proangiogenic properties in these settings. We therefore examined whether HO-1 plays a role in the beneficial effects of MSC in AKI. We isolated MSC from bone marrow of age-matched HO-1+/+ and HO-1-/- mice. Our studies indicate that while differentiation of MSC into osteo- and adipocytic lineages did not differ between cells isolated from HO-1+/+ and HO-1-/- mice, MSC from HO-1-/- mice had significantly lower angiogenic potential. Moreover, HO-1-/- MSC demonstrated reduced expression and secretion of several important growth and proangiogenic factors (stromal cell-derived factor-1, vascular endothelial growth factor-A, and hepatocyte growth factor) compared with MSC derived from HO-1+/+ mice. In addition, conditioned medium of HO-1+/+ MSC rescued functional and morphological changes associated with cisplatin-induced AKI, while the HO-1-/--conditioned medium was ineffectual. Our studies indicate that HO-1 plays an important role in MSC-mediated protection. The results expand understanding of the renoprotective effects of MSC and may provide novel strategies to better utilize MSC in various disease models.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology-Renal Physiology. - 300 : 1 (2011), p. F254-F262. -
További szerzők:Kim, Junghyun Traylor, Amie M. Sanders, Paul W. Balla József (1959-) (belgyógyász, nephrológus) Agarwal, Anupam Curtis, Lisa M.
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