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001-es BibID:	BIBFORM061589
Első szerző:	Arany István (tudományos segédmunkatárs)
Cím:	Chronic nicotine exposure exacerbates acute renal ischemic injury / Istvan Arany, Samira Grifoni, Jeb S. Clark, Eva Csongradi, Christine Maric, Luis A. Juncos
Dátum:	2011
Megjegyzések:	Chronic nicotine exposure exacerbates acute renal ischemicinjury. Am J Physiol Renal Physiol 301: F125?F133, 2011. Firstpublished April 20, 2011; doi:10.1152/ajprenal.00041.2011.?Recentepidemiological reports showed that smoking has a negative impacton renal function and elevates the renal risk not only in the renalpatient but perhaps also in the healthy population. Studies suggestedthat nicotine, a major tobacco alkaloid, links smoking to renal dysfunction.While several studies showed that smoking/chronic nicotineexposure exacerbates the progression of chronic renal diseases, itsimpact on acute kidney injury is virtually unknown. Here, we studiedthe effects of chronic nicotine exposure on acute renal ischemicinjury. We found that chronic nicotine exposure increased the extentof renal injury induced by warm ischemia-reperfusion as evidenced bymorphological changes, increase in plasma creatinine level, and kidneyinjury molecule-1 expression. We also found that chronic nicotineexposure elevated markers of oxidative stress such as nitrotyrosine aswell as malondialdehyde. Interestingly, chronic nicotine exposurealone increased oxidative stress and injury in the kidney withoutmorphological alterations. Chronic nicotine treatment not only increasedreactive oxygen species (ROS) production and injury but alsoexacerbated oxidative stress-induced ROS generation through NADPHoxidase and mitochondria in cultured renal proximal tubulecells. The resultant oxidative stress provoked injury through JNKmediatedactivation of the activator protein (AP)-1 transcription factorin vitro. This mechanism might exist in vivo as phosphorylation ofJNK and its downstream target c-jun, a component of the AP-1transcription factor, is elevated in the ischemic kidneys exposed tochronic nicotine. Our results imply that smoking may sensitize thekidney to ischemic insults and perhaps facilitates progression of acutekidney injury to chronic kidney injury.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban smoking oxidative stress JNK/AP-1 activation
Megjelenés:	American Journal Of Physiology-Renal Physiology. - 301 : 1 (2011), p. F125-F133. -
További szerzők:	Grifoni Samira (tudományos segédmunkatárs) Clark Jeb S. (tudományos segédmunkatárs) Csongrádi Éva (1969-) (szakorvos) Maric Christine (tudományos segédmunkatárs) Juncos Luis A. (orvos)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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.
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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